High- or low-salt diet from weaning to adulthood: Effect on body weight, food intake and energy balance in rats
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2006-03-01
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Coelho, M. S.
Passadore, M. D.
Gasparetti, A. L.
Bibancos, T.
Prada, P. O.
Furukawa, L. L.
Furukawa, LNS
Fukui, R. T.
Casarini, D. E.
Saad, MJA
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Objective: To get some additional insight on the mechanisms of the effect of salt intake on body weight.Design and methods: Rats were fed a tow (LSD), normal (NSD), or high (HSD) salt diet. in a first set, body weight, tail-cuff blood pressure, fasting plasma thyroid-stimulating hormone, triiodothyronine, L-thyroxine, glucose, insulin, and angiotensin II were measured. Angiotensin II content was determined in white and brown adipose tissues. Uncoupling protein 1 expression was measured in brown adipose tissue. in a second set, body weight, food intake, energy balance, and plasma leptin were determined. in a third set of rats, motor activity and body weight were evaluated.Results: Blood pressure increased on HSD. Body weight was similar among groups at weaning, but during adulthood it was tower on HSD and higher on LSD. Food intake, L-thyroxine concentration, uncoupling protein 1 expression and energy expenditure were higher in HSD rats, white non-fasting leptin concentration was lower in these groups compared to NSD and LSD animals. Plasma thyroid-stimulating hormone decreased on both HSD and LSD white plasma glucose and insulin were elevated only on LSD. A decrease in plasma angiotensin II was observed in HSD rats. On LSD, an increase in brown adipose tissue angiotensin II content was associated to decreased uncoupling protein 1 expression and energy expenditure. in this group, a low angiotensin II content in white adipose tissue was also found. Motor activity was not influenced by the dietary salt content.Conclusions: Chronic alteration in salt intake is associated with changes in body weight, food intake, hormonal profile, and energy expenditure and tissue angiotensin II content. (C) 2005 Elsevier B.V. All rights reserved.
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Nutrition Metabolism and Cardiovascular Diseases. Oxford: Elsevier B.V., v. 16, n. 2, p. 148-155, 2006.