This study examined whether propolis, which had many biological activities, affected body fat and lipid metabolism. Four-week-old Wistar rats were fed a control or propolis diet for 8 wk. The control group was fed a high-fat diet, the low and the high group were fed a high-fat diet supplemented with 0.5% (w/w) and 0.05% (w/w) propolis, respectively. The weight of total white adipose tissue of the high group was lower than that of the control group. The level of PPARgamma protein in the adipose tissues of the high group was significantly lower than that of the control group. In plasma and the liver, the high group showed a significantly reduced level of cholesterol and triglyceride compared to the control group. The liver PPARalpha protein level of the high group was significantly higher than that of the control group. The liver HMG-CoA reductase protein in the high group was also significantly lower than that in the control group. Results from rats on an olive oil loading test were used to investigate whether propolis inhibited triglyceride absorption. The serum triglyceride level of the group, which received propolis corresponding to the daily dose of the high group, was significantly lower than that of the control group. It is possible that the administration of propolis improves the accumulation of body fat and dyslipidemia via the change of the expression of proteins involved in adipose depot and lipid metabolism.

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Nobiletin enhances differentiation and lipolysis of 3T3-L1 adipocytes and improves hyperglycemia and insulin resistance in obese (ob) diabetic ob/ob mice. We investigated the effects of nobiletin on lipid metabolism and accumulation of body fat in rats. The control group was fed a 20% high-fat diet and 1% cholesterol, and the nobiletin group was fed same diet supplemented with 0.1% (w/w) nobiletin. The rats were fed for 4 weeks. Weights of epididymal, perirenal, total white adipose tissues (WAT: mesenteric, perirenal, and epididymal), and the subcutaneous WAT in the nobiletin group were significantly lower than those in the control group. This decrease was brought about by nobiletin without affecting triglyceride (TG) levels in the liver and skeletal muscle. Plasma TG levels tended to be decreased by nobiletin. The size and diameter of WAT adipocytes in the nobiletin group were significantly lower than those in the control group. This decrease may be partly due to lower lipoprotein lipase (a major determinant for the development of obesity) levels in WAT of the nobiletin group than that of the control group. Plasma levels of high density lipoprotein cholesterol and apolipoprotein A-I increased significantly with administration of nobiletin. These results suggested a beneficial effect of nobiletin on lipid metabolism. However, no significant differences were observed between the nobiletin and the control groups in proteins such as ATP-binding cassette transporter A1, and sterol regulatory element-binding protein-1 in the liver, PPARγ and tumor necrosis factor-α (TNF-α) in WAT, and adiponectin and TNF-α in plasma.