| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on July 29, 2004
Accepted on October 1, 2004
Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
* To whom correspondence should be addressed. E-mail: nihisak{at}intmed3.med.kyushu-u.ac.jp.
The adipocyte-derived hormone resistin has been proposed as a possible link between obesity and insulin resistance in murine models. Many recent studies have reported physiological roles for resistin in glucose homeostasis, one of which is enhancement of glucose production from the liver by upregulating gluconeogenic enzymes such as glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. However, its in vivo roles in lipid metabolism still remain to be clarified. In this study, we investigated the effects of resistin overexpression on insulin action and lipid metabolism in C57BL/6 mice using an adenoviral gene transfer technique. Elevated plasma resistin levels in mice treated with the resistin adenovirus (AdmRes) were confirmed by western blotting analysis and RIAs. Fasting plasma glucose levels did not differ between AdmRes-treated mice and controls, but the basal insulin concentration was significantly elevated in AdmRes-treated mice. In AdmRes-treated mice, the glucose-lowering effect of insulin was impaired, as evaluated by insulin tolerance tests. Furthermore, total cholesterol and triglyceride concentrations were significantly higher, while the high-density lipoprotein cholesterol level was significantly lower. Lipoprotein analysis revealed that low-density lipoprotein was markedly increased in AdmRes-treated mice compared with controls.
In addition, in vivo Triton WR-1339 studies showed evidence of enhanced very low-density lipoprotein production in AdmRes-treated mice. The expressions of genes involved in lipoprotein metabolism, such as LDL receptor and ApoAI in the liver, were decreased. These results suggest that resistin overexpression induces dyslipidemia in mice, which is commonly seen in the insulin-resistant state, partially through enhanced secretion of lipoproteins.
This article has been cited by other articles:
 |
|
 |
|
  H. Osawa, Y. Tabara, R. Kawamoto, J. Ohashi, M. Ochi, H. Onuma, W. Nishida, K. Yamada, J. Nakura, K. Kohara, et al. Plasma Resistin, Associated With Single Nucleotide Polymorphism -420, Is Correlated With Insulin Resistance, Lower HDL Cholesterol, and High-Sensitivity C-Reactive Protein in the Japanese General Population Diabetes Care, June 1, 2007; 30(6): 1501 - 1506. [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]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 H.-S. Liu, Y.-H. Chen, P.-F. Hung, and Y.-H. Kao Inhibitory effect of green tea (-)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway Am J Physiol Endocrinol Metab, February 1, 2006; 290(2): E273 - E281. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-H. Yu and H. N. Ginsberg Adipocyte Signaling and Lipid Homeostasis: Sequelae of Insulin-Resistant Adipose Tissue Circ. Res., May 27, 2005; 96(10): 1042 - 1052. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
