Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Potassium depletion (-K) is a common electrolyte abnormality in elderly humans, occurring after diuretic use or poor oral intake. We hypothesized that aging would result in an increase in renal membrane lipid metabolism in both control and -K, and that the Na/H exchanger's protein abundance to -K would be blunted. Young and senescent non-obese male Fisher 344 x Brown-Norway F1 rats (F344 x BNF1) were fed either a normal or a K-deficient diet for 7 days. At 24-h, 32P incorporation was measured for renal cortical brush-border (BBM) and basolateral membrane (BLM) lipid metabolism. All -K animals showed a reduction in total body potassium stores, a fall in plasma aldosterone, a urinary concentrating defect, and an increase in plasma cholesterol and urine ammonium excretion (p < .001). In BBM of both age groups, -K increased phosphatidylserine, sphingomyelin, phosphatidylcholine, and phosphatidylethanolamine concentrations, but 32P incorporation fell. In BLM of young K-depleted rats, however, only phosphatidylcholine concentration increased. In the hypokalemic aged rats, the concentration of all BLM phospholipids rose, whereas 32P incorporation fell. In both membranes, cholesterol concentration and the molar ratio of cholesterol to total phospholipid increased with -K (p < .05). Potassium depletion caused brush-border membrane NHE-3 protein abundance to rise, but only in the young rats. Neither NHE-3 nor basolateral NHE-1 protein abundance was affected in aged animals with -K. These results provide the first evidence, in non-obese aged rats, that selective age-associated modifications occur in membrane lipid metabolism and membrane transporter protein abundance during -K. That aging causes a maladaptive response in brush-border NHE-3 protein expression may have important implications for elderly humans, particularly if they are given diuretics and become potassium depleted.
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PMID:Potassium depletion: renal membrane lipid metabolism and Na/H exchanger abundance in aged F344 x BNF1 rats. 1053 41

Renal cortical brush-border (BBM), basolateral membrane (BLM), and medullary plasma membrane (mPM) preparations were analyzed to assess the effects of life-long food restriction in aged rats on membrane lipid content. Young male Fischer 344 x Brown-Norway F1 rats consumed food ad libitum (young AL) or were food-restricted (FR, 60% of AL consumption) for either 6 weeks (young FR) or until the age of 30 months old (old FR). Senescent FR rats had 50 per cent decreases in fractional excretion of Na and K (p < 0.001) as compared with the young AL rats. Long-term FR reduced phosphate and titratable acid excretion by 80 per cent (p < 0.001). These values were not significantly different from those observed in young rats during 6 weeks of FR. Food restriction decreased renal Na, K-ATPase activity by 50 per cent (p < 0.001) in both old and young FR animals. Reduction of food intake, in old and young rats, decreased all BBM phospholipid concentrations (phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin) by 50 per cent than in the AL rats (p < 0.001). In BLM, chronic FR resulted only in lower phosphatidylcholine concentration (by 21%, p < 0.05) while phosphatidylethanolamine was increased approximately 80 per cent (p < 0.001). Total phospholipid content in mPM was progressively decreased by 23 per cent (p < 0.05) in the young FR group to be 55 per cent (p < 0.001) in the old FR rats. Cholesterol content was reduced in BBM and mPM by 38 per cent and 25 per cent (p < 0.05), respectively, during long-term FR. Both total phospholipid and cholesterol contents detected in mPM of the old FR rats were significantly lower than those obtained from the young FR animals (by 42%, p < 0.001 and 12%, p < 0.05, respectively). Plasma glucose, blood urea nitrogen, and body weight maintained at significantly lower levels during chronic FR. That life-long FR could prevent renal membrane lipid deposition and could lower renal work may explain the mechanisms that FR can delay the onset and diminish the severity of age-associated renal diseases.
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PMID:Life-long food restriction prevents renal membrane lipid deposition and lowers renal work in rats. 1152 48