Disruption of the Cereblon Gene Enhances Hepatic AMPK Activity and Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice
- Authors
- Lee, Kwang Min; Yang, Seung-Joo; Kim, Yong Deuk; Choi, Yoo Duk; Nam, Jong Hee; Choi, Cheol Soo; Choi, Hueng-Sik; Park, Chul-Seung
- Issue Date
- Jun-2013
- Publisher
- AMER DIABETES ASSOC
- Citation
- DIABETES, v.62, no.6, pp.1855 - 1864
- Journal Title
- DIABETES
- Volume
- 62
- Number
- 6
- Start Page
- 1855
- End Page
- 1864
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/14498
- DOI
- 10.2337/db12-1030
- ISSN
- 0012-1797
- Abstract
- A nonsense mutation in cereblon (CRBN) causes a mild type of mental retardation in humans. An earlier study showed that CRBN negatively regulates the functional activity of AMP-activated protein kinase (AMPK) in vitro by binding directly to the alpha 1-subunit of the AMPK complex. However, the in vivo role of CRBN was not stuclied. For elucidation of the physiological functions of Crbn, a mouse strain was generated in which the Crbn gene was deleted throughout the whole body. In Crbn-deficient mice fed a normal diet, AMPK in the liver showed hyperphosphorylation, which indicated the constitutive activation of AMPK. Since Crbn-deficient mice showed significantly less weight gain when fed a high-fat diet and their insulin sensitivity was considerably improved, the functions of Crbn in the liver were primarily investigated. These results provide the first in vivo evidence that Crbn is a negative modulator of AMPK, which suggests that Crbn may be a potential target for metabolic disorders of the liver.
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