期刊
CELL METABOLISM
卷 9, 期 3, 页码 252-264出版社
CELL PRESS
DOI: 10.1016/j.cmet.2009.01.011
关键词
-
资金
- United States Public Health Service [R01 DK-40936, P30 DK-45735, K23 RR-17404, R01 DK-075772]
Peroxisome proliferator-activated receptor gamma coactivator-1 beta (PGC-1 beta) is known to be a transcriptional coactivator for SREBP-1, the master regulator of hepatic lipogenesis. Here, we evaluated the role of PGC-1 beta in the pathogenesis of fructose-induced insulin resistance by using an antisense oligonucletoide (ASO) to knockdown PGC-1 beta in liver and adipose tissue. PGC-1 beta ASO improved the metabolic phenotype induced by fructose feeding by reducing expression of SREBP-1 and downstream lipogenic genes in liver. PGC-1 beta ASO also reversed hepatic insulin resistance induced by fructose in both basal and insulin-stimulated states. Furthermore, PGC-1 beta ASO increased insulin-stimulated whole-body glucose disposal due to a threefold increase in glucose uptake in white adipose tissue. These data support an important role for PGC-1 beta in the pathogenesis of fructose-induced insulin resistance and suggest that PGC-1 0 inhibition may be a therapeutic target for treatment of NAFLD, hypertriglyceridemia, and insulin resistance associated with increased de novo lipogenesis.
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