title: Lipid metabolism of orchiectomised rats was affected by fructose ingestion and the amount of ingested fructose.
abstract: We examined whether lipid metabolism in orchiectomised (ORX) rats was affected by fructose ingestion and the amount of ingested fructose. Sucrose was used as a fructose source. Sham-operated and ORX rats were fed one of the following three diets for 28 d: a maize starch-based diet without sucrose (SU0), a diet by which half or all of maize starch was replaced by sucrose (SU50 or SU100). Body-weight gain and food intake were increased by sucrose ingestion, but decreased by ORX. Plasma total cholesterol concentration was increased by ORX and dose-dependently by sucrose ingestion. Plasma TAG concentration was decreased by ORX, but was increased dose-dependently by sucrose ingestion. Plasma insulin concentration was decreased by ORX, but was not affected by sucrose ingestion. Liver TAG was increased by sucrose ingestion and ORX; however, liver cholesterol concentration was not affected by sucrose ingestion and ORX. The hepatic activity of cholesterol 7α-hydroxylase 1 was not affected by sucrose ingestion and ORX; however, faecal excretion of bile acids was decreased. The mRNA level of microsomal TAG transfer protein, which is the gene related to hepatic VLDL production, was increased by ORX and sucrose ingestion. The mRNA level of uncoupling protein-1 was decreased by ORX, but not by sucrose ingestion. Plasma insulin concentration tended to correlate with the level of sterol-regulatory element-binding protein-1c mRNA (r 0·747, P = 0·088). These results show that lipid metabolism in ORX rats would be affected by the consumption of fructose-rich sweeteners such as sucrose and high-fructose syrup.
authors.affiliation: Department of Biological Resources, Faculty of Agriculture, Ehime University, 3-5-7 Tarumi, Matsuyama 790-8566, Japan.
authors.forename: Satoru
authors.initials: S
authors.lastname: Makino
authors.forename: Taro
authors.initials: T
authors.lastname: Kishida
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Ebihara
mesh_terms: D000375:Aging; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D005632:Fructose / Q000008:administration & dosage / Q000009:adverse effects*; D005786:Gene Expression Regulation; D006937:Hypercholesterolemia / Q000209:etiology; D015228:Hypertriglyceridemia / Q000209:etiology; D007006:Hypogonadism / Q000097:blood / Q000209:etiology / Q000378:metabolism*; D050356:Lipid Metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008297:Male; D009919:Orchiectomy / Q000009:adverse effects; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D002785:Sterol O-Acyltransferase / Q000235:genetics / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D013395:Sucrose / Q000008:administration & dosage; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001057:Apolipoproteins E; D002352:Carrier Proteins; D012333:RNA, Messenger; C497389:Srebf1 protein, rat; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; C106092:microsomal triglyceride transfer protein; D005632:Fructose; D013395:Sucrose; D002785:Sterol O-Acyltransferase