This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, C.-H. Articles by Evans, R. M. Search for Related Content PubMed PubMed Citation Articles by Lee, C.-H. Articles by Evans, R. M. Pubmed/NCBI databases Medline Plus Health Information Metabolic Disorders

Minireview: Lipid Metabolism, Metabolic Diseases, and Peroxisome Proliferator-Activated Receptors

Howard Hughes Medical Institute, Gene Expression Laboratory (C.-H.L., P.O., R.M.E.), The Salk Institute for Biological Studies, La Jolla, California 92037; and Department of Biology (P.O.), University of California, San Diego, La Jolla, California 92037

Address all correspondence and requests for reprints to: Ronald M. Evans, Ph.D., Howard Hughes Medical Institute, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037. E-mail: evans{at}salk.edu.

	Abstract

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 
Lipid and carbohydrate homeostasis in higher organisms is under the control of an integrated system that has the capacity to rapidly respond to metabolic changes. The peroxisome proliferator-activated receptors (PPARs) are nuclear fatty acid receptors that have been implicated to play an important role in obesity-related metabolic diseases such as hyperlipidemia, insulin resistance, and coronary artery disease. The three PPAR subtypes, , , and , have distinct expression patterns and evolved to sense components of different lipoproteins and regulate lipid homeostasis based on the need of a specific tissue. Recent advances in identifying selective ligands in conjunction with microarray analyses and gene targeting studies have helped delineate the subtype-specific functions and the therapeutic potential of these receptors. PPAR potentiates fatty acid catabolism in the liver and is the molecular target of the lipid-lowering fibrates (e.g. fenofibrate and gemfibrozil), whereas PPAR is essential for adipocyte differentiation and mediates the activity of the insulin-sensitizing thiazolidinediones (e.g. rosiglitazone and pioglitazone). Recent evidence suggests that PPAR may be important in controlling triglyceride levels by sensing very low-density lipoprotein. Thus, uncovering the regulatory mechanisms and transcriptional targets of the PPARs will continue to provide insight into the pathogenesis of metabolic diseases and, at the same time, offer valuable information for rational drug design.

	Introduction

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 
LIPIDS ARE ESSENTIAL for energy homeostasis, reproductive and organ physiology, and numerous aspects of cellular biology. They are also linked to many pathological processes, such as obesity, diabetes, heart disease, and inflammation. To meet the different demands from a variety of tissues, the human body has evolved a sophisticated lipoprotein transport system to deliver cholesterol and fatty acids to the periphery (Fig. 1). Lipoproteins are composed of triglycerides (TG), cholesterol esters, phospholipids, and apolipoproteins, which modulate lipoprotein catabolism. In the forward transport system, TG-rich very low-density lipoprotein (VLDL) released by the liver delivers fatty acids to adipocytes for storage and to cardiac and skeletal muscle for energy consumption. Lipoprotein lipase (LPL), secreted by the adipocyte, muscle, and macrophage, plays an important role in VLDL fatty acid release, and its subsequent conversion to low-density lipoprotein (LDL). Cholesterol ester-rich LDL, on the other hand, delivers cholesterol to peripheral tissues for steroidogenesis and maintaining cell membrane integrity. Conversely, in the reverse transport system, high-density lipoprotein (HDL) transports excess cholesterol from extrahepatic cells, such as macrophages at the vessel wall, to liver, where it can be recycled or catabolized to bile acid (1). Disturbances in this system are integral components of life-threatening diseases, best exemplified by the metabolic syndrome, or syndrome X, which refers to patients who are insulin-resistant (hyperinsulinemic), dyslipidemic (elevated TG and decreased HDL-cholesterol levels), frequently hypertensive and at high risk for developing coronary artery disease (CAD) (2).

View larger version (31K): [in this window] [in a new window]   Figure 1. Circulating lipoproteins deliver both energy substrates and endogenous activators for PPARs. In humans, TG-rich VLDL particles, released by liver, deliver fatty acids to adipocytes for storage and to muscle for energy consumption. Lipoprotein lipase, a PPAR target gene in the adipocyte, promotes fatty acid release through its TG hydrolysis activity and conversion of VLDL to cholesterol-rich LDL. Activation of PPAR and PPAR induces fatty acid (FA) catabolism in metabolically active tissues such as liver and muscle, whereas PPAR is essential for lipid storage and differentiation of fat cells. Macrophages at the vessel wall also actively take up lipids such as VLDL and ox-LDL, and excess cholesterol is fluxed out through the HDL pathway. PPAR plays an important role in the balance between lipid influx and efflux, whereas PPAR is the major sensor for VLDL in the mouse macrophage. CE, Cholesterol esters.

The fact that dietary fatty acids are natural activators of this subfamily implies that lipoproteins serve as ligand carriers for PPARs, which, in turn, modulate lipid homeostasis of the body. Consistent with this, the activities of the fibrate class of lipid-lowering drugs and the thiazolidinedione (TZD) class of insulin-sensitizing drugs are believed to be mediated by PPAR and PPAR, respectively (18, 19). In addition, these PPAR agonists have all been reported to exhibit antiinflammatory activity in macrophages and endothelial cells, which is beyond the scope of this review. Here, we will discuss how these receptors coordinately modulate lipid homeostasis in metabolically active sites, including the liver, adipocytes, muscle, and macrophage, and their roles as lipid sensors in metabolic diseases.

	PPAR

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 
Liver is the key site of metabolic integration where fatty acids are mobilized and, depending on the body’s needs, either stored or used as an energy source. In the fasting state, the fuel sources of the body shift from carbohydrates and fats to mostly fats, and fatty acids that were stored during feeding are released from the adipocyte and taken up by liver. There they are either reesterified to TGs and assembled into VLDL or broken down through ß-oxidation and used to generate ketone bodies. Earlier studies have demonstrated that in the liver, PPAR directly regulates genes involved in fatty acid uptake [fatty acid binding protein (FATP)], ß-oxidation (acyl-CoA oxidase) and -oxidation (cytochrome P450). Gene targeting studies confirmed that PPAR is essential for the up-regulation of these genes caused by fasting (20, 21) or by pharmacological stimulation with synthetic ligands such as the fibrates (10, 18, 22). Although PPAR null mice have no obvious phenotype on a normal diet, these animals accumulate massive amounts of lipid in their livers when fasted or fed a high-fat diet. Fasting also results in severe hypoglycemia, hypoketonemia, and elevated plasma levels of nonesterified fatty acid, indicating a defect in fatty acid uptake and oxidation caused by dysregulation of these genes (20, 21). In line with these observations, the fibrate class of drugs including fenofibrate and gemfibrozil, which are synthetic ligands for PPAR, lower serum TGs and slightly increase HDL cholesterol levels in patients with hyperlipidemia (23), most likely due to induction of fatty acid oxidation through activation of PPAR. PPAR has also been shown to down-regulate apolipoprotein C-III, a protein which inhibits TG hydrolysis by LPL. This activity of PPAR ligands further contributes to the lipid-lowering effect.

Unlike its function in the adaptive response to fasting, the role of PPAR in cardiovascular pathogenesis appears to be detrimental. Cardiac-specific PPAR overexpression increases fatty acid oxidation and concomitantly decreases glucose transport and use, a phenotype similar to that of the diabetic heart. When these animals are made diabetic through streptozocin treatment, they develop more severe cardiomyopathy than wild-type controls, whereas PPAR null mice do not exhibit this phenotype (24, 25). Similarly, PPAR and apoE double knockout animals are protected from high cholesterol and high-fat diet-induced insulin resistance and develop less atherosclerotic lesions (26). These results strongly indicate that PPAR senses fatty acids and induces their use, and thus plays a causative role in cardiomyopathy. The net effect, however, of fibrate intervention in cardiovascular disease is likely beneficial because systemic TG reduction should result in less fat accumulation in the heart and at the vessel wall.

	PPAR

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 
Adipocytes are the main site for lipid storage and modulate the levels of lipids in the blood stream in response to hormonal signals. PPAR has high expression in this tissue and has been shown to potentiate adipocyte differentiation from fibroblasts (27). In humans with type II diabetes, pharmacologic activators of this receptor, such as TZDs, significantly improve insulin sensitivity (28); however, the mechanism of how these compounds work remains elusive. Considering the fact that muscle is the major tissue accounting for up to 80% of insulin-stimulated glucose disposal, one of the main issues yet to be resolved is how does a receptor that has high expression in fat, low expression in liver, and very low expression in muscle improve insulin sensitivity? Attempts to answer this question have proven difficult. PPAR null embryos die at gestation d 10 due to a defect in the placenta, and tetraploid rescue only proves that PPAR is essential for adipogenesis (11). Gene expression profiling by microarray suggests that the detectable changes in expression by TZDs are mostly in the adipocyte (29). These include genes involved in glucose uptake [c-Cbl-associated protein (CAP) and glucose transporter 4 (GLUT4)], lipid uptake and storage (CD36, aP2, LPL, FATP, and acyl-CoA synthetase), and energy expenditure [glycerol kinase (GyK), uncoupling protein (UCP) 2 and UCP 3; Refs. 29, 30, 31, 32, 33, 34, 35, 36, 37 ]. From these transcriptional changes, several plausible insulin-sensitizing mechanisms emerge (Fig. 2). The increase in CAP and GLUT4 may alleviate some of the hyperglycemia, however, because adipose tissue is responsible for only a very small percentage (<5%) of total glucose disposal; this alone cannot explain the profound drug activity. On the other hand, sequestering lipids into fat stores through the induction of CD36, LPL, and aP2 should reduce the metabolic burden on liver and muscle and promote glucose use. Free fatty acids (FFA), in particular, cause insulin resistance in muscle, so lowering this metabolite is likely beneficial (38). GyK up-regulation also results in decreased FFA release by adipocytes, while at the same time increasing energy expenditure. In the fasting state, TG hydrolysis is stimulated, yielding FFAs and glycerol. These molecules normally enter the blood stream to be taken up by the liver, but GyK converts glycerol into glycerol-phosphate. The presence of glycerol-phosphate allows FFA recently hydrolyzed from TGs to be reincorporated back into TGs at an energetic cost. Similarly, UCPs allow protons to cross the mitochondrial membrane bypassing the ATPase, thus diverting potential energy into heat instead of ATP formation. Increased energy expenditure should be therapeutically beneficial in diabetic patients, especially in those with obesity. Other than genes that are directly involved in lipid and glucose homeostasis, TZDs also modulate the expression of secreted signaling molecules, or adipokines in fat. This includes down-regulation of leptin (39, 40) and TNF- (41, 42) and up-regulation of Acrp30 (43, 44, 45). TNF induces insulin resistance, whereas low levels of Acrp30 have been correlated with insulin resistance in mice, and injection of this protein improves insulin sensitivity.

View larger version (31K): [in this window] [in a new window]   Figure 2. Effects of TZDs on the three primary insulin-responsive tissues. Changes listed in red are mediated directly through the nuclear fatty acid receptor, PPAR. This receptor is most abundantly expressed in adipose tissue where the largest transcriptional effect is seen. Direct effects have also been observed in liver; however, it is unclear whether or not PPAR is activated in muscle. Alterations in adipocyte physiology as well as modulation of adipokines results in secondary effects denoted in green in other tissues. These include decreased gluconeogenesis in the liver through the down-regulation of PEPCK and increased glucose oxidation in muscle due, in part, to the down-regulation of PDK4. ACS, Acyl-CoA synthetase.

Because diabetic patients are often at high risk for cardiovascular disease, the activity of PPAR in lipid-laden macrophages has also been extensively studied. Earlier findings suggested that activation of PPAR by modified fatty acids 9-hydroxyoctadecadienoic acid (9-HODE) and 13-HODE, components of oxidized-LDL (ox-LDL), might increase lipid accumulation through the induction of the scavenger receptor CD36 (49, 50). This observation raised the question as to whether TZDs exhibit a similar activity. However, a follow-up study demonstrated that PPAR also promotes cholesterol efflux through the induction of a transcriptional cascade involving the nuclear sterol receptor LXR and its downstream target ABCA1, a membrane transporter that is important for HDL-mediated reverse cholesterol transport (51, 52, 53, 54). In this view, one would predict that in the absence of proportionately increased ox-LDL, pharmacological activation of PPAR should shift the balance from lipid loading to lipid efflux and improve the status of the atherosclerotic lesion. Indeed, a decrease in lesion formation has been observed with drug intervention in several mouse models of atherosclerosis (55, 56, 57, 58, 59). Reciprocally, macrophages lacking PPAR are defective in their efflux program and display an accelerated lesion progression (51). In aggregate, these results suggest that therapeutic intervention is beneficial in treating CAD.

	PPAR

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 
Muscle is one of the most metabolically demanding tissues and relies heavily on fatty acids as an energy source. PPAR is the most abundant receptor in the muscle among the PPARs (60). It was first implicated in fatty acid metabolism from studies using the knockout animals. Most PPAR null embryos die at an early stage due to a placental defect. The small percentage of PPAR null mice that survive exhibit a reduction in fat mass (61, 62). However, this phenotype is absent in adipocyte-specific knockout animals suggesting that PPAR may regulate systemic lipid metabolism rather than adipocyte functions (61). This idea is further strengthened by the observation that treatment with the synthetic compound GW501516 in insulin-resistant rhesus monkeys dramatically improves their serum lipid profile. The effects include a decrease in fasting TG and insulin and an increase in HDL cholesterol, while lowering the levels of small dense LDL (63). Although it is unclear which tissue is the major target for this activity, the identification of PPAR as a VLDL sensor (see below) suggests that muscle could be one of the potential candidates. In support of this, a selective PPAR ligand is capable of regulating genes important for fatty acid catabolism such as malonyl-CoA decarboxylase, CPT1, and UCP3, and increasing the fatty acid oxidation rate in muscle cells (Ref. 60 ; Wang, Y., and R. M. Evans, unpublished data). Furthermore, exercise- or starvation-induced up-regulation of these genes in muscle, but not in heart or liver, remains intact in the PPAR null mice. Thus, PPAR activity appears to be more relevant than PPAR in the adaptive response of the muscle.

As mentioned earlier, PPAR has recently been shown to mediate VLDL signaling in the macrophage (17). VLDL treatment in cultured macrophages results in lipid accumulation and up-regulation of adipose differentiation-related protein, a lipid droplet-coating protein that has been implicated in lipid storage (64). Adipose differentiation-related protein was subsequently identified as a direct PPAR target gene, and components of VLDL released by LPL serve as ligands for the receptor. Accordingly, VLDL induction of this gene is abolished in the PPAR null macrophage, whereas this regulation remains unchanged in the PPAR null cells. This intriguing result has raised the question as to how receptor activation affects atherosclerotic lesion progression, because it is becoming clear now that high TG and VLDL levels may be independent risk factors for CAD (65). With regard to foam cell formation, in vitro cholesterol-loading studies using structurally distinct synthetic PPAR activators have generated inconclusive results. In one study, PPAR activation potentiated cholesterol efflux through induction of the ABCA1 pathway, whereas the other demonstrated enhanced lipid accumulation using a different agonist (63, 66). This discrepancy is likely due to differences in the experimental system, or the fact that PPAR activates both lipid uptake and oxidation, a scenario similar to the cholesterol influx and efflux activities of PPAR. Future studies in mouse models of atherosclerosis with either drug treatment or PPAR-deficient bone marrow transplantation will help clarify the role of this receptor in CAD.

	Conclusion

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 
The use of loss-of-function mutants and high-affinity ligands for the PPARs has provided a unique opportunity to identify genes regulated by these receptors and correlate these regulatory events in the nucleus to the physiology of the animal. It is now evident that PPARs, which are activated by various lipid molecules, function in distinct target tissues and coordinately regulate different metabolic pathways. PPAR and PPAR potentiate fatty acid use in liver and muscle, respectively, whereas PPAR promotes lipid storage in adipocytes. In this dynamic system, lipids are shuttled between these tissues according to the needs of the body by lipoproteins. In this view, lipoproteins not only deliver energy substrates but also carry endogenous activators for these receptors.

Given the intimate relationship between the activity of the PPARs and lipid homeostasis, continuing the study of the regulatory mechanisms mediated by PPARs will provide valuable information for designing drugs that target these receptors in metabolic diseases. Three major challenges remain to be addressed. The first will be to define metabolic pathways regulated by these receptors and which tissues they are activated in. The apparent task will be to decipher the actual site of action for TZDs. Future experiments with tissue-specific knockout of PPAR should shed light on where the drug works and, importantly, whether loss of receptor in a specific tissue is sufficient to cause insulin resistance. PPAR is another promising candidate as a lipid and insulin modulator due to its potential role in muscle. Given the wide tissue distribution of this receptor, research focusing on its activity in other metabolically active tissues will grow exponentially, and its therapeutic value will be unmasked in the near future. The next challenge will be to identify ligands that retain their effectiveness without adverse side effects. Substantial progress has already been made in designing selective PPAR modulators and dual agonists that modulate receptor activity. For example, several reported PPAR partial agonists or PPAR/ dual agonists retain insulin-sensitizing activity without causing weight gain (67, 68, 69, 70, 71). Finally, the role of PPAR and PPAR (or/and PPAR) as lipid sensors (ox-LDL verses VLDL) in the regulation of macrophage function deserves thorough investigation. It is known that macrophages at the vessel wall actively take up lipids, and this process is essential for the formation of atherogenic foam cells. Understanding these mechanisms in conjunction with the identification of selective modulators will extend the therapeutic value of PPARs to other metabolic diseases such as CAD.

	Acknowledgments

 
We thank Jun Sonoda for valuable comments, Elaine Stevens and Lita Ong for administrative assistance, and Jamie Simon for the graphic artwork.

	Footnotes

 
This work was supported by the Howard Hughes Medical Institute (HHMI). R.M.E. is an investigator of the HHMI at The Salk Institute for Biological Studies and March of Dimes Chair in Molecular and Developmental Biology. C.-H.L. is a research fellow of the HHMI, and P.O. is supported by Cellular and Molecular Genetics training grant (Department of Biology, University of California, San Diego, CA).

C.-H.L. and P.O. contributed equally to this work.

Abbreviations: CAD, Coronary artery disease; CAP, c-Cbl-associated protein; FATP, fatty acid binding protein; FFA, free fatty acids; GLUT4, glucose transporter 4; GyK, glycerol kinase; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LPL, lipoprotein lipase; ox-LDL, oxidized-LDL; PDK4, pyruvate dehydrogenase 4; PEPCK, phosphoenolpyruvate carboxykinase; PPAR, peroxisome proliferator-activated receptors; TG, triglyceride; TZD, thiazolidinedione; UCP, uncoupling protein; VLDL, very low-density lipoprotein.

Received March 5, 2003.

Accepted for publication March 11, 2003.

	References

Top Abstract Introduction PPAR{alpha} PPAR {gamma} PPAR{delta} Conclusion References

 

1. Russell DW 1992 Cholesterol biosynthesis and metabolism. Cardiovasc Drugs Ther 6:103–110[CrossRef][Medline]
2. Reaven GM 1994 Syndrome X: 6 years later. J Intern Med Suppl 736:13–22[Medline]
3. Forman BM, Tontonoz P, Chen J, Brun RP, Spiegelman BM, Evans RM 1995 15-Deoxy- 12, 14-prostaglandin J2 is a ligand for the adipocyte determination factor PPAR . Cell 83:803–812[CrossRef][Medline]
4. Forman BM, Chen J, Evans RM 1997 Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors and . Proc Natl Acad Sci USA 94:4312–4317[Abstract/Free Full Text]
5. Kliewer SA, Lenhard JM, Willson TM, Patel I, Morris DC, Lehmann JM 1995 A prostaglandin J2 metabolite binds peroxisome proliferator-activated receptor and promotes adipocyte differentiation. Cell 83:813–819[CrossRef][Medline]
6. Kliewer SA, Sundseth SS, Jones SA, Brown PJ, Wisely GB, Koble CS, Devchand P, Wahli W, Willson TM, Lenhard JM, Lehmann JM 1997 Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors and . Proc Natl Acad Sci USA 94:4318–4323[Abstract/Free Full Text]
7. Krey G, Braissant O, L’Horset F, Kalkhoven E, Perroud M, Parker MG, Wahli W 1997 Fatty acids, eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol Endocrinol 11:779–791[Abstract/Free Full Text]
8. Chawla A, Repa JJ, Evans RM, Mangelsdorf DJ 2001 Nuclear receptors and lipid physiology: opening the X-files. Science 294:1866–1870[Abstract/Free Full Text]
9. Dreyer C, Keller H, Mahfoudi A, Laudet V, Krey G, Wahli W 1993 Positive regulation of the peroxisomal ß-oxidation pathway by fatty acids through activation of peroxisome proliferator-activated receptors (PPAR). Biol Cell 77:67–76[CrossRef][Medline]
10. Peters JM, Hennuyer N, Staels B, Fruchart JC, Fievet C, Gonzalez FJ, Auwerx J 1997 Alterations in lipoprotein metabolism in peroxisome proliferator-activated receptor -deficient mice. J Biol Chem 272:27307–27312[Abstract/Free Full Text]
11. Barak Y, Nelson MC, Ong ES, Jones YZ, Ruiz-Lozano P, Chien KR, Koder A, Evans RM 1999 PPAR is required for placental, cardiac, and adipose tissue development. Mol Cell 4:585–595[CrossRef][Medline]
12. Kubota N, Terauchi Y, Miki H, Tamemoto H, Yamauchi T, Komeda K, Satoh S, Nakano R, Ishii C, Sugiyama T, Eto K, Tsubamoto Y, Okuno A, Murakami K, Sekihara H, Hasegawa G, Naito M, Toyoshima Y, Tanaka S, Shiota K, Kitamura T, Fujita T, Ezaki O, Aizawa S, Kadowaki T 1999 PPAR mediates high-fat diet-induced adipocyte hypertrophy and insulin resistance. Mol Cell 4:597–609[CrossRef][Medline]
13. Rosen ED, Sarraf P, Troy AE, Bradwin G, Moore K, Milstone DS, Spiegelman BM, Mortensen RM 1999 PPAR is required for the differentiation of adipose tissue in vivo and in vitro. Mol Cell 4:611–617[CrossRef][Medline]
14. Michalik L, Desvergne B, Tan NS, Basu-Modak S, Escher P, Rieusset J, Peters JM, Kaya G, Gonzalez FJ, Zakany J, Metzger D, Chambon P, Duboule D, Wahli W 2001 Impaired skin wound healing in peroxisome proliferator-activated receptor (PPAR) and PPARß mutant mice. J Cell Biol 154:799–814[Abstract/Free Full Text]
15. Tan NS, Michalik L, Noy N, Yasmin R, Pacot C, Heim M, Fluhmann B, Desvergne B, Wahli W 2001 Critical roles of PPAR ß/ in keratinocyte response to inflammation. Genes Dev 15:3263–3277[Abstract/Free Full Text]
16. Di-Poi N, Tan NS, Michalik L, Wahli W, Desvergne B 2002 Antiapoptotic role of PPARß in keratinocytes via transcriptional control of the Akt1 signaling pathway. Mol Cell 10:721–733[CrossRef][Medline]
17. Chawla A, Lee CH, Barak Y, He W, Rosenfeld J, Liao D, Han J, Kang H, Evans RM 2003 PPAR is a very low-density lipoprotein sensor in macrophages. Proc Natl Acad Sci USA 100:1268–1273[Abstract/Free Full Text]
18. Lee SS, Pineau T, Drago J, Lee EJ, Owens JW, Kroetz DL, Fernandez-Salguero PM, Westphal H, Gonzalez FJ 1995 Targeted disruption of the isoform of the peroxisome proliferator-activated receptor gene in mice results in abolishment of the pleiotropic effects of peroxisome proliferators. Mol Cell Biol 15:3012–3022[Abstract]
19. Lehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson TM, Kliewer SA 1995 An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor (PPAR ). J Biol Chem 270:12953–12956[Abstract/Free Full Text]
20. Leone TC, Weinheimer CJ, Kelly DP 1999 A critical role for the peroxisome proliferator-activated receptor (PPAR) in the cellular fasting response: the PPAR-null mouse as a model of fatty acid oxidation disorders. Proc Natl Acad Sci USA 96:7473–7478[Abstract/Free Full Text]
21. Kersten S, Seydoux J, Peters JM, Gonzalez FJ, Desvergne B, Wahli W 1999 Peroxisome proliferator-activated receptor mediates the adaptive response to fasting. J Clin Invest 103:1489–1498[Medline]
22. Aoyama T, Peters JM, Iritani N, Nakajima T, Furihata K, Hashimoto T, Gonzalez FJ 1998 Altered constitutive expression of fatty acid-metabolizing enzymes in mice lacking the peroxisome proliferator-activated receptor (PPAR). J Biol Chem 273:5678–5684[Abstract/Free Full Text]
23. Watts GF, Dimmitt SB 1999 Fibrates, dyslipoproteinaemia and cardiovascular disease. Curr Opin Lipidol 10:561–574[CrossRef][Medline]
24. Finck BN, Lehman JJ, Leone TC, Welch MJ, Bennett MJ, Kovacs A, Han X, Gross RW, Kozak R, Lopaschuk GD, Kelly DP 2002 The cardiac phenotype induced by PPAR overexpression mimics that caused by diabetes mellitus. J Clin Invest 109:121–130[CrossRef][Medline]
25. Finck BN, Han X, Courtois M, Aimond F, Nerbonne JM, Kovacs A, Gross RW, Kelly DP 2003 A critical role for PPAR-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy: modulation by dietary fat content. Proc Natl Acad Sci USA 100:1226–1231[Abstract/Free Full Text]
26. Tordjman K, Bernal-Mizrachi C, Zemany L, Weng S, Feng C, Zhang F, Leone TC, Coleman T, Kelly DP, Semenkovich CF 2001 PPAR deficiency reduces insulin resistance and atherosclerosis in apoE-null mice. J Clin Invest 107:1025–1034[Medline]
27. Tontonoz P, Hu E, Spiegelman BM 1994 Stimulation of adipogenesis in fibroblasts by PPAR 2, a lipid-activated transcription factor. Cell 79:1147–1156[CrossRef][Medline]
28. Sood V, Colleran K, Burge MR 2000 Thiazolidinediones: a comparative review of approved uses. Diabetes Technol Ther 2:429–440[CrossRef][Medline]
29. Way JM, Harrington WW, Brown KK, Gottschalk WK, Sundseth SS, Mansfield TA, Ramachandran RK, Willson TM, Kliewer SA 2001 Comprehensive messenger ribonucleic acid profiling reveals that peroxisome proliferator-activated receptor gamma activation has coordinate effects on gene expression in multiple insulin-sensitive tissues. Endocrinology 142:1269–1277[Abstract/Free Full Text]
30. Tontonoz P, Hu E, Graves RA, Budavari AI, Spiegelman BM 1994 mPPAR 2: tissue-specific regulator of an adipocyte enhancer. Genes Dev 8:1224–1234[Abstract/Free Full Text]
31. Young PW, Cawthorne MA, Coyle PJ, Holder JC, Holman GD, Kozka IJ, Kirkham DM, Lister CA, Smith SA 1995 Repeat treatment of obese mice with BRL 49653, a new potent insulin sensitizer, enhances insulin action in white adipocytes. Association with increased insulin binding and cell-surface GLUT4 as measured by photoaffinity labeling. Diabetes 44:1087–1092[Abstract]
32. Sfeir Z, Ibrahimi A, Amri E, Grimaldi P, Abumrad N 1997 Regulation of FAT/CD36 gene expression: further evidence in support of a role of the protein in fatty acid binding/transport. Prostaglandins Leukot Essent Fatty Acids 57:17–21[CrossRef][Medline]
33. Schoonjans K, Peinado-Onsurbe J, Lefebvre AM, Heyman RA, Briggs M, Deeb S, Staels B, Auwerx J 1996 PPAR and PPAR activators direct a distinct tissue-specific transcriptional response via a PPRE in the lipoprotein lipase gene. EMBO J 15:5336–5348[Medline]
34. Ribon V, Johnson JH, Camp HS, Saltiel AR 1998 Thiazolidinediones and insulin resistance: peroxisome proliferator activated receptor activation stimulates expression of the CAP gene. Proc Natl Acad Sci USA 95:14751–14756[Abstract/Free Full Text]
35. Martin G, Schoonjans K, Lefebvre AM, Staels B, Auwerx J 1997 Coordinate regulation of the expression of the fatty acid transport protein and acyl-CoA synthetase genes by PPAR and PPAR activators. J Biol Chem 272:28210–28217[Abstract/Free Full Text]
36. Guan HP, Li Y, Jensen MV, Newgard CB, Steppan CM, Lazar MA 2002 A futile metabolic cycle activated in adipocytes by antidiabetic agents. Nat Med 8:1122–1128[CrossRef][Medline]
37. Aubert J, Champigny O, Saint-Marc P, Negrel R, Collins S, Ricquier D, Ailhaud G 1997 Up-regulation of UCP-2 gene expression by PPAR agonists in preadipose and adipose cells. Biochem Biophys Res Commun 238:606–611[CrossRef][Medline]
38. Randle PJ 1998 Regulatory interactions between lipids and carbohydrates: the glucose fatty acid cycle after 35 years. Diabetes Metab Rev 14:263–283[CrossRef][Medline]
39. De Vos P, Lefebvre AM, Miller SG, Guerre-Millo M, Wong K, Saladin R, Hamann LG, Staels B, Briggs MR, Auwerx J 1996 Thiazolidinediones repress ob gene expression in rodents via activation of peroxisome proliferator-activated receptor . J Clin Invest 98:1004–1009[Medline]
40. Kallen CB, Lazar MA 1996 Antidiabetic thiazolidinediones inhibit leptin (ob) gene expression in 3T3–L1 adipocytes. Proc Natl Acad Sci USA 93:5793–5796[Abstract/Free Full Text]
41. Miles PD, Romeo OM, Higo K, Cohen A, Rafaat K, Olefsky JM 1997 TNF--induced insulin resistance in vivo and its prevention by troglitazone. Diabetes 46:1678–1683[Abstract]
42. Peraldi P, Xu M, Spiegelman BM 1997 Thiazolidinediones block tumor necrosis factor--induced inhibition of insulin signaling. J Clin Invest 100:1863–1869[Medline]
43. Yamauchi T, Kamon J, Waki H, Terauchi Y, Kubota N, Hara K, Mori Y, Ide T, Murakami K, Tsuboyama-Kasaoka N, Ezaki O, Akanuma Y, Gavrilova O, Vinson C, Reitman ML, Kagechika H, Shudo K, Yoda M, Nakano Y, Tobe K, Nagai R, Kimura S, Tomita M, Froguel P, Kadowaki T 2001 The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Nat Med 7:941–946[CrossRef][Medline]
44. Maeda N, Takahashi M, Funahashi T, Kihara S, Nishizawa H, Kishida K, Nagaretani H, Matsuda M, Komuro R, Ouchi N, Kuriyama H, Hotta K, Nakamura T, Shimomura I, Matsuzawa Y 2001 PPAR ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein. Diabetes 50:2094–2099[Abstract/Free Full Text]
45. Berg AH, Combs TP, Du X, Brownlee M, Scherer PE 2001 The adipocyte-secreted protein Acrp30 enhances hepatic insulin action. Nat Med 7:947–953[CrossRef][Medline]
46. Burant CF, Sreenan S, Hirano K, Tai TA, Lohmiller J, Lukens J, Davidson NO, Ross S, Graves RA 1997 Troglitazone action is independent of adipose tissue. J Clin Invest 100:2900–2908[Medline]
47. Chao L, Marcus-Samuels B, Mason MM, Moitra J, Vinson C, Arioglu E, Gavrilova O, Reitman ML 2000 Adipose tissue is required for the antidiabetic, but not for the hypolipidemic, effect of thiazolidinediones. J Clin Invest 106:1221–1228[Medline]
48. Memon RA, Tecott LH, Nonogaki K, Beigneux A, Moser AH, Grunfeld C, Feingold KR 2000 Up-regulation of peroxisome proliferator-activated receptors (PPAR-) and PPAR- messenger ribonucleic acid expression in the liver in murine obesity: troglitazone induces expression of PPAR--responsive adipose tissue-specific genes in the liver of obese diabetic mice. Endocrinology 141:4021–4031[Abstract/Free Full Text]
49. Nagy L, Tontonoz P, Alvarez JG, Chen H, Evans RM 1998 Oxidized LDL regulates macrophage gene expression through ligand activation of PPAR. Cell 93:229–240[CrossRef][Medline]
50. Tontonoz P, Nagy L, Alvarez JG, Thomazy VA, Evans RM 1998 PPAR promotes monocyte/macrophage differentiation and uptake of oxidized LDL. Cell 93:241–252[CrossRef][Medline]
51. Chawla A, Boisvert WA, Lee CH, Laffitte BA, Barak Y, Joseph SB, Liao D, Nagy L, Edwards PA, Curtiss LK, Evans RM, Tontonoz P 2001 A PPAR -LXR-ABCA1 pathway in macrophages is involved in cholesterol efflux and atherogenesis. Mol Cell 7:161–171[CrossRef][Medline]
52. Repa JJ, Turley SD, Lobaccaro JA, Medina J, Li L, Lustig K, Shan B, Heyman RA, Dietschy JM, Mangelsdorf DJ 2000 Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers. Science 289:1524–1529[Abstract/Free Full Text]
53. Venkateswaran A, Laffitte BA, Joseph SB, Mak PA, Wilpitz DC, Edwards PA, Tontonoz P 2000 Control of cellular cholesterol efflux by the nuclear oxysterol receptor LXR . Proc Natl Acad Sci USA 97:12097–12102[Abstract/Free Full Text]
54. Costet P, Luo Y, Wang N, Tall AR 2000 Sterol-dependent transactivation of the ABC1 promoter by the liver X receptor/retinoid X receptor. J Biol Chem 275:28240–28245[Abstract/Free Full Text]
55. Li AC, Brown KK, Silvestre MJ, Willson TM, Palinski W, Glass CK 2000 Peroxisome proliferator-activated receptor ligands inhibit development of atherosclerosis in LDL receptor-deficient mice. J Clin Invest 106:523–531[Medline]
56. Collins AR, Meehan WP, Kintscher U, Jackson S, Wakino S, Noh G, Palinski W, Hsueh WA, Law RE 2001 Troglitazone inhibits formation of early atherosclerotic lesions in diabetic and nondiabetic low density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol 21:365–371[Abstract/Free Full Text]
57. Chen Z, Ishibashi S, Perrey S, Osuga Ji, Gotoda T, Kitamine T, Tamura Y, Okazaki H, Yahagi N, Iizuka Y, Shionoiri F, Ohashi K, Harada K, Shimano H, Nagai R, Yamada N 2001 Troglitazone inhibits atherosclerosis in apolipoprotein E-knockout mice: pleiotropic effects on CD36 expression and HDL. Arterioscler Thromb Vasc Biol 21:372–377[Abstract/Free Full Text]
58. Claudel T, Leibowitz MD, Fievet C, Tailleux A, Wagner B, Repa JJ, Torpier G, Lobaccaro JM, Paterniti JR, Mangelsdorf DJ, Heyman RA, Auwerx J 2001 Reduction of atherosclerosis in apolipoprotein E knockout mice by activation of the retinoid X receptor. Proc Natl Acad Sci USA 98:2610–2615[Abstract/Free Full Text]
59. Lee CH, Evans RM 2002 Peroxisome proliferator-activated receptor- in macrophage lipid homeostasis. Trends Endocrinol Metab 13:331–335[CrossRef][Medline]
60. Muoio DM, MacLean PS, Lang DB, Li S, Houmard JA, Way JM, Winegar DA, Corton JC, Dohm GL, Kraus WE 2002 Fatty acid homeostasis and induction of lipid regulatory genes in skeletal muscles of peroxisome proliferator-activated receptor (PPAR) knock-out mice. Evidence for compensatory regulation by PPAR . J Biol Chem 277:26089–26097[Abstract/Free Full Text]
61. Barak Y, Liao D, He W, Ong ES, Nelson MC, Olefsky JM, Boland R, Evans RM 2002 Effects of peroxisome proliferator-activated receptor on placentation, adiposity, and colorectal cancer. Proc Natl Acad Sci USA 99:303–308[Abstract/Free Full Text]
62. Peters JM, Lee SS, Li W, Ward JM, Gavrilova O, Everett C, Reitman ML, Hudson LD, Gonzalez FJ 2000 Growth, adipose, brain, and skin alterations resulting from targeted disruption of the mouse peroxisome proliferator-activated receptor ß(). Mol Cell Biol 20:5119–5128[Abstract/Free Full Text]
63. Oliver Jr WR, Shenk JL, Snaith MR, Russell CS, Plunket KD, Bodkin NL, Lewis MC, Winegar DA, Sznaidman ML, Lambert MH, Xu HE, Sternbach DD, Kliewer SA, Hansen BC, Willson TM 2001 A selective peroxisome proliferator-activated receptor agonist promotes reverse cholesterol transport. Proc Natl Acad Sci USA 98:5306–5311[Abstract/Free Full Text]
64. Londos C, Brasaemle DL, Schultz CJ, Segrest JP, Kimmel AR 1999 Perilipins, ADRP, and other proteins that associate with intracellular neutral lipid droplets in animal cells. Semin Cell Dev Biol 10:51–58[CrossRef][Medline]
65. Ginsberg HN 2002 New perspectives on atherogenesis: role of abnormal triglyceride-rich lipoprotein metabolism. Circulation 106:2137–2142[Free Full Text]
66. Vosper H, Patel L, Graham TL, Khoudoli GA, Hill A, Macphee CH, Pinto I, Smith SA, Suckling KE, Wolf CR, Palmer CN 2001 The peroxisome proliferator-activated receptor promotes lipid accumulation in human macrophages. J Biol Chem 276:44258–44265[Abstract/Free Full Text]
67. Oberfield JL, Collins JL, Holmes CP, Goreham DM, Cooper JP, Cobb JE, Lenhard JM, Hull-Ryde EA, Mohr CP, Blanchard SG, Parks DJ, Moore LB, Lehmann JM, Plunket K, Miller AB, Milburn MV, Kliewer SA, Willson TM 1999 A peroxisome proliferator-activated receptor ligand inhibits adipocyte differentiation. Proc Natl Acad Sci USA 96:6102–6106[Abstract/Free Full Text]
68. Rocchi S, Picard F, Vamecq J, Gelman L, Potier N, Zeyer D, Dubuquoy L, Bac P, Champy MF, Plunket KD, Leesnitzer LM, Blanchard SG, Desreumaux P, Moras D, Renaud JP, Auwerx J 2001 A unique PPAR ligand with potent insulin-sensitizing yet weak adipogenic activity. Mol Cell 8:737–747[CrossRef][Medline]
69. Berger JP, Petro AE, MacNaul KL, Kelly LJ, Zhang BB, Richards K, Elbrecht A, Johnson BA, Zhou G, Doebber TW, Biswas C, Parikh M, Sharma N, Tanen MR, Thompson GM, Ventre J, Adams AD, Mosley R, Surwit RS, Moller DE 2003 Distinct properties and advantages of a novel PPAR selective modulator. Mol Endocrinol 17:662–676[Abstract/Free Full Text]
70. Sauerberg P, Petterson I, Jeppesen L, Bury PS, Mogensen JP, Wassermann K, Brand CL, Sturis J, Woldike HF, Fleckner J, Andersen AS, Mortensen SB, Svensson LA, Rasmussen HB, Lehmann SV, Polivka Z, Sindelar K, Panajotova V, Ynddal L, Wulff EM 2002 Novel tricyclic--alkyloxyphenylpropionic acids: dual PPAR/ agonists with hypolipidemic and antidiabetic activity. J Med Chem 45:789–804[CrossRef][Medline]
71. Ye JM, Iglesias MA, Watson DG, Ellis B, Wood L, Jensen PB, Sorensen RV, Larsen PJ, Cooney GJ, Wassermann K, Kraegen EW 2003 PPAR/ ragaglitazar eliminates fatty liver and enhances insulin action in fat-fed rats in the absence of hepatomegaly. Am J Physiol Endocrinol Metab 284:E531–E540

This article has been cited by other articles:

				A. Taube, K. Eckardt, and J. Eckel Role of lipid-derived mediators in skeletal muscle insulin resistance Am J Physiol Endocrinol Metab, November 1, 2009; 297(5): E1004 - E1012. [Abstract] [Full Text] [PDF]

				K. R. Feingold, A. Moser, S. M. Patzek, J. K. Shigenaga, and C. Grunfeld Infection decreases fatty acid oxidation and nuclear hormone receptors in the diaphragm J. Lipid Res., October 1, 2009; 50(10): 2055 - 2063. [Abstract] [Full Text] [PDF]

				K. Kappert, O. Tsuprykov, J. Kaufmann, J. Fritzsche, I. Ott, M. Goebel, I. N. Bahr, P.-L. Hassle, R. Gust, E. Fleck, et al. Chronic Treatment With Losartan Results in Sufficient Serum Levels of the Metabolite EXP3179 for PPAR{gamma} Activation Hypertension, October 1, 2009; 54(4): 738 - 743. [Abstract] [Full Text] [PDF]

				G. P. Rossi Losartan Metabolite EXP3179: An AT1-Receptor-Independent Treatment Strategy for Patients With the Metabolic Syndrome? Hypertension, October 1, 2009; 54(4): 710 - 712. [Full Text] [PDF]

				S. Lkhagvadorj, L. Qu, W. Cai, O. P. Couture, C. R. Barb, G. J. Hausman, D. Nettleton, L. L. Anderson, J. C. M. Dekkers, and C. K. Tuggle Microarray gene expression profiles of fasting induced changes in liver and adipose tissues of pigs expressing the melanocortin-4 receptor D298N variant Physiol Genomics, June 10, 2009; 38(1): 98 - 111. [Abstract] [Full Text] [PDF]

				T. Ohta, N. Masutomi, N. Tsutsui, T. Sakairi, M. Mitchell, M. V. Milburn, J. A. Ryals, K. D. Beebe, and L. Guo Untargeted Metabolomic Profiling as an Evaluative Tool of Fenofibrate-Induced Toxicology in Fischer 344 Male Rats Toxicol Pathol, June 1, 2009; 37(4): 521 - 535. [Abstract] [Full Text] [PDF]

				D. M. Selva and G. L. Hammond Peroxisome-Proliferator Receptor {gamma} Represses Hepatic Sex Hormone-Binding Globulin Expression Endocrinology, May 1, 2009; 150(5): 2183 - 2189. [Abstract] [Full Text] [PDF]

				F. Y. Ali, P. C.J. Armstrong, A.-R. A. Dhanji, A. T. Tucker, M. J. Paul-Clark, J. A. Mitchell, and T. D. Warner Antiplatelet Actions of Statins and Fibrates Are Mediated by PPARs Arterioscler Thromb Vasc Biol, May 1, 2009; 29(5): 706 - 711. [Abstract] [Full Text] [PDF]

				L. L. Y. Chan, S. P. Sebert, M. A. Hyatt, T. Stephenson, H. Budge, M. E. Symonds, and D. S. Gardner Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2009; 296(5): R1455 - R1463. [Abstract] [Full Text] [PDF]

				A. Mencarelli, B. Renga, E. Distrutti, and S. Fiorucci Antiatherosclerotic effect of farnesoid X receptor Am J Physiol Heart Circ Physiol, February 1, 2009; 296(2): H272 - H281. [Abstract] [Full Text] [PDF]

				L. Matthews, A. Berry, M. Tersigni, F. D'Acquisto, A. Ianaro, and D. Ray Thiazolidinediones Are Partial Agonists for the Glucocorticoid Receptor Endocrinology, January 1, 2009; 150(1): 75 - 86. [Abstract] [Full Text] [PDF]

				M. T. Bility, M. K. Devlin-Durante, N. Blazanin, A. B. Glick, J. M. Ward, B. H. Kang, M. J. Kennett, F. J. Gonzalez, and J. M. Peters Ligand activation of peroxisome proliferator-activated receptor {beta}/{delta} (PPAR{beta}/{delta}) inhibits chemically induced skin tumorigenesis Carcinogenesis, December 1, 2008; 29(12): 2406 - 2414. [Abstract] [Full Text] [PDF]

				H. N. Suh, H. T. Huong, C. H. Song, J. H. Lee, and H. J. Han Linoleic acid stimulates gluconeogenesis via Ca2+/PLC, cPLA2, and PPAR pathways through GPR40 in primary cultured chicken hepatocytes Am J Physiol Cell Physiol, December 1, 2008; 295(6): C1518 - C1527. [Abstract] [Full Text] [PDF]

				M. J. Holness, G. K. Greenwood, N. D. Smith, and M. C. Sugden PPAR{alpha} activation and increased dietary lipid oppose thyroid hormone signaling and rescue impaired glucose-stimulated insulin secretion in hyperthyroidism Am J Physiol Endocrinol Metab, December 1, 2008; 295(6): E1380 - E1389. [Abstract] [Full Text] [PDF]

				M. G. Borland, J. E. Foreman, E. E. Girroir, R. Zolfaghari, A. K. Sharma, S. Amin, F. J. Gonzalez, A. C. Ross, and J. M. Peters Ligand Activation of Peroxisome Proliferator-Activated Receptor-{beta}/{delta} Inhibits Cell Proliferation in Human HaCaT Keratinocytes Mol. Pharmacol., November 1, 2008; 74(5): 1429 - 1442. [Abstract] [Full Text] [PDF]

				S. Chikahisa, K. Tominaga, T. Kawai, K. Kitaoka, K. Oishi, N. Ishida, K. Rokutan, and H. Sei Bezafibrate, a Peroxisome Proliferator-Activated Receptors Agonist, Decreases Body Temperature and Enhances Electroencephalogram Delta-Oscillation during Sleep in Mice Endocrinology, October 1, 2008; 149(10): 5262 - 5271. [Abstract] [Full Text] [PDF]

				S. Hummasti and P. Tontonoz Adopting New Orphans into the Family of Metabolic Regulators Mol. Endocrinol., August 1, 2008; 22(8): 1743 - 1753. [Abstract] [Full Text] [PDF]

				E. Capobianco, V. White, R. Higa, N. Martinez, and A. Jawerbaum Effects of natural ligands of PPAR{gamma} on lipid metabolism in placental tissues from healthy and diabetic rats Mol. Hum. Reprod., August 1, 2008; 14(8): 491 - 499. [Abstract] [Full Text] [PDF]

				J. B. Lockridge, M. L. Sailors, D. J. Durgan, O. Egbejimi, W. J. Jeong, M. S. Bray, W. C. Stanley, and M. E. Young Bioinformatic profiling of the transcriptional response of adult rat cardiomyocytes to distinct fatty acids J. Lipid Res., July 1, 2008; 49(7): 1395 - 1408. [Abstract] [Full Text] [PDF]

				H. Sun, I. M. Berquin, R. T. Owens, J. T. O'Flaherty, and I. J. Edwards Peroxisome Proliferator-Activated Receptor {gamma}-Mediated Up-regulation of Syndecan-1 by n-3 Fatty Acids Promotes Apoptosis of Human Breast Cancer Cells Cancer Res., April 15, 2008; 68(8): 2912 - 2919. [Abstract] [Full Text] [PDF]

				J. Bastin, F. Aubey, A. Rotig, A. Munnich, and F. Djouadi Activation of Peroxisome Proliferator-Activated Receptor Pathway Stimulates the Mitochondrial Respiratory Chain and Can Correct Deficiencies in Patients' Cells Lacking Its Components J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1433 - 1441. [Abstract] [Full Text] [PDF]

				G. D. Barish, A. R. Atkins, M. Downes, P. Olson, L.-W. Chong, M. Nelson, Y. Zou, H. Hwang, H. Kang, L. Curtiss, et al. PPAR{delta} regulates multiple proinflammatory pathways to suppress atherosclerosis PNAS, March 18, 2008; 105(11): 4271 - 4276. [Abstract] [Full Text] [PDF]

				S. Z. Duan, M. G. Usher, and R. M. Mortensen Peroxisome Proliferator-Activated Receptor-{gamma}-Mediated Effects in the Vasculature Circ. Res., February 15, 2008; 102(3): 283 - 294. [Abstract] [Full Text] [PDF]

				S. Papineni, S. Chintharlapalli, and S. Safe Methyl 2-Cyano-3,11-dioxo-18{beta}-olean-1,12-dien-30-oate Is a Peroxisome Proliferator-Activated Receptor-{gamma} Agonist That Induces Receptor-Independent Apoptosis in LNCaP Prostate Cancer Cells Mol. Pharmacol., February 1, 2008; 73(2): 553 - 565. [Abstract] [Full Text] [PDF]

				D. Fliegner, D. Westermann, A. Riad, C. Schubert, E. Becher, J. Fielitz, C. Tschope, and V. Regitz-Zagrosek Up-regulation of PPAR{gamma} in myocardial infarction Eur J Heart Fail, January 1, 2008; 10(1): 30 - 38. [Abstract] [Full Text] [PDF]

				M. York, M. Abdelrahim, S. Chintharlapalli, S. D. Lucero, and S. Safe 1,1-Bis(3'-Indolyl)-1-(p-Substitutedphenyl)methanes Induce Apoptosis and Inhibit Renal Cell Carcinoma Growth Clin. Cancer Res., November 15, 2007; 13(22): 6743 - 6752. [Abstract] [Full Text] [PDF]

				S. Qin, T. Liu, V. S. Kamanna, and M. L. Kashyap Pioglitazone Stimulates Apolipoprotein A-I Production Without Affecting HDL Removal in HepG2 Cells: Involvement of PPAR-{alpha} Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2428 - 2434. [Abstract] [Full Text] [PDF]

				L. A. Cogburn, T. E. Porter, M. J. Duclos, J. Simon, S. C. Burgess, J. J. Zhu, H. H. Cheng, J. B. Dodgson, and J. Burnside Functional Genomics of the Chicken A Model Organism Poult. Sci., October 1, 2007; 86(10): 2059 - 2094. [Abstract] [Full Text] [PDF]

				M. A. Gorocica-Buenfil, F. L. Fluharty, C. K. Reynolds, and S. C. Loerch Effect of dietary vitamin A concentration and roasted soybean inclusion on marbling, adipose cellularity, and fatty acid composition of beef J Anim Sci, September 1, 2007; 85(9): 2230 - 2242. [Abstract] [Full Text] [PDF]

				D. Constantin, D. Constantin-Teodosiu, R. Layfield, K. Tsintzas, A. J. Bennett, and P. L. Greenhaff PPAR{delta} agonism induces a change in fuel metabolism and activation of an atrophy programme, but does not impair mitochondrial function in rat skeletal muscle J. Physiol., August 15, 2007; 583(1): 381 - 390. [Abstract] [Full Text] [PDF]

				D. Debevec, M. Christian, D. Morganstein, A. Seth, B. Herzog, M. Parker, and R. White Receptor Interacting Protein 140 Regulates Expression of Uncoupling Protein 1 in Adipocytes through Specific Peroxisome Proliferator Activated Receptor Isoforms and Estrogen-Related Receptor {alpha} Mol. Endocrinol., July 1, 2007; 21(7): 1581 - 1592. [Abstract] [Full Text] [PDF]

				H. Hellmold, H. Zhang, U. Andersson, B. Blomgren, T. Holland, A.-L. Berg, M. Elebring, N. Sjogren, K. Bamberg, B. Dahl, et al. Tesaglitazar, a PPAR{alpha}/{gamma} Agonist, Induces Interstitial Mesenchymal Cell DNA Synthesis and Fibrosarcomas in Subcutaneous Tissues in Rats Toxicol. Sci., July 1, 2007; 98(1): 63 - 74. [Abstract] [Full Text] [PDF]

				A. Pozzi, M. R. Ibanez, A. E. Gatica, S. Yang, S. Wei, S. Mei, J. R. Falck, and J. H. Capdevila Peroxisomal Proliferator-activated Receptor-{alpha}-dependent Inhibition of Endothelial Cell Proliferation and Tumorigenesis J. Biol. Chem., June 15, 2007; 282(24): 17685 - 17695. [Abstract] [Full Text] [PDF]

				G. Kronke, A. Kadl, E. Ikonomu, S. Bluml, A. Furnkranz, I. J. Sarembock, V. N. Bochkov, M. Exner, B. R. Binder, and N. Leitinger Expression of Heme Oxygenase-1 in Human Vascular Cells Is Regulated by Peroxisome Proliferator-Activated Receptors Arterioscler Thromb Vasc Biol, June 1, 2007; 27(6): 1276 - 1282. [Abstract] [Full Text] [PDF]

				C. A. Stuart, M. E.A. Howell, and D. Yin Overexpression of GLUT5 in Diabetic Muscle Is Reversed by Pioglitazone Diabetes Care, April 1, 2007; 30(4): 925 - 931. [Abstract] [Full Text] [PDF]

				A. Rodrigue-Way, A. Demers, H. Ong, and A. Tremblay A Growth Hormone-Releasing Peptide Promotes Mitochondrial Biogenesis and a Fat Burning-Like Phenotype through Scavenger Receptor CD36 in White Adipocytes Endocrinology, March 1, 2007; 148(3): 1009 - 1018. [Abstract] [Full Text] [PDF]

				E. Dyroy, T. H. Rost, R. J. Pettersen, B. Halvorsen, O. A. Gudbrandsen, T. Ueland, Z. Muna, F. Muller, J. E. Nordrehaug, P. Aukrust, et al. Tetradecylselenoacetic Acid, a PPAR Ligand With Antioxidant, Antiinflammatory, and Hypolipidemic Properties Arterioscler Thromb Vasc Biol, March 1, 2007; 27(3): 628 - 634. [Abstract] [Full Text] [PDF]

				D. L. Sprecher, C. Massien, G. Pearce, A. N. Billin, I. Perlstein, T. M. Willson, D. G. Hassall, N. Ancellin, S. D. Patterson, D. C. Lobe, et al. Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor {delta} Agonist Arterioscler Thromb Vasc Biol, February 1, 2007; 27(2): 359 - 365. [Abstract] [Full Text] [PDF]

				S. Chintharlapalli, S. Papineni, and S. Safe 1,1-Bis(3'-Indolyl)-1-(p-substitutedphenyl)methanes Inhibit Growth, Induce Apoptosis, and Decrease the Androgen Receptor in LNCaP Prostate Cancer Cells through Peroxisome Proliferator-Activated Receptor {gamma}-Independent Pathways Mol. Pharmacol., February 1, 2007; 71(2): 558 - 569. [Abstract] [Full Text] [PDF]

				S. Qu, D. Su, J. Altomonte, A. Kamagate, J. He, G. Perdomo, T. Tse, Y. Jiang, and H. H. Dong PPAR{alpha} mediates the hypolipidemic action of fibrates by antagonizing FoxO1 Am J Physiol Endocrinol Metab, February 1, 2007; 292(2): E421 - E434. [Abstract] [Full Text] [PDF]

				X. Yang, K. A. Lamia, and R. M. Evans Nuclear Receptors, Metabolism, and the Circadian Clock Cold Spring Harb Symp Quant Biol, January 1, 2007; 72(0): 387 - 394. [Abstract] [PDF]

				T. Degenhardt, M. Matilainen, K.-H. Herzig, T. W. Dunlop, and C. Carlberg The Insulin-like Growth Factor-binding Protein 1 Gene Is a Primary Target of Peroxisome Proliferator-activated Receptors J. Biol. Chem., December 22, 2006; 281(51): 39607 - 39619. [Abstract] [Full Text] [PDF]

				L. Michalik, J. Auwerx, J. P. Berger, V. K. Chatterjee, C. K. Glass, F. J. Gonzalez, P. A. Grimaldi, T. Kadowaki, M. A. Lazar, S. O'Rahilly, et al. International Union of Pharmacology. LXI. Peroxisome Proliferator-Activated Receptors Pharmacol. Rev., December 1, 2006; 58(4): 726 - 741. [Abstract] [Full Text] [PDF]

				K. Tsintzas, K. Jewell, M. Kamran, D. Laithwaite, T. Boonsong, J. Littlewood, I. Macdonald, and A. Bennett Differential regulation of metabolic genes in skeletal muscle during starvation and refeeding in humans J. Physiol., August 15, 2006; 575(1): 291 - 303. [Abstract] [Full Text] [PDF]

				A. G. Smith and G. E. O. Muscat Orphan nuclear receptors: therapeutic opportunities in skeletal muscle Am J Physiol Cell Physiol, August 1, 2006; 291(2): C203 - C217. [Abstract] [Full Text] [PDF]

				K. L.E. Klos, C. F. Sing, E. Boerwinkle, S. C. Hamon, T. J. Rea, A. Clark, M. Fornage, and J. E. Hixson Consistent Effects of Genes Involved in Reverse Cholesterol Transport on Plasma Lipid and Apolipoprotein Levels in CARDIA Participants Arterioscler Thromb Vasc Biol, August 1, 2006; 26(8): 1828 - 1836. [Abstract] [Full Text] [PDF]

				M. I. Iruretagoyena, S. E. Sepulveda, J. P. Lezana, M. Hermoso, M. Bronfman, M. A. Gutierrez, S. H. Jacobelli, and A. M. Kalergis Inhibition of Nuclear Factor-{kappa}B Enhances the Capacity of Immature Dendritic Cells to Induce Antigen-Specific Tolerance in Experimental Autoimmune Encephalomyelitis J. Pharmacol. Exp. Ther., July 1, 2006; 318(1): 59 - 67. [Abstract] [Full Text] [PDF]

				J. H. Lee, J. L. Chan, E. Sourlas, V. Raptopoulos, and C. S. Mantzoros Recombinant Methionyl Human Leptin Therapy in Replacement Doses Improves Insulin Resistance and Metabolic Profile in Patients with Lipoatrophy and Metabolic Syndrome Induced by the Highly Active Antiretroviral Therapy J. Clin. Endocrinol. Metab., July 1, 2006; 91(7): 2605 - 2611. [Abstract] [Full Text] [PDF]

				S. Hummasti and P. Tontonoz The Peroxisome Proliferator-Activated Receptor N-Terminal Domain Controls Isotype-Selective Gene Expression and Adipogenesis Mol. Endocrinol., June 1, 2006; 20(6): 1261 - 1275. [Abstract] [Full Text] [PDF]

				L. Qiao, P. S. MacLean, H. You, J. Schaack, and J. Shao Knocking Down Liver CCAAT/Enhancer-Binding Protein {alpha} by Adenovirus-Transduced Silent Interfering Ribonucleic Acid Improves Hepatic Gluconeogenesis and Lipid Homeostasis in db/db Mice Endocrinology, June 1, 2006; 147(6): 3060 - 3069. [Abstract] [Full Text] [PDF]

				T. R. Sweeney, A. H. Moser, J. K. Shigenaga, C. Grunfeld, and K. R. Feingold Decreased nuclear hormone receptor expression in the livers of mice in late pregnancy Am J Physiol Endocrinol Metab, June 1, 2006; 290(6): E1313 - E1320. [Abstract] [Full Text] [PDF]

				Q. Wu, A. M. Ortegon, B. Tsang, H. Doege, K. R. Feingold, and A. Stahl FATP1 Is an Insulin-Sensitive Fatty Acid Transporter Involved in Diet-Induced Obesity. Mol. Cell. Biol., May 1, 2006; 26(9): 3455 - 3467. [Abstract] [Full Text] [PDF]

				J. Lopez-Soriano, C. Chiellini, M. Maffei, P. A. Grimaldi, and J. M. Argiles Roles of Skeletal Muscle and Peroxisome Proliferator-Activated Receptors in the Development and Treatment of Obesity Endocr. Rev., May 1, 2006; 27(3): 318 - 329. [Abstract] [Full Text] [PDF]

				D. M. Kendall, C. J. Rubin, P. Mohideen, J.-M. Ledeine, R. Belder, J. Gross, P. Norwood, M. O'Mahony, K. Sall, G. Sloan, et al. Improvement of Glycemic Control, Triglycerides, and HDL Cholesterol Levels With Muraglitazar, a Dual ({alpha}/{gamma}) Peroxisome Proliferator-Activated Receptor Activator, in Patients With Type 2 Diabetes Inadequately Controlled With Metformin Monotherapy: A double-blind, randomized, pioglitazone-comparative study Diabetes Care, May 1, 2006; 29(5): 1016 - 1023. [Abstract] [Full Text] [PDF]

				P. Zahradka, B. Wright, M. Fuerst, N. Yurkova, K. Molnar, and C. G. Taylor Peroxisome Proliferator-Activated Receptor {alpha} and {gamma} Ligands Differentially Affect Smooth Muscle Cell Proliferation and Migration J. Pharmacol. Exp. Ther., May 1, 2006; 317(2): 651 - 659. [Abstract] [Full Text] [PDF]

				S. Chintharlapalli, S. Papineni, and S. Safe 1,1-Bis(3'-indolyl)-1-(p-substituted phenyl)methanes inhibit colon cancer cell and tumor growth through PPAR{gamma}-dependent and PPAR{gamma}-independent pathways Mol. Cancer Ther., May 1, 2006; 5(5): 1362 - 1370. [Abstract] [Full Text] [PDF]

				C. Caldari-Torres, C. Rodriguez-Sallaberry, E. S. Greene, and L. Badinga Differential effects of n-3 and n-6 fatty acids on prostaglandin F2alpha production by bovine endometrial cells. J Dairy Sci, March 1, 2006; 89(3): 971 - 977. [Abstract] [Full Text] [PDF]

				M. Schupp, L. D. Lee, N. Frost, S. Umbreen, B. Schmidt, T. Unger, and U. Kintscher Regulation of Peroxisome Proliferator-Activated Receptor {gamma} Activity by Losartan Metabolites Hypertension, March 1, 2006; 47(3): 586 - 589. [Abstract] [Full Text] [PDF]

				C.-H. Lee, P. Olson, A. Hevener, I. Mehl, L.-W. Chong, J. M. Olefsky, F. J. Gonzalez, J. Ham, H. Kang, J. M. Peters, et al. PPAR{delta} regulates glucose metabolism and insulin sensitivity PNAS, February 28, 2006; 103(9): 3444 - 3449. [Abstract] [Full Text] [PDF]

				C.-H. Lee, K. Kang, I. R. Mehl, R. Nofsinger, W. A. Alaynick, L.-W. Chong, J. M. Rosenfeld, and R. M. Evans Peroxisome proliferator-activated receptor {delta} promotes very low-density lipoprotein-derived fatty acid catabolism in the macrophage PNAS, February 14, 2006; 103(7): 2434 - 2439. [Abstract] [Full Text] [PDF]

				A. R. Nawrocki, M. W. Rajala, E. Tomas, U. B. Pajvani, A. K. Saha, M. E. Trumbauer, Z. Pang, A. S. Chen, N. B. Ruderman, H. Chen, et al. Mice Lacking Adiponectin Show Decreased Hepatic Insulin Sensitivity and Reduced Responsiveness to Peroxisome Proliferator-activated Receptor {gamma} Agonists J. Biol. Chem., February 3, 2006; 281(5): 2654 - 2660. [Abstract] [Full Text] [PDF]

				S.-i. Oka, H. Masutani, W. Liu, H. Horita, D. Wang, S. Kizaka-Kondoh, and J. Yodoi Thioredoxin-Binding Protein-2-Like Inducible Membrane Protein Is a Novel Vitamin D3 and Peroxisome Proliferator-Activated Receptor (PPAR){gamma} Ligand Target Protein that Regulates PPAR{gamma} Signaling Endocrinology, February 1, 2006; 147(2): 733 - 743. [Abstract] [Full Text] [PDF]

				W. Kassouf, S. Chintharlapalli, M. Abdelrahim, G. Nelkin, S. Safe, and A. M. Kamat Inhibition of Bladder Tumor Growth by 1,1-Bis(3'-Indolyl)-1-(p-Substitutedphenyl)Methanes: A New Class of Peroxisome Proliferator-Activated Receptor {gamma} Agonists Cancer Res., January 1, 2006; 66(1): 412 - 418. [Abstract] [Full Text] [PDF]

				A. K. Berfield, A. Chait, J. F. Oram, R. A. Zager, A. C. Johnson, and C. K. Abrass IGF-1 induces rat glomerular mesangial cells to accumulate triglyceride Am J Physiol Renal Physiol, January 1, 2006; 290(1): F138 - F147. [Abstract] [Full Text] [PDF]

				E. A. Hanniman, G. Lambert, T. C. McCarthy, and C. J. Sinal Loss of functional farnesoid X receptor increases atherosclerotic lesions in apolipoprotein E-deficient mice J. Lipid Res., December 1, 2005; 46(12): 2595 - 2604. [Abstract] [Full Text] [PDF]

				F. Djouadi, F. Aubey, D. Schlemmer, J.P.N. Ruiter, R.J.A. Wanders, A.W. Strauss, and J. Bastin Bezafibrate increases very-long-chain acyl-CoA dehydrogenase protein and mRNA expression in deficient fibroblasts and is a potential therapy for fatty acid oxidation disorders Hum. Mol. Genet., September 15, 2005; 14(18): 2695 - 2703. [Abstract] [Full Text] [PDF]

				A. I. Shulman and D. J. Mangelsdorf Retinoid X Receptor Heterodimers in the Metabolic Syndrome N. Engl. J. Med., August 11, 2005; 353(6): 604 - 615. [Full Text] [PDF]

				E. Compe, P. Drane, C. Laurent, K. Diderich, C. Braun, J. H. J. Hoeijmakers, and J.-M. Egly Dysregulation of the Peroxisome Proliferator-Activated Receptor Target Genes by XPD Mutations Mol. Cell. Biol., July 15, 2005; 25(14): 6065 - 6076. [Abstract] [Full Text] [PDF]

				J. Kim, P. Yang, M. Suraokar, A. L. Sabichi, N. D. Llansa, G. Mendoza, V. Subbarayan, C. J. Logothetis, R. A. Newman, S. M. Lippman, et al. Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase-Derived Products Cancer Res., July 15, 2005; 65(14): 6189 - 6198. [Abstract] [Full Text] [PDF]

				F. Molnar, M. Matilainen, and C. Carlberg Structural Determinants of the Agonist-independent Association of Human Peroxisome Proliferator-activated Receptors with Coactivators J. Biol. Chem., July 15, 2005; 280(28): 26543 - 26556. [Abstract] [Full Text] [PDF]

				H. Sun, I. M. Berquin, and I. J. Edwards Omega-3 Polyunsaturated Fatty Acids Regulate Syndecan-1 Expression in Human Breast Cancer Cells Cancer Res., May 15, 2005; 65(10): 4442 - 4447. [Abstract] [Full Text] [PDF]

				J. M. Wallace, M. Schwarz, P. Coward, J. Houze, J. K. Sawyer, K. L. Kelley, A. Chai, and L. L. Rudel Effects of peroxisome proliferator-activated receptor {alpha}/{delta} agonists on HDL-cholesterol in vervet monkeys J. Lipid Res., May 1, 2005; 46(5): 1009 - 1016. [Abstract] [Full Text] [PDF]

				A. Xu, M. C. Lam, K. W. Chan, Y. Wang, J. Zhang, R. L. C. Hoo, J. Y. Xu, B. Chen, W.-S. Chow, A. W. K. Tso, et al. Angiopoietin-like protein 4 decreases blood glucose and improves glucose tolerance but induces hyperlipidemia and hepatic steatosis in mice PNAS, April 26, 2005; 102(17): 6086 - 6091. [Abstract] [Full Text] [PDF]

				M. F. Simon, D. Daviaud, J. P. Pradere, S. Gres, C. Guigne, M. Wabitsch, J. Chun, P. Valet, and J. S. Saulnier-Blache Lysophosphatidic Acid Inhibits Adipocyte Differentiation via Lysophosphatidic Acid 1 Receptor-dependent Down-regulation of Peroxisome Proliferator-activated Receptor {gamma}2 J. Biol. Chem., April 15, 2005; 280(15): 14656 - 14662. [Abstract] [Full Text] [PDF]

				D. K. Kramer, L. Al-Khalili, S. Perrini, J. Skogsberg, P. Wretenberg, K. Kannisto, H. Wallberg-Henriksson, E. Ehrenborg, J. R. Zierath, and A. Krook Direct Activation of Glucose Transport in Primary Human Myotubes After Activation of Peroxisome Proliferator-Activated Receptor {delta} Diabetes, April 1, 2005; 54(4): 1157 - 1163. [Abstract] [Full Text] [PDF]

				H.-L. Fang, S. C. Strom, H. Cai, C. N. Falany, T. A. Kocarek, and M. Runge-Morris Regulation of Human Hepatic Hydroxysteroid Sulfotransferase Gene Expression by the Peroxisome Proliferator-Activated Receptor {alpha} Transcription Factor Mol. Pharmacol., April 1, 2005; 67(4): 1257 - 1267. [Abstract] [Full Text] [PDF]

				F. Djouadi, F. Aubey, D. Schlemmer, and J. Bastin Peroxisome Proliferator Activated Receptor {delta} (PPAR{delta}) Agonist But Not PPAR{alpha} Corrects Carnitine Palmitoyl Transferase 2 Deficiency in Human Muscle Cells J. Clin. Endocrinol. Metab., March 1, 2005; 90(3): 1791 - 1797. [Abstract] [Full Text] [PDF]

				L. Julan, H. Guan, J. P. van Beek, and K. Yang Peroxisome Proliferator-Activated Receptor {delta} Suppresses 11{beta}-Hydroxysteroid Dehydrogenase Type 2 Gene Expression in Human Placental Trophoblast Cells Endocrinology, March 1, 2005; 146(3): 1482 - 1490. [Abstract] [Full Text] [PDF]

				S. Lee, D.-K. Lee, E. Choi, and J. W. Lee Identification of a Functional Vitamin D Response Element in the Murine Insig-2 Promoter and Its Potential Role in the Differentiation of 3T3-L1 Preadipocytes Mol. Endocrinol., February 1, 2005; 19(2): 399 - 408. [Abstract] [Full Text] [PDF]

				S. A. Balaguer, R. A. Pershing, C. Rodriguez-Sallaberry, W. W. Thatcher, and L. Badinga Effects of Bovine Somatotropin on Uterine Genes Related to the Prostaglandin Cascade in Lactating Dairy Cows J Dairy Sci, February 1, 2005; 88(2): 543 - 552. [Abstract] [Full Text] [PDF]

				U. Kintscher and R. E. Law PPAR{gamma}-mediated insulin sensitization: the importance of fat versus muscle Am J Physiol Endocrinol Metab, February 1, 2005; 288(2): E287 - E291. [Abstract] [Full Text] [PDF]

				A. Y.Y. Cheng and I. G. Fantus Oral antihyperglycemic therapy for type 2 diabetes mellitus Can. Med. Assoc. J., January 18, 2005; 172(2): 213 - 226. [Abstract] [Full Text] [PDF]

				H. Patel, R. Truant, R. A. Rachubinski, and J. P. Capone Activity and subcellular compartmentalization of peroxisome proliferator-activated receptor {alpha} are altered by the centrosome-associated protein CAP350 J. Cell Sci., January 1, 2005; 118(1): 175 - 186. [Abstract] [Full Text] [PDF]

				T. Hays, I. Rusyn, A. M. Burns, M. J. Kennett, J. M. Ward, F. J. Gonzalez, and J. M. Peters Role of peroxisome proliferator-activated receptor-{alpha} (PPAR{alpha}) in bezafibrate-induced hepatocarcinogenesis and cholestasis Carcinogenesis, January 1, 2005; 26(1): 219 - 227. [Abstract] [Full Text] [PDF]

				P. R. Devchand, O. Ziouzenkova, and J. Plutzky Oxidative Stress and Peroxisome Proliferator-Activated Receptors: Reversing the Curse? Circ. Res., December 10, 2004; 95(12): 1137 - 1139. [Full Text] [PDF]

				S. S. T. Lee, W.-Y. Chan, C. K. C. Lo, D. C. C. Wan, D. S. C. Tsang, and W.-T. Cheung Requirement of PPAR{alpha} in maintaining phospholipid and triacylglycerol homeostasis during energy deprivation J. Lipid Res., November 1, 2004; 45(11): 2025 - 2037. [Abstract] [Full Text] [PDF]

				V. E. Richards, B. Chau, M. R. White, and C. A. McQueen Hepatic Gene Expression and Lipid Homeostasis in C57Bl/6 Mice Exposed to Hydrazine or Acetylhydrazine Toxicol. Sci., November 1, 2004; 82(1): 318 - 332. [Abstract] [Full Text] [PDF]

				Y. Guan Peroxisome Proliferator-Activated Receptor Family and Its Relationship to Renal Complications of the Metabolic Syndrome J. Am. Soc. Nephrol., November 1, 2004; 15(11): 2801 - 2815. [Abstract] [Full Text] [PDF]

				J. M. Huss, I. P. Torra, B. Staels, V. Giguere, and D. P. Kelly Estrogen-Related Receptor {alpha} Directs Peroxisome Proliferator-Activated Receptor {alpha} Signaling in the Transcriptional Control of Energy Metabolism in Cardiac and Skeletal Muscle Mol. Cell. Biol., October 15, 2004; 24(20): 9079 - 9091. [Abstract] [Full Text] [PDF]

				B. Brunmair, A. Lest, K. Staniek, F. Gras, N. Scharf, M. Roden, H. Nohl, W. Waldhausl, and C. Furnsinn Fenofibrate Impairs Rat Mitochondrial Function by Inhibition of Respiratory Complex I J. Pharmacol. Exp. Ther., October 1, 2004; 311(1): 109 - 114. [Abstract] [Full Text] [PDF]

				J. M. Huss and D. P. Kelly Nuclear Receptor Signaling and Cardiac Energetics Circ. Res., September 17, 2004; 95(6): 568 - 578. [Abstract] [Full Text] [PDF]

				S. Chintharlapalli, R. Smith III, I. Samudio, W. Zhang, and S. Safe 1,1-Bis(3'-indolyl)-1-(p-substitutedphenyl)methanes Induce Peroxisome Proliferator-Activated Receptor {gamma}-Mediated Growth Inhibition, Transactivation, and Differentiation Markers in Colon Cancer Cells Cancer Res., September 1, 2004; 64(17): 5994 - 6001. [Abstract] [Full Text] [PDF]

				P. Yubero, E. Hondares, M. C. Carmona, M. Rossell, F. J. Gonzalez, R. Iglesias, M. Giralt, and F. Villarroya The Developmental Regulation of Peroxisome Proliferator-Activated Receptor-{gamma} Coactivator-1{alpha} Expression in the Liver Is Partially Dissociated from the Control of Gluconeogenesis and Lipid Catabolism Endocrinology, September 1, 2004; 145(9): 4268 - 4277. [Abstract] [Full Text] [PDF]

				Y. Liu, Y. Zhu, F. Rannou, T.-S. Lee, K. Formentin, L. Zeng, X. Yuan, N. Wang, S. Chien, B. M. Forman, et al. Laminar Flow Activates Peroxisome Proliferator-Activated Receptor-{gamma} in Vascular Endothelial Cells Circulation, August 31, 2004; 110(9): 1128 - 1133. [Abstract] [Full Text] [PDF]

				K. Kitajka, A. J. Sinclair, R. S. Weisinger, H. S. Weisinger, M. Mathai, A. P. Jayasooriya, J. E. Halver, and L. G. Puskas Effects of dietary omega-3 polyunsaturated fatty acids on brain gene expression PNAS, July 27, 2004; 101(30): 10931 - 10936. [Abstract] [Full Text] [PDF]

				W. Khovidhunkit, M.-S. Kim, R. A. Memon, J. K. Shigenaga, A. H. Moser, K. R. Feingold, and C. Grunfeld Thematic review series: The Pathogenesis of Atherosclerosis. Effects of infection and inflammation on lipid and lipoprotein metabolism mechanisms and consequences to the host J. Lipid Res., July 1, 2004; 45(7): 1169 - 1196. [Abstract] [Full Text] [PDF]

				Y.-m. Liu, M. Moldes, J.-P. Bastard, E. Bruckert, N. Viguerie, B. Hainque, A. Basdevant, D. Langin, J. Pairault, and K. Clement Adiponutrin: A New Gene Regulated by Energy Balance in Human Adipose Tissue J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 2684 - 2689. [Abstract] [Full Text] [PDF]

				Y. Shidoji and H. Ogawa Natural occurrence of cancer-preventive geranylgeranoic acid in medicinal herbs J. Lipid Res., June 1, 2004; 45(6): 1092 - 1103. [Abstract] [Full Text] [PDF]

				G. Leonardsson, J. H. Steel, M. Christian, V. Pocock, S. Milligan, J. Bell, P.-W. So, G. Medina-Gomez, A. Vidal-Puig, R. White, et al. Nuclear receptor corepressor RIP140 regulates fat accumulation PNAS, June 1, 2004; 101(22): 8437 - 8442. [Abstract] [Full Text] [PDF]

				C. K. Sung, H. She, S. Xiong, and H. Tsukamoto Tumor necrosis factor-{alpha} inhibits peroxisome proliferator-activated receptor {gamma} activity at a posttranslational level in hepatic stellate cells Am J Physiol Gastrointest Liver Physiol, May 1, 2004; 286(5): G722 - G729. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, C.-H. Articles by Evans, R. M. Search for Related Content PubMed PubMed Citation Articles by Lee, C.-H. Articles by Evans, R. M. Pubmed/NCBI databases Medline Plus Health Information Metabolic Disorders