title: A high-fructose diet induces insulin resistance but not blood pressure changes in normotensive rats.
abstract: Rats fed a high-fructose diet represent an animal model for insulin resistance and hypertension. We recently showed that a high-fructose diet containing vegetable oil but a normal sodium/potassium ratio induced mild insulin resistance with decreased insulin receptor substrate-1 tyrosine phosphorylation in the liver and muscle of normal rats. In the present study, we examined the mean blood pressure, serum lipid levels and insulin sensitivity by estimating in vivo insulin activity using the 15-min intravenous insulin tolerance test (ITT, 0.5 ml of 6 microg insulin, iv) followed by calculation of the rate constant for plasma glucose disappearance (Kitt) in male Wistar-Hannover rats (110-130 g) randomly divided into four diet groups: control, 1:3 sodium/potassium ratio (R Na:K) diet (C 1:3 R Na:K); control, 1:1 sodium/potassium ratio diet (CNa 1:1 R Na:K); high-fructose, 1:3 sodium/potassium ratio diet (F 1:3 R Na:K), and high-fructose, 1:1 sodium/potassium ratio diet (FNa 1:1 R Na:K) for 28 days. The change in R Na:K for the control and high-fructose diets had no effect on insulin sensitivity measured by ITT. In contrast, the 1:1 R Na:K increased blood pressure in rats receiving the control and high-fructose diets from 117 +/- 3 and 118 +/- 3 mmHg to 141 +/- 4 and 132 +/- 4 mmHg (P < 0.05), respectively. Triacylglycerol levels were higher in both groups treated with a high-fructose diet when compared to controls (C 1:3 R Na:K: 1.2 +/- 0.1 mmol/l vs F 1:3 R Na:K: 2.3 +/- 0.4 mmol/l and CNa 1:1 R Na:K: 1.2 +/- 0.2 mmol/l vs FNa 1:1 R Na:K: 2.6 +/- 0.4 mmol/l, P < 0.05). These data suggest that fructose alone does not induce hyperinsulinemia or hypertension in rats fed a normal R Na:K diet, whereas an elevation of sodium in the diet may contribute to the elevated blood pressure in this animal model.
authors.affiliation: Departamento de Planejamento Alimentar e Nutrição, Faculdade de Economia e Administração, Universidade Estadual de Campinas, Campinas, SP, Brasil.
authors.forename: R M
authors.initials: RM
authors.lastname: Bezerra
authors.forename: M
authors.initials: M
authors.lastname: Ueno
authors.forename: M S
authors.initials: MS
authors.lastname: Silva
authors.forename: D Q
authors.initials: DQ
authors.lastname: Tavares
authors.forename: C R
authors.initials: CR
authors.lastname: Carvalho
authors.forename: M J
authors.initials: MJ
authors.lastname: Saad
authors.forename: J A
authors.initials: JA
authors.lastname: Gontijo
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects*; D004032:Diet; D005632:Fructose / Q000008:administration & dosage / Q000494:pharmacology*; D006946:Hyperinsulinism / Q000209:etiology; D006973:Hypertension / Q000209:etiology; D015228:Hypertriglyceridemia / Q000209:etiology; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome; D011188:Potassium / Q000008:administration & dosage; D051381:Rats; D017208:Rats, Wistar; D012982:Sodium, Dietary / Q000008:administration & dosage
chemical_list: D001786:Blood Glucose; D008055:Lipids; D012982:Sodium, Dietary; D005632:Fructose; D011188:Potassium