title: High- or low-salt diet from weaning to adulthood: effect on insulin sensitivity in Wistar rats.
abstract: Because of conflicting results in the literature, further studies are needed to confirm an association between the degree of salt consumption and insulin sensitivity. The aim of this study was to measure insulin sensitivity in rats fed from weaning to adulthood with a low (LSD), normal (NSD), or high (HSD) salt diet. Body weight, carcass lipid content, blood glucose, nonesterified fatty acids, plasma insulin, plasma renin activity, and a glucose transporter (GLUT4) were measured. A euglycemic hyperinsulinemic clamp was used in 52 anesthetized rats. Body weight was higher in rats on LSD than in those on NSD (P<0.05) or HSD (P<0.001). Percentage fat carcass content was higher (P<0.05) in rats on LSD than in those on NSD. Basal plasma insulin and glucose levels were not altered (P>0.05) by salt consumption. Nonesterified fatty acids were lower in rats on HSD than in those on LSD (P<0.05) or NSD (P<0.01). Glucose uptake was lower in rats on LSD than in those on NSD (P<0.05) or HSD (P<0. 001). When a euglycemic hyperinsulinemic clamp was used on pair-weight rats, similar results were obtained, which suggests that the effect of LSD on insulin sensitivity was not due to higher body weight. GLUT4 in insulin-sensitive tissues was increased in rats on HSD except in the cardiac muscle. Captopril treatment partially reversed low insulin sensitivity in LSD rats, whereas losartan did not change it, which indicates that the effect of LSD on insulin sensitivity is angiotensin independent. In conclusion, the present results demonstrate that chronic dietary salt restriction induces a decrease in insulin sensitivity not associated with renin-angiotensin system activity or body weight changes.
authors.affiliation: Nephrology Department, Laboratory of Hypertension, University of São Paulo School of Medicine, Brazil.
authors.forename: P
authors.initials: P
authors.lastname: Prada
authors.forename: M M
authors.initials: MM
authors.lastname: Okamoto
authors.forename: L N
authors.initials: LN
authors.lastname: Furukawa
authors.forename: U F
authors.initials: UF
authors.lastname: Machado
authors.forename: J C
authors.initials: JC
authors.lastname: Heimann
authors.forename: M S
authors.initials: MS
authors.lastname: Dolnikoff
mesh_terms: D000375:Aging / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D001835:Body Weight; D002216:Captopril / Q000494:pharmacology; D004039:Diet, Sodium-Restricted; D005947:Glucose / Q000493:pharmacokinetics; D051275:Glucose Transporter Type 4; D006946:Hyperinsulinism / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology*; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000032:analysis; D009124:Muscle Proteins; D051381:Rats; D017208:Rats, Wistar; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D014886:Weaning
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D051275:Glucose Transporter Type 4; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495694:Slc2a4 protein, rat; D017673:Sodium Chloride, Dietary; D002216:Captopril; D005947:Glucose; D019808:Losartan