) compared with wild-type mice.
When CB2-/- mice were maintained on a high-fat diet, their weight gain was not different from wild-type mice (gaining 19 and 21 g, respectively), whereas CB-DKO mice gained only 5 g. There were no significant differences in food intake or locomotor activity between the three groups. Respiratory exchange rate and heat production were elevated in CB-DKO mice, with upregulation of adipose tissue thermogenic genes. Glucose tolerance test and insulin levels indicated increased insulin sensitivity in CB-DKO mice, whereas CB2-/- displayed signs of impaired glucose clearance.
These results indicate that lacking both CB1R and CB2R protected mice from diet-induced obesity, possibly through the prominent role of CB1R in obesity or through an interactive effect of both receptors.
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