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Insights into insulin resistance and type 2 diabetes from knockout mouse models
Takashi Kadowaki
Takashi Kadowaki
Published August 15, 2000
Citation Information: J Clin Invest. 2000;106(4):459-465. https://doi.org/10.1172/JCI10830.
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Perspective

Insights into insulin resistance and type 2 diabetes from knockout mouse models

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Abstract

Authors

Takashi Kadowaki

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Figure 1

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Roles of PPARγ in the adipocyte. In this model, PPARγ acts at two steps ...
Roles of PPARγ in the adipocyte. In this model, PPARγ acts at two steps to regulate adipocyte size and insulin sensitivity. First, PPARγ promotes the differentiation of pre-adipocytes (P) to normal, insulin-sensitive, small adipocytes (S), a step that can be activated by providing artificial PPARγ agonists, the thiazolidinediones (TZD). PPARγ also plays a critical role in adipocyte hypertrophy and development of insulin resistance under a high-fat diet. In wild-type mice, such a diet promotes adipocyte hypertrophy, which converts small adipocytes (S) into large adipocytes (L). These latter cells, in turn, induce factors such as TNF-α and FFAs, which promote insulin resistance. PPARγ+/– animals therefore enjoy some protection from adipocyte hypertrophy and the development of insulin resistance under a high-fat diet. Adapted from ref. 38.

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