BACKGROUND: Leptin, produced by adipose tissue, apart from regulating food intake and energy expenditure, also has natriuretic activity. In this study we examined the effect of leptin on renal Na+, K+-ATPase responsible for active tubular sodium reabsorption, and compared the renal effects of leptin in lean and obese rats. MATERIAL/ METHODS: Male Wistar rats were either kept on normal laboratory chow or made obese by a high-calorie diet. The animals were placed in metabolic cages and urine was collected in 2-hour periods. RESULTS: In lean animals, leptin (1 mg/kg i.p.) caused a 139.5% increase in urine output, a 112.4% increase in natriuresis, and a 57.2% increase in the fractional excretion of sodium, but had no effect on the glomerular filtration rate. Leptin at this dose decreased renal medullary Na+, K+-ATPase activity at 30 minutes, 1 hour and 2 hours by 31%, 34.3% and 21.2%, respectively. The effect of leptin on Na+, K+-ATPase at 1 hour was dose-dependent; the lowest dose inducing significant inhibition was 0.25 mg/kg. By contrast, leptin had no effect on either cortical Na+, K+-ATPase or the ouabain-resistant fraction of ATPase. In obese rats, leptin increased urine output by only 29.1% and natriuresis by 28.9%, and had no significant effect on medullary Na+, K+-ATPase. CONCLUSIONS: Leptin stimulates natriuresis primarily by inhibiting tubular sodium reabsorption. This effect is mediated, at least partially, by decreased Na+, K+-ATPase activity in the renal medulla, and is impaired in obese rats.
BACKGROUND:Leptin, produced by adipose tissue, apart from regulating food intake and energy expenditure, also has natriuretic activity. In this study we examined the effect of leptin on renal Na+, K+-ATPase responsible for active tubular sodium reabsorption, and compared the renal effects of leptin in lean and obeserats. MATERIAL/ METHODS: Male Wistar rats were either kept on normal laboratory chow or made obese by a high-calorie diet. The animals were placed in metabolic cages and urine was collected in 2-hour periods. RESULTS: In lean animals, leptin (1 mg/kg i.p.) caused a 139.5% increase in urine output, a 112.4% increase in natriuresis, and a 57.2% increase in the fractional excretion of sodium, but had no effect on the glomerular filtration rate. Leptin at this dose decreased renal medullary Na+, K+-ATPase activity at 30 minutes, 1 hour and 2 hours by 31%, 34.3% and 21.2%, respectively. The effect of leptin on Na+, K+-ATPase at 1 hour was dose-dependent; the lowest dose inducing significant inhibition was 0.25 mg/kg. By contrast, leptin had no effect on either cortical Na+, K+-ATPase or the ouabain-resistant fraction of ATPase. In obeserats, leptin increased urine output by only 29.1% and natriuresis by 28.9%, and had no significant effect on medullary Na+, K+-ATPase. CONCLUSIONS:Leptin stimulates natriuresis primarily by inhibiting tubular sodium reabsorption. This effect is mediated, at least partially, by decreased Na+, K+-ATPase activity in the renal medulla, and is impaired in obeserats.
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