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Department of Cell Biology (M.W.R., P.E.S.) and Diabetes Research and Training Center (P.E.S.), Albert Einstein College of Medicine, Bronx, New York 10461
Address all correspondence and requests for reprints to: Philipp E. Scherer, Diabetes Research and Training Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. E-mail: scherer{at}aecom.yu.edu.
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Abstract |
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 Top Abstract IntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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Introduction |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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). These adipocyte-specific or enriched proteins, termed adipokines, have been shown to have a variety of local, peripheral, and central effects that will be discussed below. Adipose tissue is therefore able to integrate signals from other organs and respond by regulating secretion of multiple proteins. As an active participant in whole body energy homeostasis, adipose tissue can negatively influence other systems when dysregulated. Although adipocytes are capable of increasing in size, the cellular homeostasis and the secretory profile of larger adipocytes becomes altered and increasingly dysregulated compared with adipocytes of smaller size (1). Although the total number of adipocytes is increased with increasing fat mass, the increased number and percentage of these large adipocytes may partially account for the inability of adipose tissue to function properly and contribute to some of the problems associated with obesity.
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The Adipocyte and Energy Homeostasis |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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Leptin injection can reduce body weight and fat mass by increasing energy expenditure and decreasing food intake (15). The weight loss induced by leptin administration differs from simple reduction in food intake (15, 16, 17). Additionally, leptin-administered animals do not display a rise in serum free fatty acids or ketones associated with rapid weight loss in food-restricted animals (18).
The mechanism by which leptin is capable of exerting its metabolic affects has been an area of intense research. A recently reported mechanism is based on the observation that leptin is capable of activating 5'-AMP-activated protein kinase (AMPK) in muscle and liver both by acting directly on these tissues and by acting centrally through the central nervous system (19, 20). When activated, AMPK decreases ATP-consuming anabolic pathways such as glucose-regulated transcription, protein synthesis, cholesterol synthesis, and fatty acid and triglyceride synthesis, and it also increases ATP-producing catabolic pathways such as increased glucose transport, ß oxidation, glycolysis, and mitochondrial biogenesis. Patients with lipodystrophy have significant lipid droplets in liver and muscle. Administration of leptin to these patients significantly increases insulin sensitivity, improves serum lipid profiles, and decreases lipid accumulation in liver and muscle (21, 22).
Beyond its central metabolic functions, leptin has profound effects on a number of other physiologic processes, such as fertility and normal immune function (23). The influence of leptin in immune function can be clearly seen in the context of nutritional status. Normal immune function is suppressed during times of nutritional deprivation, a state associated with low levels of circulating leptin. The immunosuppression associated with acute starvation is reversed when leptin is exogenous administered (24). In line with these observations, ob/ob mice have impaired T cell immunity (25). Leptin also alters the regulation of hormones in the hypothalamus-pituitary-adrenal axis and affects GH, prolactin, and a number of other anterior pituitary hormones (26). Similar to other hormones, diurnal and ultradian leptin rhythms have been identified with peak circulating levels at night reaching the nadir in the morning. This rhythm can be altered by meal timing but does not seem to be entrained by the circadian clock (27).
The relevance of leptin in normal human metabolic function is evident from leptin replacement therapy to a small number of individuals with leptin deficiency due to chromosomal mutations (see accompanying review by O’Rahilly et al., Ref. 28). Studies with diet-induced obese mice showed that these mice were resistant to the effects of leptin administration (29). It has been postulated that a leptin resistance can develop in the face of high circulating levels of the hormone. This is supported by the fact that leptin levels are increased in most mouse models of insulin resistance associated with obesity. The effectiveness of intracerebral ventricular injections of leptin in a number of models of genetic and diet induced obesity suggest that leptin resistance can occur at several levels, from the transport across the blood brain barrier, to downstream targets of the receptor (reviewed in Ref. 30). The inability of high endogenous leptin to prevent weight gain may partly be explained by the reduced cerebrospinal fluid:peripheral ratio of leptin in obese individuals (31). Leptin may have evolved to deal with limited energy availability, and its main function may be to mediate responses necessary to increase those energy stores, i.e. including effects on feeding behavior (12). As such, it is unfortunately not capable of preventing overconsumption or obesity and does not appear to be a viable treatment for obesity at this stage.
Adiponectin
Adiponectin is a 30-kDa adipose-specific secreted protein that circulates in human serum at 5–30 nM concentrations, with circulating levels approximately two to three times higher in females than in males (32, 33). The mature protein consists of an amino-terminal collagen-like domain and a carboxy-terminal head domain with structural similarities to complement factor C1q. Serum adiponectin (FL-Ad) is found as a low-molecular-weight complex consisting of a dimer of trimers as well as a high-molecular-weight complex consisting of up to six trimers (34). A third form, generated by cleavage of the collagenous stalk region that results in globular trimer (gAd), has not conclusively been shown to exist as a physiological intermediate but has potent pharmacological activity (35).
An analysis of obesity-prone rhesus monkeys that often progress to type 2 diabetes examined the plasma concentration of adiponectin longitudinally (36). A decrease in circulating FL-Ad was seen with increasing BMI (37). This decrease in FL-Ad strongly correlated with the concomitant decrease in insulin sensitivity. Although the relationship between insulin action and adiponectin plasma levels is independent of body adiposity, the levels of FL-Ad are almost always decreased in obesity. Human studies focusing on Pima Indian and Japanese cohorts demonstrated an association between low plasma adiponectin levels and obesity and type 2 diabetes (38, 39). Adiponectin levels were negatively correlated with the degree of hyperinsulinemia and insulin resistance in both ethnic groups. Moreover, relatively moderate weight loss can lead to a significant increase in circulating FL-Ad levels, demonstrating that the decrease in adiponectin serum concentration is reversible (40). Importantly, this rise in serum FL-Ad mirrors the increase in insulin sensitivity seen with reduction in adipose tissue mass. Spranger et al. (41) have recently shown that baseline plasma adiponectin levels in apparently healthy individuals are independently associated with future risk for the development of type 2 diabetes.
Further genetic studies examined whether polymorphisms in the locus for adiponectin, 3q27, could affect the circulating levels of adiponectin and whether these polymorphisms were associated with increased risk for the development of type 2 diabetes. The results of one study showed evidence of linkage with metabolic syndrome (42), whereas another showed evidence of a type 2 diabetes susceptibility locus at 3q27-qter in a French population with early-onset diabetes. Polymorphisms within the adiponectin locus were also linked with increased risk for type 2 diabetes in a Japanese cohort (43). Study of a missense mutation in the globular head domain of FL-Ad found in another Japanese cohort was associated with low plasma adiponectin and type 2 diabetes. All carriers of one of these missense mutations exhibited at least one feature of metabolic syndrome (44). A concise summary of the available genetic data is provided by Vasseur et al. (45).
Peroxisome proliferator-activated receptor (PPAR) 
agonists increase expression and plasma concentrations of adiponectin (46, 47) as well as decrease plasma TNF
concentration. TNF is increased locally in adipose tissue in obesity, and it is possible that the higher levels of TNF may be due to suppressed adiponectin levels in vivo (48). TNF has been shown to reduce adiponectin expression in adipocytes in a dose-dependent manner (49). Elevated TNF levels have been reported in the adiponectin knockout mouse. Introduction of adiponectin by adenoviral infection normalized serum TNF in these mice. Overexpression of gAd in the apolipoprotein E (ApoE) -/- mouse model demonstrated that overexpression of gAd reduces the severe atherosclerosis and increased TNF and class A scavenger receptors typically seen in apolipoprotein E (ApoE) -/- mouse (50). Similarly, an increase in atherosclerotic plaque formation can be observed in adiponectin null mice compared with wild-type mice after induced vascular injury (51). Furthermore, diabetics with CAD have been shown to have less adiponectin than diabetics without CAD (38).
Impairment of insulin secretion and a decrease in peripheral sensitivity to insulin characterize the pathogenesis of type 2 diabetes. Together, they result in increased hepatic glucose production and impaired peripheral glucose clearance by muscle and fat. Mouse models that carry specific genetic lesions that affect insulin sensitivity directly at the level of the fat cell often have altered adipokine profiles that may partially explain their phenotype. Fat cell-specific ablation of the insulin receptor (FIRKO) causes increased serum adiponectin levels (1). Conversely, the massive down-regulation of the insulin receptor observed in adipocytes isolated from caveolin-1 knockout mice (52) results in a dramatic reduction of adiponectin levels in serum (53). The ablation of insulin-stimulated glucose uptake in adipocytes by tissue-specific ablation of the glucose transporter GLUT4 results in impaired insulin sensitivity in muscle and liver, with evidence pointing at an adipokine (or lack thereof) as a causative factor for the insulin resistance seen in liver and muscle (54). All of these mouse models that interfere with insulin signaling or downstream events (such as glucose transport) in the adipocyte have profound effects on adiponectin levels in serum and emphasize the importance of insulin signaling in the feedback loop that controls serum levels of adiponectin.
Studies in mice examined the effect of recombinant adiponectin on insulin sensitivity and lipid metabolism. Injection of mice with FL-Ad was found to decrease gluconeogenesis in the liver and peripheral lipid accumulation in nonadipose tissues (55). The reduction in gluconeogenesis was due to decreased expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) and resulted in reduced hepatic glucose production (47). The ability of FL-Ad to acutely lower serum glucose was independent of any change in insulin secretion (47). Additionally, this suppression of glucose production was reproduced in vitro in isolated primary hepatocytes. The treatment of mice with gAd increased glucose uptake and fatty acid oxidation in muscle and decreased lipid accumulation in muscle. gAd injection into mice exposed to a high-fat, high-sucrose diet induced weight loss without decreasing food intake (35). Overexpression of gAd in transgenic mice in the background of the ob/ob mutation reverses insulin resistance without affecting body weight (50). Fatty acid oxidation was increased in skeletal muscle and expression of uncoupling proteins-2 and -3 were up-regulated (50).
Similar to the peripheral effects of leptin, it is possible that gAd increases insulin sensitivity in muscle by increasing FA oxidation, thereby decreasing intramyocellular lipid accumulation. Adiponectin affects glucose metabolism and insulin sensitivity through activation of AMPK. Treatment of muscle cells in vitro with Ad leads to stimulation of ß oxidation and glucose uptake. Dominant-negative AMPK transfected into myocytes blocked adiponectin-mediated phosphorylation of acetyl-CoA carboxylase 1 (ACC1), a downstream target of AMPK (56). Adenoviral infection of dominant-negative AMPK significantly decreased the glucose-lowering effect of FL-Ad in vivo and blunted the FL-Ad-mediated repression of gluconeogenic enzymes. Even though some light has been shed on the intracellular events taking place upon adiponectin treatment, major gaps still exist with respect to the identification of a receptor and which membrane-proximal signaling modules are used to trigger the transcriptional changes observed.
Resistin
Resistin is a 10-kDa adipose tissue-specific hormone that was recently identified in a screen designed to enrich for transcripts that were up-regulated during adipogenesis but decreased with PPAR agonist treatment (57). Injection of resistin into wild-type mice resulted in reduced glucose tolerance and insulin action, whereas injection of neutralizing antibodies into diabetic obese mice improved insulin action (57). We recently published the acute in vivo effects of resistin on glucose production, glucose clearance, and insulin action in insulin-clamped rats (58). When resistin was infused at near physiological levels in the presence of physiologically high circulating insulin, lower rates of glucose infusion were necessary to maintain basal glucose levels. The insulin resistance caused by resistin infusion was completely attributed to an increase in the rate of glucose production and not to an increase in glucose uptake. This indicates that resistin has a clear and rapid effect on hepatic, but not peripheral, insulin sensitivity (58). However, other groups have shown resistin mRNA in most mouse models of insulin resistance to actually be down-regulated (59). Additionally, although the human resistin gene promoter has been shown to have binding sites for ADD-1/SREBP-1c (adipocyte determination and differentiation factor 1/sterol regulatory element binding protein 1c) and C/EBP (CCAAT/enhancer-binding protein ), two transcription factors that have important roles in adipogenesis (60), resistin expression in human adipocytes was very low within human adipose tissue explants (61, 62). In fact, human resistin expression was higher in monocytes (62) and other nonadipocyte cells of adipose tissue (63) than in adipocytes. Furthermore, some studies have failed to show a link between resistin levels and BMI or insulin sensitivity (61, 64, 65) whereas others argue for such a connection (66, 67, 68).
Although these studies shed doubt on a role of resistin in insulin resistance associated with obesity, it is possible that serum levels do not correlate with tissue mRNA or protein levels, a phenomenon observed for other adipokines under certain conditions (32). The majority of published papers on resistin make conclusions based only on resistin transcript levels and lack serum concentrations of the secreted, mature protein due to the difficulty in measuring serum resistin. Caution should therefore be used in interpreting studies ruling out a role for resistin based only on mRNA or cellular protein levels. Further studies focusing on serum resistin concentrations, as well as development of knockout and transgenic mouse models and the identification of a receptor, will be necessary to determine the clinical relevance of resistin in obesity and in the development of insulin resistance.
Acylation-stimulating protein (ASP)
ASP is produced by a two-step process involving three proteins of the alternate complement system: C3, factor B, and adipsin. All three of these precursor proteins are produced and secreted by adipocytes (69). ASP increases lipogenesis locally in adipocytes and inhibits hormone-sensitive lipase-mediated lipolysis. Mice lacking complement factor C3 (and therefore deficient in ASP) display greater caloric intake with normal fat absorption but are significantly leaner (70). These mice are therefore resistant to diet-induced weight gain and display increased postprandial free fatty acid levels. ASP levels are elevated in obese humans and decrease after fasting or weight loss (71).
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Adipokine Secretion |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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The Adipocyte as a Source and Target for Inflammation |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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production in adipose tissue (74). The locally elevated TNF directly interferes with proper insulin signal transduction through specific phosphorylation of critical serine residues in the insulin receptor and insulin receptor substrate-1, thereby leading to a local desensitization to insulin signaling (75). In addition to local increases in TNF, a systemic increase in inflammatory markers has been shown to be associated with obesity. C-reactive protein (CRP) is an unspecific acute phase reactant that serves as an excellent indicator of systemic inflammation (76). Insulin resistance is not only associated with a significant increase in CRP, but a whole host of additional acute phase reactants that are elevated as well. Many of these additional factors including IL-6, 1 acid glycoprotein, and serum amyloid A (SAA) are expressed in adipose tissue (77). All of these proteins (with the exception of CRP) are up-regulated in adipose tissue in the insulin-resistant state. Increased serum IL-6 is predictive of future cardiovascular problems (78). SAA can effectively compete for binding of apolipoprotein A-I on high-density lipoprotein particles, thereby altering trafficking of these particles (79). Additional acute phase reactants produced in adipocytes include the pentraxin family member PTX-3 (80), which is closely related to CRP, as well as the lipocalin 24p3 (77), whose roles in the innate immune response and as an iron binding protein have recently been established (81, 82). Additionally, ceruloplasmin and macrophage migration inhibitory factor have also been identified as secretory products of adipocytes, albeit it is not known whether expression of these proteins is altered with the development of insulin resistance (83, 84). Interestingly, the antiinflammatory factor IL-1 receptor antagonist (IL-1Ra) is also expressed in adipose tissue where it is significantly up-regulated in obesity, concomitant with an increase in systemic IL-1 receptor antagonist levels (85).
It is technically difficult to gauge the relative contribution of adipocytes to the systemic levels of these proteins in any given metabolic state. However, in a direct comparison, adipocytes have a proinflammatory potential equal or superior to that of macrophages with respect to a subset of inflammatory markers (86). Combined with the highly significant biomass that adipocytes can contribute to whole body weight, particularly in obese individuals, there is little doubt that the systemic contribution of adipose tissue is significant. As an example, increased systemic TNF was seen in the recently described adiponectin knockout mouse with adipose tissue being the only tissue examined with a significant increase in TNF expression (48). This demonstrates that an adipose-specific increase in an inflammatory cytokine was capable of translating into a significant systemic increase in concentration.
The potential of the adipocyte as a potent source for acute phase reactants can be understood on the basis of the specific transcription factors that are expressed. Many of the general factors involved in the acute phase reactant response in the liver, such as the members of the C/EBP family, are also abundantly expressed in the adipocyte. Specific transcription factors, such as SAA-enhancing factor that has been shown to play an important role in the dramatic induction of SAA in the liver (87), are also strongly induced during adipogenesis (our unpublished observations). Although we can phenomenologically describe the close functional relationship between the adipocyte, macrophage, and some specialized hepatocyte functions, we struggle to explain the teleological rationale for coupling the innate immune response with energy homeostasis. Nevertheless, it seems to be desirable across species and phyla, to use a single cell as an integrator for both immune and metabolic function. In flies, the fat body not only serves for energy storage and assumes primitive liver functions but also serves as primary coordinator of the innate immune response (88). Analogous to these evolutionarily more primitive systems, we expect that mammalian adipocytes produce a host of bacteriostatic and bacteriocidal factors, an area that has remained vastly unexplored thus far. It is likely that a complex cross-talk exists between adipocytes and the closely juxtaposed cells within the stroma of adipose tissue, such as macrophages. A recent paper by Charriere et al. (89) calls attention to the close relationship between the adipocyte and macrophages lineages. Injection of the well-established 3T3-L1 preadipocyte cell line into the peritoneum of nude mice resulted in the induction of a number of highly macrophage-specific surface markers, indicating that these cells effectively trans-differentiate into macrophages in vivo (89).
Although PPAR agonists, such as the thiazolidinediones (TZDs), may exert their antidiabetic effects at least in part on the basis of gene induction of adipocyte-specific polypeptides with beneficial activity on insulin sensitivity, the antiinflammatory effects of TZDs on adipocytes may be equally important. TZDs significantly reduce the production of SAA in adipocytes of diabetic mice and prevent the TNF-mediated repression of adiponectin production (77).
The close connection between inflammation and insulin resistance has been further underscored by recent findings of the Shoelson and Hotamisligil groups. Treatment with high doses of salicylates can reverse the insulin resistance in obese and diet-induced diabetic mouse models by inhibiting IKKß. They have further shown these positive antiinflammatory effects on insulin sensitivity in humans and point to IKKß as a new therapeutic target for type 2 diabetes (90, 91, 92). The proinflammatory c-Jun amino-terminal kinase (JNK) pathway has been implicated in insulin resistance in cultured cells. In vivo, JNK activity is abnormally elevated in obesity. Mice carrying a chromosomal deletion of JNK1 display reduced adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signaling (93). Future studies will have to determine the importance of these proinflammatory cascades in adipose tissue vis-à-vis the adipokine profile and systemic insulin sensitivity.
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Effects on Vasculature and Additional Stromal Interactions |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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Adipokines and Cancer |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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Potential for Additional Factors |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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Conclusion and Future Perspectives |
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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Future work will hopefully shed additional mechanistic insights into the underlying reasons why an excess of adipose tissue is associated with a higher propensity toward insulin resistance. The receptors for many of the recently identified adipokines, including adiponectin and resistin, have yet to be identified. Serum cofactors that associate with these adipokines and potentially stimulate proteolytic cleavage to activate them also need to be isolated and identified.
Due to the large number of factors influencing insulin sensitivity and the development of insulin resistance, it is exceedingly unlikely that levels of any one factor will enable us to explain the development of insulin resistance. In light of this complexity, it is surprising how well the correlations between adiponectin and insulin sensitivity have consistently held up in a large number of clinical studies. Nevertheless, it is likely that an index will need to be developed that takes levels of a number of these adipokines (adiponectin, resistin, inflammatory cytokines) as well as free fatty acids and triglycerides into account before a complete model can take shape.
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Footnotes |
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Abbreviations: AMPK, 5'-AMP-activated protein kinase; ASP, acylation-stimulating protein; BMI, body mass index; CAD, coronary artery disease; CRP, C-reactive protein; FL-Ad, serum adiponectin; gAD, globular trimer; JNK, c-Jun amino-terminal kinase; PPAR, peroxisome proliferator-activated receptor; SAA, serum amyloid A; TZD, thiazolidinedione.
Received May 9, 2003.
Accepted for publication June 3, 2003.
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TopAbstractIntroductionThe Adipocyte and Energy...Adipokine SecretionThe Adipocyte as a...Effects on Vasculature and...Adipokines and CancerPotential for Additional FactorsConclusion and Future...References |
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agonists: a potential mechanism of insulin sensitization. Endocrinology 143:998–1007 agonists. J Biol Chem 276:25651–25653. Mol Endocrinol 17:1522–1533 activators. Biochem Biophys Res Commun 300:472–476[CrossRef][Medline]
action in humans. Diabetes 50:2199–2202: a key component of the obesity-diabetes link. Diabetes 43:1271–1278[Abstract]
. J Clin Invest 94:1543–1549
-induced, secreted protein of adipose cells. J Lipid Res 44:994–1000. Biochem Biophys Res Commun 235:94–98[CrossRef][Medline]
B interacts with SEF to synergistically activate mouse serum amyloid A3 gene transcription. J Biol Chem 275:31616–31623This article has been cited by other articles:
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 |
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|
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|
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|
|
|
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|
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 |
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 R. Summer, F. F. Little, N. Ouchi, Y. Takemura, T. Aprahamian, D. Dwyer, K. Fitzsimmons, B. Suki, H. Parameswaran, A. Fine, et al. Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice Am J Physiol Lung Cell Mol Physiol, June 1, 2008; 294(6): L1035 - L1042. [Abstract] [Full Text] [PDF]
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 B.-W. Wang, H.-F. Hung, H. Chang, P. Kuan, and K.-G. Shyu Mechanical stretch enhances the expression of resistin gene in cultured cardiomyocytes via tumor necrosis factor-{alpha} Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2305 - H2312. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Bullo, M. R Peeraully, P. Trayhurn, J Folch, and J. Salas-Salvado Circulating nerve growth factor levels in relation to obesity and the metabolic syndrome in women Eur. J. Endocrinol., September 1, 2007; 157(3): 303 - 310. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. T. Campbell, M. Cotterchio, E. Dicks, P. Parfrey, S. Gallinger, and J. R. McLaughlin Excess Body Weight and Colorectal Cancer Risk in Canada: Associations in Subgroups of Clinically Defined Familial Risk of Cancer Cancer Epidemiol. Biomarkers Prev., September 1, 2007; 16(9): 1735 - 1744. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Vu, W. Kim, X. Fang, Y.-T. Liu, A. Xu, and G. Sweeney Coculture with Primary Visceral Rat Adipocytes from Control But Not Streptozotocin-Induced Diabetic Animals Increases Glucose Uptake in Rat Skeletal Muscle Cells: Role of Adiponectin Endocrinology, September 1, 2007; 148(9): 4411 - 4419. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. M. De Taeye, T. Novitskaya, O. P. McGuinness, L. Gleaves, M. Medda, J. W. Covington, and D. E. Vaughan Macrophage TNF-{alpha} contributes to insulin resistance and hepatic steatosis in diet-induced obesity Am J Physiol Endocrinol Metab, September 1, 2007; 293(3): E713 - E725. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Weiss Fat distribution and storage: how much, where, and how? Eur. J. Endocrinol., August 1, 2007; 157(suppl_1): S39 - S45. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. G. McTernan and S. Kumar Retinol Binding Protein 4 and Pathogenesis of Diabetes J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2430 - 2432. [Full Text] [PDF]
|
|
|
|
|
|
G. Murdolo, A. Hammarstedt, M. Sandqvist, M. Schmelz, C. Herder, U. Smith, and P.-A. Jansson Monocyte Chemoattractant Protein-1 in Subcutaneous Abdominal Adipose Tissue: Characterization of Interstitial Concentration and Regulation of Gene Expression by Insulin J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2688 - 2695. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Adachi, C. Kumar, Y. Zhang, and M. Mann In-depth Analysis of the Adipocyte Proteome by Mass Spectrometry and Bioinformatics Mol. Cell. Proteomics, July 1, 2007; 6(7): 1257 - 1273. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Barazzoni, A. Bernardi, F. Biasia, A. Semolic, A. Bosutti, M. Mucci, F. Dore, M. Zanetti, and G. Guarnieri Low fat adiponectin expression is associated with oxidative stress in nondiabetic humans with chronic kidney disease--impact on plasma adiponectin concentration Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R47 - R54. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Desoye and S. Hauguel-de Mouzon The Human Placenta in Gestational Diabetes Mellitus: The insulin and cytokine network Diabetes Care, July 1, 2007; 30(Supplement_2): S120 - S126. [Full Text] [PDF]
|
|
|
|
 |
|
 M. Qatanani and M. A. Lazar Mechanisms of obesity-associated insulin resistance: many choices on the menu Genes & Dev., June 15, 2007; 21(12): 1443 - 1455. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Si, J. Yoon, and K. Lee Flux profile and modularity analysis of time-dependent metabolic changes of de novo adipocyte formation Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1637 - E1646. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. K. Saxena, P. M. Vertino, F. A. Anania, and D. Sharma Leptin-induced Growth Stimulation of Breast Cancer Cells Involves Recruitment of Histone Acetyltransferases and Mediator Complex to CYCLIN D1 Promoter via Activation of Stat3 J. Biol. Chem., May 4, 2007; 282(18): 13316 - 13325. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Stefan, A. M. Hennige, H. Staiger, J. Machann, F. Schick, E. Schleicher, A. Fritsche, and H.-U. Haring High Circulating Retinol-Binding Protein 4 Is Associated With Elevated Liver Fat but Not With Total, Subcutaneous, Visceral, or Intramyocellular Fat in Humans Diabetes Care, May 1, 2007; 30(5): 1173 - 1178. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Alvarez-Llamas, E. Szalowska, M. P. de Vries, D. Weening, K. Landman, A. Hoek, B. H. R. Wolffenbuttel, H. Roelofsen, and R. J. Vonk Characterization of the Human Visceral Adipose Tissue Secretome Mol. Cell. Proteomics, April 1, 2007; 6(4): 589 - 600. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Flowers, A. T. Oler, S. T. Nadler, Y. Choi, K. L. Schueler, B. S. Yandell, C. M. Kendziorski, and A. D. Attie Abdominal obesity in BTBR male mice is associated with peripheral but not hepatic insulin resistance Am J Physiol Endocrinol Metab, March 1, 2007; 292(3): E936 - E945. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G D Norata, M Ongari, K Garlaschelli, S Raselli, L Grigore, and A L Catapano Plasma resistin levels correlate with determinants of the metabolic syndrome Eur. J. Endocrinol., February 1, 2007; 156(2): 279 - 284. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Sharma and B. Staels Peroxisome Proliferator-Activated Receptor {gamma} and Adipose Tissue--Understanding Obesity-Related Changes in Regulation of Lipid and Glucose Metabolism J. Clin. Endocrinol. Metab., February 1, 2007; 92(2): 386 - 395. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Kusminski, N. F. da Silva, S. J. Creely, F. M. Fisher, A. L. Harte, A. R. Baker, S. Kumar, and P. G. McTernan The in Vitro Effects of Resistin on the Innate Immune Signaling Pathway in Isolated Human Subcutaneous Adipocytes J. Clin. Endocrinol. Metab., January 1, 2007; 92(1): 270 - 276. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Rodriguez-Pacheco, A. J. Martinez-Fuentes, S. Tovar, L. Pinilla, M. Tena-Sempere, C. Dieguez, J. P. Castano, and M. M. Malagon Regulation of Pituitary Cell Function by Adiponectin Endocrinology, January 1, 2007; 148(1): 401 - 410. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Ghosh, Y. Lu, A. Katz, Y. Hu, and R. Li Tumor suppressor BRCA1 inhibits a breast cancer-associated promoter of the aromatase gene (CYP19) in human adipose stromal cells Am J Physiol Endocrinol Metab, January 1, 2007; 292(1): E246 - E252. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Phillips, O. A. Hatoum, and D. D. Gutterman The mechanism of flow-induced dilation in human adipose arterioles involves hydrogen peroxide during CAD Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H93 - H100. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Chung, K. LaPoint, K. Martinez, A. Kennedy, M. Boysen Sandberg, and M. K. McIntosh Preadipocytes Mediate Lipopolysaccharide-Induced Inflammation and Insulin Resistance in Primary Cultures of Newly Differentiated Human Adipocytes Endocrinology, November 1, 2006; 147(11): 5340 - 5351. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. T. C. Yang, H. Y. Suk, X. Yang, O. Olabisi, R. Y. L. Yu, J. Durand, L. A. Jelicks, J.-Y. Kim, P. E. Scherer, Y. Wang, et al. Role of Transcription Factor NFAT in Glucose and Insulin Homeostasis Mol. Cell. Biol., October 15, 2006; 26(20): 7372 - 7387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Turgeon, M. C. Carr, P. M. Maki, M. E. Mendelsohn, and P. M. Wise Complex Actions of Sex Steroids in Adipose Tissue, the Cardiovascular System, and Brain: Insights from Basic Science and Clinical Studies Endocr. Rev., October 1, 2006; 27(6): 575 - 605. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Bodles, V. Varma, A. Yao-Borengasser, B. Phanavanh, C. A. Peterson, R. E. McGehee Jr., N. Rasouli, M. Wabitsch, and P. A. Kern Pioglitazone induces apoptosis of macrophages in human adipose tissue J. Lipid Res., September 1, 2006; 47(9): 2080 - 2088. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Trayhurn and C. Bing Appetite and energy balance signals from adipocytes Phil Trans R Soc B, July 29, 2006; 361(1471): 1237 - 1249. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Trayhurn, C. Bing, and I. S. Wood Adipose Tissue and Adipokines--Energy Regulation from the Human Perspective J. Nutr., July 1, 2006; 136(7): 1935S - 1939S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. H. Treiber, D. S. Kronfeld, and R. J. Geor Insulin Resistance in Equids: Possible Role in Laminitis J. Nutr., July 1, 2006; 136(7): 2094S - 2098S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. R. Srinivasan, L. Myers, and G. S. Berenson Changes in Metabolic Syndrome Variables Since Childhood in Prehypertensive and Hypertensive Subjects: The Bogalusa Heart Study Hypertension, July 1, 2006; 48(1): 33 - 39. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. P. Nunez, W.-J. Oh, J. Rozenberg, C. Perella, M. Anver, J. C. Barrett, S. N. Perkins, D. Berrigan, J. Moitra, L. Varticovski, et al. Accelerated Tumor Formation in a Fatless Mouse with Type 2 Diabetes and Inflammation. Cancer Res., May 15, 2006; 66(10): 5469 - 5476. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Sell, D. Dietze-Schroeder, U. Kaiser, and J. Eckel Monocyte Chemotactic Protein-1 Is a Potential Player in the Negative Cross-Talk between Adipose Tissue and Skeletal Muscle Endocrinology, May 1, 2006; 147(5): 2458 - 2467. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Ehling, A. Schaffler, H. Herfarth, I. H. Tarner, S. Anders, O. Distler, G. Paul, J. Distler, S. Gay, J. Scholmerich, et al. The Potential of Adiponectin in Driving Arthritis J. Immunol., April 1, 2006; 176(7): 4468 - 4478. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. E. Wolins, B. K. Quaynor, J. R. Skinner, A. Tzekov, C. Park, K. Choi, and P. E. Bickel OP9 mouse stromal cells rapidly differentiate into adipocytes: characterization of a useful new model of adipogenesis J. Lipid Res., February 1, 2006; 47(2): 450 - 460. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Gary-Bobo, G. Elachouri, B. Scatton, G. Le Fur, F. Oury-Donat, and M. Bensaid The Cannabinoid CB1 Receptor Antagonist Rimonabant (SR141716) Inhibits Cell Proliferation and Increases Markers of Adipocyte Maturation in Cultured Mouse 3T3 F442A Preadipocytes Mol. Pharmacol., February 1, 2006; 69(2): 471 - 478. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. R. Hugo, T. D. Brandebourg, C. E. S. Comstock, K. S. Gersin, J. J. Sussman, and N. Ben-Jonathan LS14: A Novel Human Adipocyte Cell Line that Produces Prolactin Endocrinology, January 1, 2006; 147(1): 306 - 313. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. K. LeBrasseur and N. B. Ruderman Why Might Thiazolidinediones Increase Exercise Capacity in Patients With Type 2 Diabetes? Diabetes Care, December 1, 2005; 28(12): 2975 - 2977. [Full Text] [PDF]
|
|
|
|
|
|
G. M. van der Vleuten, L. J. H. van Tits, M. den Heijer, H. Lemmers, A. F. H. Stalenhoef, and J. de Graaf Decreased adiponectin levels in familial combined hyperlipidemia patients contribute to the atherogenic lipid profile J. Lipid Res., November 1, 2005; 46(11): 2398 - 2404. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Engeli Is there a pathophysiological role for perivascular adipocytes? Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1794 - H1795. [Full Text] [PDF]
|
|
|
|
|
|
C. Barandier, J.-P. Montani, and Z. Yang Mature adipocytes and perivascular adipose tissue stimulate vascular smooth muscle cell proliferation: effects of aging and obesity Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1807 - H1813. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. P. Keenan, C.-M. Hoe, L. Mixson, C. L. Mccoy, J. B. Coleman, B. A. Mattson, G. A. Ballam, L. A. Gumprecht, and K. A. Soper Diabesity: A Polygenic Model of Dietary-Induced Obesity from Ad Libitum Overfeeding of Sprague-Dawley Rats and Its Modulation by Moderate and Marked Dietary Restriction Toxicol Pathol, October 1, 2005; 33(6): 650 - 674. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Kampf, B. Bodin, O. Kallskog, C. Carlsson, and L. Jansson Marked Increase in White Adipose Tissue Blood Perfusion in the Type 2 Diabetic GK Rat Diabetes, September 1, 2005; 54(9): 2620 - 2627. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J Morris, E. Velkoska, and T. J Cole Central and peripheral contributions to obesity-associated hypertension: impact of early overnourishment Exp Physiol, September 1, 2005; 90(5): 697 - 702. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Trayhurn White adipose tissue grafts--keeping in contact Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2005; 289(2): R297 - R298. [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Grundy Point: The Metabolic Syndrome Still Lives Clin. Chem., August 1, 2005; 51(8): 1352 - 1354. [Full Text] [PDF]
|
|
|
|
|
|
G. B. Di Gregorio, A. Yao-Borengasser, N. Rasouli, V. Varma, T. Lu, L. M. Miles, G. Ranganathan, C. A. Peterson, R. E. McGehee, and P. A. Kern Expression of CD68 and Macrophage Chemoattractant Protein-1 Genes in Human Adipose and Muscle Tissues: Association With Cytokine Expression, Insulin Resistance, and Reduction by Pioglitazone Diabetes, August 1, 2005; 54(8): 2305 - 2313. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Lappas, M. Permezel, and G. E. Rice Leptin and Adiponectin Stimulate the Release of Proinflammatory Cytokines and Prostaglandins from Human Placenta and Maternal Adipose Tissue via Nuclear Factor-{kappa}B, Peroxisomal Proliferator-Activated Receptor-{gamma} and Extracellularly Regulated Kinase 1/2 Endocrinology, August 1, 2005; 146(8): 3334 - 3342. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Hamerman Osteoporosis and atherosclerosis: biological linkages and the emergence of dual-purpose therapies QJM, July 1, 2005; 98(7): 467 - 484. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Dietze-Schroeder, H. Sell, M. Uhlig, M. Koenen, and J. Eckel Autocrine Action of Adiponectin on Human Fat Cells Prevents the Release of Insulin Resistance-Inducing Factors Diabetes, July 1, 2005; 54(7): 2003 - 2011. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Bullo, M. R. Peeraully, and P. Trayhurn Stimulation of NGF expression and secretion in 3T3-L1 adipocytes by prostaglandins PGD2, PGJ2, and {Delta}12-PGJ2 Am J Physiol Endocrinol Metab, July 1, 2005; 289(1): E62 - E67. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. P. Combs, Nagajyothi, S. Mukherjee, C. J. G. de Almeida, L. A. Jelicks, W. Schubert, Y. Lin, D. S. Jayabalan, D. Zhao, V. L. Braunstein, et al. The Adipocyte as an Important Target Cell for Trypanosoma cruzi Infection J. Biol. Chem., June 24, 2005; 280(25): 24085 - 24094. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Park, H. K. Rho, K. H. Kim, S. S. Choe, Y. S. Lee, and J. B. Kim Overexpression of Glucose-6-Phosphate Dehydrogenase Is Associated with Lipid Dysregulation and Insulin Resistance in Obesity Mol. Cell. Biol., June 15, 2005; 25(12): 5146 - 5157. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Schaffler and H Herfarth Creeping fat in Crohn's disease: travelling in a creeper lane of research? Gut, June 1, 2005; 54(6): 742 - 744. [Full Text] [PDF]
|
|
|
|
|
|
E. Bugianesi, U. Pagotto, R. Manini, E. Vanni, A. Gastaldelli, R. de Iasio, E. Gentilcore, S. Natale, M. Cassader, M. Rizzetto, et al. Plasma Adiponectin in Nonalcoholic Fatty Liver Is Related to Hepatic Insulin Resistance and Hepatic Fat Content, Not to Liver Disease Severity J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3498 - 3504. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Linscheid, D. Seboek, H. Zulewski, U. Keller, and B. Muller Autocrine/Paracrine Role of Inflammation-Mediated Calcitonin Gene-Related Peptide and Adrenomedullin Expression in Human Adipose Tissue Endocrinology, June 1, 2005; 146(6): 2699 - 2708. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Capozza, T. P. Combs, A. W. Cohen, Y.-R. Cho, S.-Y. Park, W. Schubert, T. M. Williams, D. L. Brasaemle, L. A. Jelicks, P. E. Scherer, et al. Caveolin-3 knockout mice show increased adiposity and whole body insulin resistance, with ligand-induced insulin receptor instability in skeletal muscle Am J Physiol Cell Physiol, June 1, 2005; 288(6): C1317 - C1331. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Velkoska, T. J. Cole, and M. J. Morris Early dietary intervention: long-term effects on blood pressure, brain neuropeptide Y, and adiposity markers Am J Physiol Endocrinol Metab, June 1, 2005; 288(6): E1236 - E1243. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. H. Berg and P. E. Scherer Adipose Tissue, Inflammation, and Cardiovascular Disease Circ. Res., May 13, 2005; 96(9): 939 - 949. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. McGillis White Adipose Tissue, Inert No More! Endocrinology, May 1, 2005; 146(5): 2154 - 2156. [Full Text] [PDF]
|
|
|
|
|
|
J. A. Sennello, R. Fayad, A. M. Morris, R. H. Eckel, E. Asilmaz, J. Montez, J. M. Friedman, C. A. Dinarello, and G. Fantuzzi Regulation of T Cell-Mediated Hepatic Inflammation by Adiponectin and Leptin Endocrinology, May 1, 2005; 146(5): 2157 - 2164. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Sjoholm, J. Palming, L. E. Olofsson, A. Gummesson, P.-A. Svensson, T. C. Lystig, E. Jennische, J. Brandberg, J. S. Torgerson, B. Carlsson, et al. A Microarray Search for Genes Predominantly Expressed in Human Omental Adipocytes: Adipose Tissue as a Major Production Site of Serum Amyloid A J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 2233 - 2239. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Wang, J. R. Jenkins, and P. Trayhurn Expression and secretion of inflammation-related adipokines by human adipocytes differentiated in culture: integrated response to TNF-{alpha} Am J Physiol Endocrinol Metab, April 1, 2005; 288(4): E731 - E740. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Trayhurn Adipose Tissue in Obesity--An Inflammatory Issue Endocrinology, March 1, 2005; 146(3): 1003 - 1005. [Full Text] [PDF]
|
|
|
|
|
|
S. A. Summers and D. H. Nelson A Role for Sphingolipids in Producing the Common Features of Type 2 Diabetes, Metabolic Syndrome X, and Cushing's Syndrome Diabetes, March 1, 2005; 54(3): 591 - 602. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Lappas, K. Yee, M. Permezel, and G. E. Rice Sulfasalazine and BAY 11-7082 Interfere with the Nuclear Factor-{kappa}B and I{kappa}B Kinase Pathway to Regulate the Release of Proinflammatory Cytokines from Human Adipose Tissue and Skeletal Muscle in Vitro Endocrinology, March 1, 2005; 146(3): 1491 - 1497. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Skurk, C. Herder, I. Kraft, S. Muller-Scholze, H. Hauner, and H. Kolb Production and Release of Macrophage Migration Inhibitory Factor from Human Adipocytes Endocrinology, March 1, 2005; 146(3): 1006 - 1011. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. P. Reilly, M. Lehrke, M. L. Wolfe, A. Rohatgi, M. A. Lazar, and D. J. Rader Resistin Is an Inflammatory Marker of Atherosclerosis in Humans Circulation, February 22, 2005; 111(7): 932 - 939. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A M Diehl, Z P Li, H Z Lin, and S Q Yang Cytokines and the pathogenesis of non-alcoholic steatohepatitis Gut, February 1, 2005; 54(2): 303 - 306. [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Lazar How Obesity Causes Diabetes: Not a Tall Tale Science, January 21, 2005; 307(5708): 373 - 375. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. T. Page, K. L. Herbst, J. K. Amory, A. D. Coviello, B. D. Anawalt, A. M. Matsumoto, and W. J. Bremner Testosterone Administration Suppresses Adiponectin Levels in Men J Androl, January 1, 2005; 26(1): 85 - 92. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Verreth, D. De Keyzer, M. Pelat, P. Verhamme, J. Ganame, J. K. Bielicki, A. Mertens, R. Quarck, N. Benhabiles, G. Marguerie, et al. Weight Loss-Associated Induction of Peroxisome Proliferator-Activated Receptor-{alpha} and Peroxisome Proliferator-Activated Receptor-{gamma} Correlate With Reduced Atherosclerosis and Improved Cardiovascular Function in Obese Insulin-Resistant Mice Circulation, November 16, 2004; 110(20): 3259 - 3269. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Rochford, R. K. Semple, M. Laudes, K. B. Boyle, C. Christodoulides, C. Mulligan, C. J. Lelliott, S. Schinner, D. Hadaschik, M. Mahadevan, et al. ETO/MTG8 Is an Inhibitor of C/EBP{beta} Activity and a Regulator of Early Adipogenesis Mol. Cell. Biol., November 15, 2004; 24(22): 9863 - 9872. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Klein, S. Westphal, D. Kraus, B. Meier, N. Perwitz, V. Ott, M. Fasshauer, and H H. Klein Metformin inhibits leptin secretion via a mitogen-activated protein kinase signalling pathway in brown adipocytes J. Endocrinol., November 1, 2004; 183(2): 299 - 307. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S.-k. Park, S.-Y. Oh, M.-Y. Lee, S. Yoon, K.-S. Kim, and J.-w. Kim CCAAT/Enhancer Binding Protein and Nuclear Factor-Y Regulate Adiponectin Gene Expression in Adipose Tissue Diabetes, November 1, 2004; 53(11): 2757 - 2766. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Schelling and J. R. Sedor The Metabolic Syndrome as a Risk Factor for Chronic Kidney Disease: More than a Fat Chance? J. Am. Soc. Nephrol., November 1, 2004; 15(11): 2773 - 2774. [Full Text] [PDF]
|
|
|
|
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B. E. Wisse The Inflammatory Syndrome: The Role of Adipose Tissue Cytokines in Metabolic Disorders Linked to Obesity J. Am. Soc. Nephrol., November 1, 2004; 15(11): 2792 - 2800. [Abstract] [Full Text] [PDF]
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K. E. Davis, M. Moldes, and S. R. Farmer The Forkhead Transcription Factor FoxC2 Inhibits White Adipocyte Differentiation J. Biol. Chem., October 8, 2004; 279(41): 42453 - 42461. [Abstract] [Full Text] [PDF]
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