期刊
BIOCHEMICAL JOURNAL
卷 438, 期 -, 页码 283-289出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20110263
关键词
activating transcription factor 4 (ATF4); glucose tolerance; hepatic steatosis; high-carbohydrate diet (HCD); insulin sensitivity; stearoyl-CoA desaturase 1 (SCD1)
资金
- Ministry of Science and Technology of China [2009CB919001, 2010CB912502]
- National Natural Science Foundation [30871208, 30890043]
- Shanghai Institutes for Biological Sciences
- Chinese Academy of Sciences [SIBS2008006, CRC2010005]
- Science and Technology Commission of Shanghai Municipality [08DJ1400601]
- Clinical Research Center, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences
- Shanghai Scientific and Technological Innovation Action Plan [10JC1416900]
- Chinese Academy of Sciences
- Shanghai Municipality [08PJ1410700]
- China Postdoctoral Science Foundation
- K.C. Wong Education Foundation, Hong Kong
Chronic feeding of HCD (high-carbohydrate diet) is one of the major contributors to the prevailing of metabolic diseases. ATF4 (activating transcription factor 4) has been shown to play an important role in the regulation of glucose metabolism and obesity development; however, it is unclear how ATF4(-/-) mice respond to HCD. in the present study, we show that 8 weeks of HCD results in significant higher accumulation of TAGs (triacylglycerols) in livers and impairment in glucose tolerance in ATF4(+/+) mice, but not in ATF4(-/-) mice, compared with those on a normal diet. Meanwhile, energy expenditure is further enhanced by HCD in AM mice. Moreover, we show that ATF4 deficiency suppresses HCD-induced SCD1 (stearoyl-CoA desaturase 1) expression, furthermore, oral supplementation of the main product of SCD1 oleate (18:1) increases TAG accumulation in livers of ATF4(-/-) mice. Taken together, these results suggest that ATF4 deficiency is protective for HCD-induced hepatic steatosis and impairment of glucose tolerance and insulin sensitivity. Furthermore, the resistance to hepatic steatosis is at least in part due to suppression of SCD1 expression under HCD.
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