Resistance to diet-induced adiposity in cannabinoid receptor-1 deficient mice is not due to impaired adipocyte function

Nutrition & Metabolism

Gertjan van Dijk²  Pieter JJ Sauer³  Folkert Kuipers¹  Vincent W Bloks³  Theo H van Dijk¹  Aycha Bleeker³  Trijnie Bos¹  Pieter T de Boer³  Anniek H Koolman²  Maaike H Oosterveer³ 

[1] Department of Laboratory Medicine, Center for Liver Digestive and Metabolic Diseases, University Medical Center Groningen; University of Groningen, P.O. Box 30.001 9700 RB Groningen, The Netherlands;Center for Behavior and Neurosciences, Unit Neuroendocrinology, University of Groningen, Nijenborgh 7, 9747 AG Groningen, The Netherlands;Department of Pediatrics, University Medical Center Groningen; University of Groningen, P.O. Box 30.001 9700 RB Groningen, The Netherlands

关键词: lipolysis;    lipogenesis;    fat tissue;    diet-induced adiposity;    CB₁-receptor;   

Others  :  820161
DOI  :  10.1186/1743-7075-8-93

 received in 2011-08-01, accepted in 2011-12-27,  发布年份 2011

【 摘 要 】

Background

Overactivity and/or dysregulation of the endocannabinoid system (ECS) contribute to development of obesity. In vitro studies indicate a regulatory role for the cannabinoid receptor 1 (CB₁) in adipocyte function and CB₁-receptor deficient (CB₁^-/-) mice are resistant to high fat diet-induced obesity. Whether this phenotype of CB₁^-/- mice is related to altered fat metabolism in adipose tissue is unknown.

Methods

We evaluated adipose tissue differentiation/proliferation markers and quantified lipogenic and lipolytic activities in fat tissues of CB₁^-/- and CB₁^+/+ mice fed a high-fat (HF) or a high-fat/fish oil (HF/FO) diet as compared to animals receiving a low-fat chow diet. Comparison between HF diet and HF/FO diet allowed to investigate the influence of dietary fat quality on adipose tissue biology in relation to CB₁ functioning.

Results

The adiposity-resistant phenotype of the CB₁^-/- mice was characterized by reduced fat mass and adipocyte size in HF and HF/FO-fed CB₁^-/- mice in parallel to a significant increase in energy expenditure as compared to CB₁^+/+ mice. The expression levels of adipocyte differentiation and proliferation markers were however maintained in these animals. Consistent with unaltered lipogenic gene expression, the fatty acid synthesis rates in adipose tissues from CB₁^-/- and CB₁^+/+ mice were unchanged. Whole-body and adipose-specific lipoprotein lipase (LPL) activities were also not altered in CB₁^-/- mice.

Conclusions

These findings indicate that protection against diet-induced adiposity in CB₁-deficient mice is not related to changes in adipocyte function per se, but rather results from increased energy dissipation by oxidative and non-oxidative pathways.

【 授权许可】

   
2011 Oosterveer et al; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

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