| Deficient of a clock gene, brain and muscle Arnt-like protein-1 (BMAL1), induces dyslipidemia and ectopic fat formation. | |
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MedLine Citation:
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PMID: 21966465 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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A link between circadian rhythm and metabolism has long been discussed. Circadian rhythm is controlled by positive and negative transcriptional and translational feedback loops composed of several clock genes. Among clock genes, the brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor output cycles kaput (CLOCK) play important roles in the regulation of the positive rhythmic transcription. In addition to control of circadian rhythm, we have previously shown that BMAL1 regulates adipogenesis. In metabolic syndrome patients, the function of BMAL1 is dysregulated in visceral adipose tissue. In addition, analysis of SNPs has revealed that BMAL1 is associated with susceptibility to hypertension and type II diabetes. Furthermore, the significant roles of BMAL1 in pancreatic β cells proliferation and maturation were recently reported. These results suggest that BMAL1 regulates energy homeostasis. Therefore, in this study, we examined whether loss of BMAL1 function is capable of inducing metabolic syndrome. Deficient of the Bmal1 gene in mice resulted in elevation of the respiratory quotient value, indicating that BMAL1 is involved in the utilization of fat as an energy source. Indeed, lack of Bmal1 reduced the capacity of fat storage in adipose tissue, resulting in an increase in the levels of circulating fatty acids, including triglycerides, free fatty acids, and cholesterol. Elevation of the circulating fatty acids level induced the formation of ectopic fat in the liver and skeletal muscle in Bmal1 -/- mice. Interestingly, ectopic fat formation was not observed in tissue-specific (liver or skeletal muscle) Bmal1 -/- mice even under high fat diet feeding condition. Therefore, we were led to conclude that BMAL1 is a crucial factor in the regulation of energy homeostasis, and disorders of the functions of BMAL1 lead to the development of metabolic syndrome. |
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Authors:
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Shigeki Shimba; Tomohiro Ogawa; Shunsuke Hitosugi; Yuya Ichihashi; Yuki Nakadaira; Munehiro Kobayashi; Masakatsu Tezuka; Yasuhiro Kosuge; Kumiko Ishige; Yoshihisa Ito; Kazuo Komiyama; Yuko Okamatsu-Ogura; Kazuhiro Kimura; Masayuki Saito |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-09-22 |
Journal Detail:
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Title: PloS one Volume: 6 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2011 |
Date Detail:
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Created Date: 2011-10-03 Completed Date: 2012-02-10 Revised Date: 2012-05-07 |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e25231 Citation Subset: IM |
Affiliation:
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Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba, Japan. shimba.shigeki@nihon-u.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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ARNTL Transcription Factors
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deficiency*,
genetics Adipose Tissue / metabolism Animals Cholesterol / metabolism Dyslipidemias / etiology*, genetics, metabolism* Fatty Acids / metabolism Liver / metabolism Male Mice Mice, Mutant Strains Muscle, Skeletal / metabolism Triglycerides / metabolism |
| Chemical | |
Reg. No./Substance:
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0/ARNTL Transcription Factors; 0/Arntl protein, mouse; 0/Fatty Acids; 0/Triglycerides; 57-88-5/Cholesterol |
| Comments/Corrections | |
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