Abstract
The role of adipocytes as protein secreting cells has been known for almost 15 years. Most of these proteins have known biological activity and are called adipokines. However, only a few of the adipokines have been shown to regulate insulin sensitivity. The latter effects are direct or indirect. The adipokines regulating insulin sensitivity are tumor necrosis factor alpha, adiponectin, interleukin-6, resistin and leptin. This review examines the mechanism how these adipokines influence insulin sensitivity, how the adipocyte production of the adipokines is regulated and if genetic variance in the genes encoding for adipokines is important for the development of type 2 diabetes mellitus.
Keywords: adipose tissue, endothelial cells, tumor necrosis factor alpha, glucose metabolism, gi protein, lipolytic, interleukin, glucocorticoids, inflammatory genes, single nucleotide polymorphisms
Current Molecular Medicine
Title: Insulin Resistance in Type 2 Diabetes - Role of the Adipokines
Volume: 5 Issue: 3
Author(s): P. Arner
Affiliation:
Keywords: adipose tissue, endothelial cells, tumor necrosis factor alpha, glucose metabolism, gi protein, lipolytic, interleukin, glucocorticoids, inflammatory genes, single nucleotide polymorphisms
Abstract: The role of adipocytes as protein secreting cells has been known for almost 15 years. Most of these proteins have known biological activity and are called adipokines. However, only a few of the adipokines have been shown to regulate insulin sensitivity. The latter effects are direct or indirect. The adipokines regulating insulin sensitivity are tumor necrosis factor alpha, adiponectin, interleukin-6, resistin and leptin. This review examines the mechanism how these adipokines influence insulin sensitivity, how the adipocyte production of the adipokines is regulated and if genetic variance in the genes encoding for adipokines is important for the development of type 2 diabetes mellitus.
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Cite this article as:
Arner P., Insulin Resistance in Type 2 Diabetes - Role of the Adipokines, Current Molecular Medicine 2005; 5 (3) . https://dx.doi.org/10.2174/1566524053766022
DOI https://dx.doi.org/10.2174/1566524053766022 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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