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Obesity (Silver Spring). 2011 Mar;19(3):659-61. doi: 10.1038/oby.2010.266. Epub 2010 Oct 28.

Impact of clock gene Bmal1 deficiency on nutritionally induced obesity in mice.

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  • 1Center for Molecular and Vascular Biology, KU Leuven, Leuven, Belgium.


To evaluate the hypothesis that the clock gene Bmal1 (brain and muscle arnt like protein-1) plays a role in the development of obesity, 5-week-old male Bmal1-deficient (Bmal1(-/-)) mice and wild-type littermates (Bmal1(+/+)) were kept on a high-fat diet (HFD) for 15 weeks. Despite an initial accelerated weight gain of Bmal1(-/-) mice, body weight and subcutaneous (SC) and gonadal (GON) adipose tissue mass were comparable to Bmal1(+/+) mice at the end of the diet period. Noninvasive magnetic resonance imaging scanning revealed a modest increase in fat content in Bmal1(-/-) mice after 10 weeks of HFD, whereas at the start and the end of the HFD feeding no differences were observed between both genotypes. After 15 weeks of HFD, adipocyte and blood vessel size and density were similar for Bmal1(+/+) and Bmal1(-/-) mice. However, the weight of major organs was significantly reduced in Bmal1(-/-) mice, confirming the premature ageing phenotype. Thus, we hypothesize that an initial accelerated increase in body weight and fat mass of Bmal1(-/-) mice on HFD may have been offset by the effect of premature ageing on organ weight, resulting in comparable weights after 15 weeks of HFD.

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