期刊
SCIENCE
卷 322, 期 5907, 页码 1539-1543出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1160794
关键词
-
资金
- NIH
- American Diabetes Association [1-04-RA-47]
- Pennsylvania State Department of Health
- Core facilities at the University of Massachusetts
- National Institute of Diabetes and Digestive and Kidney Diseases
- Diabetes and Endocrinology Research Center [DK52530]
A high-fat diet causes activation of the regulatory protein c-Jun NH(2)-terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high- fat diet- induced insulin resistance in the liver. JNK1- dependent secretion of the inflammatory cytokine interleukin- 6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.
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