期刊
CELL METABOLISM
卷 7, 期 5, 页码 421-433出版社
CELL PRESS
DOI: 10.1016/j.cmet.2008.04.005
关键词
-
资金
- NIDDK NIH HHS [R01 DK067509, DK067509, F32 DK075249-02, DK075249, F32 DK075249] Funding Source: Medline
Insulin resistance is a common disorder caused by a wide variety of physiological insults, some of which include poor diet, inflammation, anti-inflammatory steroids, hyperinsulinemia, and dyslipidemia. The common link between these diverse insults and insulin resistance is widely considered to involve impaired insulin signaling, particularly at the level of the insulin receptor substrate (IRS). To test this model, we utilized a heterologous system involving the platelet-derived growth factor (PDGF) pathway that recapitulates many aspects of insulin action independently of IRS. We comprehensively analyzed six models of insulin resistance in three experimental systems and consistently observed defects in both insulin and PDGF action despite a range of insult-specific defects within the IRS-Akt nexus. These findings indicate that while insulin resistance is associated with multiple deficiencies, the most deleterious defects and the origin of insulin resistance occur independently of IRS.
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