Abstract
BackgroundOveractivity 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.MethodsWe 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.ResultsThe 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.ConclusionsThese 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.
Highlights
Overactivity and/or dysregulation of the endocannabinoid system (ECS) contribute to development of obesity
The resistance against high-fat diet-induced adiposity in cannabinoid receptor 1 (CB1)-/- mice is associated with increased energy expenditure and reduced adipocyte size We first evaluated the adiposity-inducing effects of two high-fat diets in young CB1+/+ and CB1-/- mice
HF and high-fat/fish oil (HF/FO) feeding resulted in a comparable increase in fat mass compared to chow in CB1+/+ mice, while CB1-/- mice remained relatively lean on the HF and HF/FO diets (Figure 1B)
Summary
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. Adipose tissue represents an important peripheral node of the ECS and several in vitro studies indicate that CB1-receptor activity is critical for adipocyte function [5,6,7]. ECS signalling in adipocytes supposedly promotes lipid storage [6,11,12,13]via the induction of lipogenic genes and by increasing fatty acid uptake [5,6]. Since growth retardation in CB1-/mice is already apparent during the first weeks of life [5], appropriate CB1-receptor functioning may be critical for adipose tissue development in vivo
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