English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

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 (CB 1 ) in adipocyte function and CB 1 -receptor deficient ( CB 1  -/-  ) mice are resistant to high fat diet-induced obesity. Whether this phenotype of  CB 1  -/-   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  CB 1  -/-   and  CB 1  +/+   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 CB 1  functioning.    Results  The adiposity-resistant phenotype of the  CB 1  -/-   mice was characterized by reduced fat mass and adipocyte size in HF and HF/FO-fed  CB 1  -/-   mice in parallel to a significant increase in energy expenditure as compared to  CB 1  +/+   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  CB 1  -/-   and  CB 1  +/+   mice were unchanged. Whole-body and adipose-specific lipoprotein lipase (LPL) activities were also not altered in  CB 1  -/-   mice.    Conclusions  These findings indicate that protection against diet-induced adiposity in  CB 1  -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.

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