Effect Of Resistant Starch On Lipid Metabolism And Its Related Gene Express Level In Obese Mice Induced By High-fat-diet

Resistant starch is functional food similar with dietary fiber; it has a wide range of application in food additive and health food market for its good characteristics. Nowadays the research of resistant starch is in the ascendant. So our study started from its absorption and metabolism characteristics to discuss the physiological function of resistant starch.Objective:The study in our article is going to find out molecular mechanisms of resistant starch (RS) in weight and serum lipid level control, to investigate the effects of RS starch on the lipid metabolism-related mRNA in mice which were diet-induced obesity, thereby providing basic study for the development of RS foods.Methods:72Weight-and age-matched male C57BL/6J mice were choosed as subjects and randomly divided into7groups. They were fed for12week on a high-fat diet containing unmodified sweet potato starch, hydroxypropylated distarch phosphate, cross-linking and Octenyl Succinic Anhydride starch, and citric acid acetylated starch. After12weeks, serum lipid levels, weight and morphological changes of mice liver tissue were examined. Likewise, fatty acid synthese, sterol regulatory element binding protein1-c,3-hydroxy-3-methylglutary coenzyme A reductase mRNA levels were examined.Results:1. Impacts of RS on weight control of mice:After the mice were fed with high-fat-diet respectively which contained HPCL-SPS, CLOSA-SPS, SPS and CAAC-SPS for12weeks, their weights decreased. In comparison with the high-fat-diet group, the decrease of HPCL-SPS、CLOSA-SPS、CAAC-SPS group in weight was statistically significant (p<0.05), but RS group has no significant difference (p>0.05). There was no significantly different between SPS group and HF group in weight, however, compared with different RS group, it was statistically significant (p<0.05).2. The kidney, liver and spleen index of the mice fed with RS-containing group has no significant difference compared with mice in the high-fat-diet group and control group (p>0.05);but the fat index in HPCL-SPS, CLOSA-SPS, SPS and CAAC-SPS group was significantly decreased compared with HF group (p<0.05). It shows RS can surpress obese to some extent. 3. Impacts of RS on the serum lipid level of mice:The TG and VLDL level in HF group was significantly higher than other groups (p<0.05). Although the TG and VLDL level in every RS group has no significant difference, they were statistically significant among SPS group and RS group (p<0.05).However, TC、HDL-C和LDL-C level in mice with RS-containing high-fat-diet almost has no change.4. Morphological changes of mice liver tissue:SPS、HPCL-SPS、CLOSA-SPS、 CAAC-SPS group liver tissue has steatosis in different degrees. But compared with HF group, the hepatic lobule cell amount decreases, fat vacuoles in liver significantly reduced and had light degeneration and liver cell cord arranged in neat in these groups.5. Impacts of RS on the expression of FAS, SREBP-1C, HMGCR gene:The expression of FAS gene in CAAC-SPS、HPCL-SPS group was significantly different compared with HF group(p<0.05), the remaining has no significant difference (p>0.05). The expression of SREBP-1C gene in CAAC-SPS、HPCL-SPS, CLOSA group was significantly different compared with HF group(p<0.05), the remaining has no significant difference (p>0.05). The expression of HMGCR gene in CLOSA-SPS、 CAAC-SPS group was significantly different compared with HF group(p<0.05). There was slight change between HPCL-SPS and SPS group, the change has no significant difference (p<0.05).Conclusion:With the change of related gene expression level, those fed the RS diet had a significantly lower hepatic lipogenesis capacity in HF-diet induced obesity mice. In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively, which may be attributable to decreased fat lipogenesis in the liver. Its mechanism probably was that digestibility of starch influences hepatic glucose metabolism and absorption of cholesterol and tyiglycerides. So it affects the expression of SREBP-1C, thereby induced FAS down regulation, but also affects the expression of HMGCR.