To understand the molecular mechanisms underlying the influence of quercetin on the physiological effects of hyperlipidemia, we investigated its role in the prevention of high-fat diet (HFD)-induced obesity and found that it regulated hepatic gene expression related to lipid metabolism. Quercetin supplementation in mice significantly reduced the HFD-induced gains in body weight, liver weight, and white adipose tissue weight compared with the mice fed only with HFD. It also significantly reduced HFD-induced increases in serum lipids, including cholesterol, triglyceride, and thiobarbituric acid-reactive substance (TBARS). Consistent with the reduced liver weight and white adipose tissue weight, hepatic lipid accumulation and the size of lipid droplets in the epididymal fat pads were also reduced by quercetin supplementation. To further investigate how quercetin may reduce obesity, we analyzed lipid metabolism-related genes in the liver. Quercetin supplementation altered expression profiles of several lipid metabolism-related genes, including Fnta, Pon1, Pparg, Aldh1b1, Apoa4, Abcg5, Gpam, Acaca, Cd36, Fdft1, and Fasn, relative to those in HFD control mice. The expression patterns of these genes observed by quantitative reverse transcriptase-polymerase chain reaction were confirmed by immunoblot assays. Collectively, our results indicate that quercetin prevents HFD-induced obesity in C57B1/6 mice, and its anti-obesity effects may be related to the regulation of lipogenesis at the level of transcription.

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Cassia tora fiber supplement consisting of 2 g of soluble fiber extracted from Cassia semen (C. tora L.), 200 mg of alpha-tocopherol, 500 mg of ascorbic acid, and 300 mg of maltodextrin was formulated in a pack, and given to 15 type II diabetic subjects (seven men and eight women 57.1 +/- 2.9 years old) with instructions to take two packs per day for 2 months. Placebo contained maltodextrin only with a little brown caramel color. Lifestyle factors and dietary intakes of the subjects were not altered during the 2-month period. Serum total cholesterol was moderately (P < .1) decreased in the C. tora group compared with the age- and gender-matched placebo group, as was the ratio of apolipoprotein B to apolipoprotein A1 (P < .1). Levels of serum triglycerides and low-density lipoprotein-cholesterol tended to decrease more in the C. tora-supplemented group than in the placebo group. Serum alpha-tocopherol was increased (P < .01) but lipid peroxides were not significantly lower in the C. tora group. Fasting blood glucose, hemoglobin A1c, blood urea nitrogen, creatinine, and activities of serum aspartate aminotransferase and alanine aminotransferase were not changed by the fiber supplement. We concluded that C. tora supplements can help improve serum lipid status in type II diabetic subjects without serious adverse effects.