Red mold rice prevents the development of obesity, dyslipidemia and hyperinsulinemia induced by high-fat diet

Abstract

Objective: To investigate the influences of red mold rice (RMR) on obesity and related metabolic abnormalities. Methods and results:The 3T3-L1 cell line was used to examine the effects of RMR extracts on preadipocytes and on mature adipocytes. Both water and ethanol extracts of RMR had inhibitory effects on 3T3-L1 preadipocyte proliferation and differentiation. Water extracts of RMR enhanced the lipolysis activity in mature adipocytes, which negatively correlated with the triglyceride content within cells. RMR treatment did not affect heparin-releasable lipoprotein lipase activity in mature adipocytes. Furthermore, animal studies were carried out to explore the antiobesity effects of RMR. The control group of male Wistar rats were fed regular laboratory feed, whereas the other groups were fed the high-fat (HF) diet supplemented with lovastatin, rice or RMR (0.4 and 2%, w w À1 ). The relative caloric intakes of the control and HF groups were 3.34 and 4.85 kcal g À1 , respectively. After 6 weeks, rats treated with RMR at the 0.4 and 2% doses had lower weight gain and less fat pads mass accompanied with smaller fat cells than did the HF-diet rats. These effects probably resulted from an increase in the lipolysis activity of adipose tissue and a reduction in food/energy consumption. On the other hand, the RMR supplement significantly reduced serum total cholesterol, serum low-density lipoprotein (LDL) cholesterol, the ratio of LDL to high-density lipoprotein (HDL) cholesterol and serum insulin in the HF group. Moreover, the 2% RMR treatment significantly increased serum HDL cholesterol. Conclusion: This study reveals for the first time that RMR can prevent body fat accumulation and improve dyslipidemia. The antiobesity effects of RMR mainly derive from the lipolytic activity and mild antiappetite potency of RMR. In addition, extracts of RMR suppressed the proliferation and differentiation in 3T3-L1 preadipocytes, which might have contributed to the inhibition of new adipocyte formation or hyperplasia in adipose tissue.

A high-fat diet as a model of fatty liver disease in rats

“…However, since the energy density of the HF diet was higher than the energy density of the control diet, i.e., 6.57 kcal/g versus 4.17 kcal/g, both groups consumed the same amount of calories. The present data agree with those reported by Chen et al 21 , who also observed a reduced food consumption in animals receiving an HF+ diet compared to control.…”

“…Also, Akagiri Akagiri et al 22 , in a 14 week study, did not detect significant differences in weight gain between animals fed the HF diet and controls, although the first one tended to gain more weight. In contrast, Chen et al 21 , after six weeks of study, observed that rats receiving a high-calorie HF diet (22.4% more energy than the control diet) gained more weight than rats receiving a normal diet. The same result was obtained by Matsuzawa-Nagataa et al 23 , after 24 weeks of administration of the HF diet.…”

Influence of dietary macronutrient composition on adiposity and cellularity of different fat depots in Wistar rats

“…The enlargement of this fat depot may be the result of an increase in the number of adipocytes (hyperplasia) or an increase in adipocyte size by lipid accumulation (hypertrophy). Moreover, hyperplasia can be due to the presence of new preadipocytes or to an induction of its differentiation (8). It is known that the most severe form of obesity is characterized by an adipose tissue enlargement as a consequence of adipocyte hyperplasia (18) and that it is related with an early age of onset (10).…”

Nutraceuticals and dyslipidaemia: Beyond the common therapeutics

“…Many studies have evaluated the potential role of nutraceuticals in the prevention of dyslipidaemia both in animal models (Alshatwi et al, 2011;Chen et al, 2008;Dvir et al, 2009;Huang & Lin, 2012a, 2012b and in humans (Becker et al, 2009;CasasAgustench et al, 2012;Demonty et al, 2006;Dulin et al, 2006;Garaiova et al, 2013;Gonç alves et al, 2006;Guardamagna et al, 2011;Izzo et al, 2010;Maki et al, 2012;Marazzi et al, 2011;Pá rraga et al, 2011;Qin et al, 2009;Rayman et al, 2011;Sirtori et al, 2009;Tomé -Carneiro et al, 2012;Weingä rtner, Bö hm, & Laufs, 2009;Wofford et al, 2012;Wong et al, 2010;Zhao et al, 2011).…”