期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 286, 期 43, 页码 37458-37469出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.242651
关键词
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资金
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- National Center for Global Health and Medicine [21S116]
- Takeda Science Foundation
- Takeda Medical Science Foundation
- Grants-in-Aid for Scientific Research [21591151, 23126520, 23300257, 24651055, 23500971] Funding Source: KAKEN
Kruppel-like factor 15 (KLF15), a member of the Kruppel-like factor family of transcription factors, has been found to play diverse roles in adipocytes in vitro. However, little is known of the function of KLF15 in adipocytes in vivo. We have now found that the expression of KLF15 in adipose tissue is down-regulated in obese mice, and we therefore generated adipose tissue-specific KLF15 transgenic (aP2-KLF15Tg) mice to investigate the possible contribution of KLF15 to various pathological conditions associated with obesity in vivo. The aP2-KLF15 Tg mice manifest insulin resistance and are resistant to the development of obesity induced by maintenance on a high fat diet. However, they also exhibit improved glucose tolerance as a result of enhanced insulin secretion. Furthermore, this enhancement of insulin secretion was shown to result from down-regulation of the expression of stearoyl-CoA desaturase 1 (SCD1) in white adipose tissue and a consequent reduced level of oxidative stress. This is supported by the findings that restoration of SCD1 expression in white adipose tissue of aP2-KLF15 Tg mice exhibited increased oxidative stress in white adipose tissue and reduced insulin secretion with hyperglycemia. Our data thus provide an example of cross-talk between white adipose tissue and pancreatic beta cells mediated through modulation of oxidative stress.
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