Genetic disruption of protein phosphatase 5 in mice prevents high-fat diet feeding-induced weight gain

被引：15
|
作者：
Grankvist, N. [1 ]
Honkanen, R. E. [1 ,2 ]
Sjoholm, A. [1 ,2 ]
Ortsater, H. [1 ]
机构：
[1] Karolinska Inst, Sodersjukhuset, Dept Clin Sci & Educ, Stockholm, Sweden
[2] Univ S Alabama, Coll Med, Dept Biochem & Mol Biol, Mobile, AL USA
来源：
FEBS LETTERS | 2013年 / 587卷 / 23期
关键词：
Diabetes; Protein phosphatase 5; High-fat diet; Knockout mouse; Obesity; Insulin sensitivity; PANCREATIC BETA-CELLS; GLUCOCORTICOID-RECEPTOR; INSULIN-RESISTANCE; C57BL/6J MICE; GLUCOSE; PP5; OBESITY; ISLETS; MOUSE; ATHEROSCLEROSIS;
D O I：
10.1016/j.febslet.2013.10.022
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The role of serine/threonine protein phosphatase 5 (PP5) in the development of obesity and insulin resistance associated with high-fat diet-feeding (HFD) was examined using PP5-deficient mice (Ppp5c(-/-)). Despite similar caloric intake, Ppp5c(-/-) mice on HFD gained markedly less weight and did not accumulate visceral fat compared to wild-type littermates (Ppp5c(+/+)). On a control diet, Ppp5c(-/-) mice had markedly improved glucose control compared to Ppp5c(+/+) mice, an effect diminished by HFD. However, even after 10 weeks of HFD glucose control in Ppp5c(-/-) mice was similar to that observed in Ppp5c(+/+) mice on the control diet. Thus, PP5 deficiency confers protection against HFD-induced weight gain in mice. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码：3869 / 3874
页数：6
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