The effect of high-amylose cornstarch on lipid metabolism in OVX rats is affected by fructose feeding.
We examined whether the effects of high-amylose cornstarch (HACS) on lipid metabolism in ovariectomized (OVX) rats were affected by high-fructose feeding. Sucrose (482 g/kg diet) was used as fructose source. OVX rats were fed one of the following four diets for 21 days: a sucrose-based or cornstarch-based cholesterol-free diet with or without HACS (150 g/kg diet). Body weight and food intake were increased by sucrose. Plasma total cholesterol and low-density lipoprotein cholesterol concentrations were increased by sucrose and decreased by HACS in cornstarch-fed rats, but not in sucrose-fed rats. Liver total lipids and concentrations of plasma and liver triacylglycerol (TAG) were increased by sucrose, whereas plasma TAG concentration was decreased by HACS, in sucrose-fed rats. However, liver cholesterol concentration was not affected by diet. The amount of cholesterol in small-intestinal contents was increased in sucrose-fed rats, but not in cornstarch-fed rats, but that of bile acids was not affected by diet. Fecal excretions of bile acids and neutral sterols were increased by HACS. The level of sterol-regulatory element-binding protein-1c mRNA was increased by sucrose and decreased by HACS in sucrose-fed rats, but not in cornstarch-fed rats. The level of farnesoid X receptor mRNA was decreased by sucrose and increased by HACS in cornstarch-fed rats, but not in sucrose-fed rats, as was the level of cholesterol 7alpha-hydroxylase mRNA. These results show that the effect of HACS on hyperlipidemia induced by ovarian hormone deficiency would be affected by the consumption of fructose-rich sweeteners such as sucrose and high-fructose syrup.
Liu
Xiong
X
Department of Biological Resources, Faculty of Agriculture, Ehime University, Matsuyama 790-8566, Japan.
Ogawa
Hiroshi
H
Kishida
Taro
T
Ebihara
Kiyoshi
K
D000688:Amylose / Q000008:administration & dosage*; D000818:Animals; D001647:Bile Acids and Salts / Q000032:analysis; D001835:Body Weight; D002790:Cholesterol 7-alpha-Hydroxylase / Q000235:genetics / Q000378:metabolism; D004032:Diet; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D005243:Feces / Q000737:chemistry; D005260:Female; D005632:Fructose / Q000008:administration & dosage*; D005766:Gastrointestinal Contents / Q000737:chemistry; D005786:Gene Expression Regulation; D006937:Hypercholesterolemia / Q000139:chemically induced / Q000517:prevention & control*; D050356:Lipid Metabolism / Q000235:genetics; D008055:Lipids / Q000032:analysis / Q000097:blood; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D010052:Ovariectomy; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics / Q000378:metabolism; D013213:Starch / Q000008:administration & dosage* / Q000737:chemistry; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D000099150:Receptor, Farnesoid X-Activated
D000688:Amylose; D001647:Bile Acids and Salts; D002790:Cholesterol 7-alpha-Hydroxylase; D004040:Dietary Carbohydrates; D005632:Fructose; D008055:Lipids; D018160:Receptors, Cytoplasmic and Nuclear; D013213:Starch; D051780:Sterol Regulatory Element Binding Protein 1; D000099150:Receptor, Farnesoid X-Activated; C532838:CYP7A1 protein, rat