Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 23, Pages 9888-9893Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0702448104
Keywords
mRNA; clock; diabetes; posttranscriptional; lipid
Categories
Funding
- NEI NIH HHS [EY11489, EY02414, R01 EY011489, R01 EY002414] Funding Source: Medline
- NIDDK NIH HHS [P30 DK063609, DK063609] Funding Source: Medline
- NIGMS NIH HHS [T32 GM008136, R01 GM076626, 2T32 GM008136-21, GM076626] Funding Source: Medline
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The mammalian circadian system consists of a central oscillator in the suprachiasmatic nucleus of the hypothalamus, which coordinates peripheral clocks in organs throughout the body. Although circadian clocks control the rhythmic expression of a large number of genes involved in metabolism and other aspects of circadian physiology, the consequences of genetic disruption of circadian-controlled pathways remain poorly defined. Here we report that the targeted disruption of Nocturnin (Ccrn41) in mice, a gene that encodes a circadian deadenylase, confers resistance to diet-induced obesity. Mice lacking Nocturnin remain lean on high-fat diets, with lower body weight and reduced visceral fat. However, unlike lean lipodystrophic mouse models, these mice do not have fatty livers and do not exhibit increased activity or reduced food intake. Gene expression data suggest that Nocturnin knockout mice have deficits in lipid metabolism or uptake, in addition to changes in glucose and insulin sensitivity. Our data support a pivotal role for Nocturnin downstream of the circadian clockwork in the posttranscriptional regulation of genes necessary for nutrient uptake, metabolism, and storage.
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