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Identifying the links between obesity, insulin resistance and β‐cell function: potential role of adipocyte‐derived cytokines in the pathogenesis of type 2 diabetes
Author(s) -
Greenberg A. S.,
McDaniel M. L.
Publication year - 2002
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.32.s3.4.x
Subject(s) - insulin resistance , endocrinology , medicine , diabetes mellitus , beta cell , type 2 diabetes , pathogenesis , insulin , adipose tissue , tumor necrosis factor alpha , glucose homeostasis , adipocyte , immunology , biology , islet
A combination of insulin resistance and pancreatic β‐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 β‐cell dysfunction in the pathogenesis of type 2 diabetes mellitus. Pro‐inflammatory cytokines such as tumour necrosis factor‐α (TNF‐α) have deleterious effects on both glucose homeostasis and β‐cell function, and can disrupt insulin signalling pathways in both pancreatic β 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 β‐cell dysfunction.