Identifying the links between obesity, insulin resistance and β-cell function:: potential role of adipocyte-derived cytokines in the pathogenesis of type 2 diabetes

被引：229
作者：
Greenberg, AS
McDaniel, ML [1 ]
机构：
[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA
[2] Tufts Univ, USDA, Jean Mayer Human Nutr Res Ctr Aging, Boston, MA 02111 USA
[3] Tufts Univ New England Med Ctr, Tupper Res Inst, Div Endocrinol, Boston, MA 02111 USA
来源：
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION | 2002年 / 32卷
关键词：
diabetes mellitus type 2; PPAR gamma; tumour necrosis factor-alpha; pathogenesis;
D O I：
10.1046/j.1365-2362.32.s3.4.x
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
A combination of insulin resistance and pancreatic beta-cell dysfunction underlies most cases of type 2 diabetes. While the interplay of these two impairments is believed to be important in the development and progression of type 2 diabetes, the mechanisms involved are unclear. A number of factors have been suggested as possibly linking insulin resistance and beta-cell dysfunction in the pathogenesis of type 2 diabetes mellitus. Pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNF-alpha) have deleterious effects on both glucose homeostasis and beta-cell function, and can disrupt insulin signalling pathways in both pancreatic beta cells and liver and adipose tissue. The anti-inflammatory activity of the thiazolidinedione anti-diabetic agents is potentially beneficial, given the possible role of pro-inflammatory cytokines in linking insulin resistance with beta-cell dysfunction.
引用
收藏
页码：24 / 34
页数：11
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