Background: Most obesities are known low in sympathetic activity, and brain neurotransmitters may play roles in the defective exhibitions of obesity. Caffeine, a stimulant, which can prompt lipolysis, has been applied on the therapy of obesity. Although the interactive combinations between caffeine and certain neurotransmitters has been appreciated recently, but its regulatory mechanisms are still obscure. This study investigated the effect of caffeine on the body fat deposition, and its interactions with brain serotonin and catecholamine in the genetically obese (ob/ob) mice.
Methods: At 12-week of age, obese mice and their lean counterparts (+/?) were administered with caffeine (4 mg/d) in water for 4 weeks. The brain neurotransmitters levels and body fat content were measured.
Results: The obese mice without caffeine treatment had lower brain norepinephrine and epinephrine levels than the lean controls. And there had no difference between obese and lean mice in brain levels of serotonin, tryptophan, and 5-hydroxyindoleacetic acid. Caffeine treatment showed no effect on the food intake, but decreased the body fat content significantly in obese mice. Mice with caffeine treatment showed increase of the levels of brain neurotransmitters in both phenotypes; this effect was more predominant in obese mice.
Conclusions: This study indicated that the effect of caffeine to decrease body fat deposition in the obese mice might be associated with the recovered increases of sympathetic activity.