期刊
CELL METABOLISM
卷 14, 期 2, 页码 242-253出版社
CELL PRESS
DOI: 10.1016/j.cmet.2011.05.013
关键词
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资金
- FIMA
- UTE
- Department of Health of Gobierno de Navarra
- Linea Especial Nutricion, Obesidad y Salud Universidad de Navarra
- National Research Program Torres Quevedo
- Fundacion Pedro Barrie de la Maza y Condesa de Fenosa and Fundacion Echebano
- [FIS PI041321]
- [Mutua Madrilena]
Cardiotrophin-1 (CT-1) is a member of the gp130 family of cytokines. We observed that ct-1(-/-) mice develop mature-onset obesity, insulin resistance, and hypercholesterolemia despite reduced calorie intake. Decreased energy expenditure preceded and accompanied the development of obesity. Acute treatment with rCT-1 decreased blood glucose in an insulin-independent manner and increased insulin-stimulated AKT phosphorylation in muscle. These changes were associated with stimulation of fatty acid oxidation, an effect that was absent in AMPK alpha 2(-/-) mice. Chronic rCT-1 treatment reduced food intake, enhanced energy expenditure, and induced white adipose tissue remodeling characterized by upregulation of genes implicated in the control of lipolysis, fatty acid oxidation, and mitochondrial biogenesis and genes typifying brown fat phenotype. Moreover, rCT-1 reduced body weight and corrected insulin resistance in ob/ob and in high-fat-fed obese mice. We conclude that CT-1 is a master regulator of fat and glucose metabolism with potential applications for treatment of obesity and insulin resistance.
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