Metabolik Sendromda Adiponektin

Abstract

Derlememizde insülin direnci, diyabet ve metabolik sendromda adiponektin ve adiponektin reseptörlerinin patofizyolojisi tanımlanmaktadır. Adiposit biyolojisindeki son gelişmeler adipositlerin enerji depolayan hücreler olmaktan öte çeşitli hormonlar sitokinler, growth faktörler ve diğer biyoaktif maddeleri salgıladığını göstermektedir. Adiponektin adipöz dokudan büyük miktarlarda salgılanan ve vücudu insüline duyarlılaştıran bir adipokindir. Bu adipositokin antidiyabetik, antiaterosklerotik ve antiinflamatuvar fonksiyonlara sahiptir. Adiponektin reseptörleri, AdipoR1 ve AdipoR2 adiponektinin metabolik etkilerine aracılık etmektedir. Bu nedenle adiponektin ve adiponektin reseptörleri insülin direnci ile karakterize obezite ile ilişkili hastalıklar ile mücadele için çok yönlü potansiyel terapötik hedeflerdir

Keywords

• Adiponektin,İnsülin Direnci,Metabolik Sendrom,Diabet

Adıponectın In Metabolıc Syndrome

Abstract

This review describes the pathophysiology of adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome. Recent progress in adipocyte biology shows thatadipocytes are not merely energy-storing cells but that theysecrete a variety of hormones cytokines, growth factors, andother bioactive substances. Adiponectin is an adipokine that is abundantly expressed in adipose tissue and directly sensitizes the body to insulin. This adipocytokine has various biofunctions,such as antidiabetic, antiatherosclerotic, and antiinflammatoryfunctions. The adiponectin receptors, AdipoR1 and AdipoR2, mediate the metabolic actions of adiponectin. Therefore, adiponectin and adiponectin receptors represent potential therapeutic targets to combat obesity-linked diseases characterized by insulin resistance

Keywords

• Adiponectin,Insuline Resistance,Metabolic Syndrome,Diabetes

References

1. Flier JS. Obesity wars: molecular progress confronts an expanding epidemic. Cell, 2004; 116:337-350.
2. Matsuzawa Y. Pathophysiology and molecular mechanisms of visceral fat syndrome: the Japanese experience. Diabetes Metab Rev, 1997; 13:3-13.
3. National Cholesterol Education Program. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP)
4. Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA, 2001; 285:2486-2497.
5. Taniguchi CM, Emanuelli B, Kahn CR. Critical nodes in signaling pathways: insights into insulin action. Nat Rev Mol Cell Biol, 2006; 7:85-96
6. Saltiel AR, Kahn CR. Insulin signaling and the regulation of glucose and lipid metabolism. Nature, 2001; 414:799-806.
7. Spiegelman BM, Flier JS. Obesity and regulation of energy balance. Cell, 2001; 104:531-543.
8. Chawla A, Saez E, Evans RM. Don’t know much bile-ology. Cell, 2000; 103:1-4.

9. Obici S, Feng Z, Arduini A, et al. Inhibition of palmitoyltransferase-1 decreases food intake and glucose production. Nat Med, 2003; 9:756- 761.
10. Lazar MA. The humoral side of insulin resistance. Nat Med, 2006; 12:43-44.
11. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab, 2004; 89:2548-2556.
12. Kadowaki T, Yamauchi T. Adiponectin and adiponectin receptors. Endocr Rev, 2005; 26:439-451.
13. Scherer PE, Williams S, Fogliano M, et al. A novel serum protein similar to C1q, produced exclusively in adipocytes. J Biol Chem, 1995; 270: 26746-26749.
14. Das K, Lin Y, Widen E, et al. Chromosomal localization, expression pattern and promoter analysis of the mouse gene encoding adipocyte-specific secretory protein Acrp30. Biochem Biophys Res Commun, 2001; 280:1120-1129.
15. Shapiro L, Scherer PE. The crystal structure of a complement-1q family protein suggests an evolutionary link to tumor necrosis factor. Curr Biol, 1998; 8:335-338.