Biomedical subjects

M B Zemel

Publications and source records attributed to M B Zemel.

80 records · Page 5Linked to original sources

PubMed1988

Salt sensitivity in blacks. Salt intake and natriuretic substances.

Accumulating evidence suggests that hypertension in blacks is manifested in part by impaired renal excretion of salt. Consequently, this study was performed to determine if hypertensive and normotensive black subjects differ in their ability to generate known natriuretic substances. Fourteen normotensive and 11 hypertensive blacks were maintained on constant metabolic diets containing either 40 or 180 mmol of salt per day for 14 days each. During the last 4 days of each salt intake period, urine was collected for measurement of sodium, dopamine, and norepinephrine. On the last day of each 14-day dietary period, blood pressures were measured, blood was collected for measurement of plasma atrial natriuretic factor (ANF) and aldosterone, and urine was collected over 2 hours for measurement of prostaglandin E2 (PGE2). Both the normotensive and the hypertensive groups manifested salt sensitivity; their mean arterial pressure rose by 7 +/- 0.2 and 6 +/- 0.2%, respectively, when salt intake was increased from 40 to 180 mmol/day. The hypertensive group exhibited decreased (p less than 0.05) dopamine excretion as compared with the normotensive group for both dietary salt intakes. Plasma ANF levels increased (p less than 0.05) in the hypertensive group, but not in the normotensive group, with increasing dietary salt. Plasma aldosterone and urinary norepinephrine and PGE2 were comparable in the two groups for both dietary salt intakes. These data suggest that salt sensitivity is not unique to hypertensive blacks but occurs in normotensive blacks as well. Decreased renal production of dopamine may be a pathogenic factor in the development and maintenance of hypertension in blacks.

Adult↗

PubMed1987

Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans.

Impaired glucose tolerance results from Cr restriction in animals, and Cr supplementation improves glucose tolerance in diabetic animals. These effects are presumably due to the role of Cr in glucose tolerance factor (GTF), a complex of Cr and nicotinic acid believed to facilitate insulin binding. Humans, however, do not uniformly respond to Cr supplementation. The present study was designed to evaluate the possibility that the failure results from inadequate levels of dietary nicotinic acid to serve as substrate for GTF synthesis. Sixteen healthy elderly volunteers were divided into three groups and given either 200 micrograms Cr, 100 mg nicotinic acid, or 200 micrograms Cr + 100 mg nicotinic acid daily for 28 days and evaluated on days 0 and 28. Fasting glucose and glucose tolerance were unaffected by either chromium or nicotinic acid alone. In contrast, the combined chromium-nicotinic acid supplement caused a 15% decrease in a glucose area integrated total (p less than .025) and a 7% decrease in fasting glucose. None of the treatments exerted any effect on fasting or one-hour insulin levels. Thus, these data suggest that the inability to respond to chromium supplementation may result from suboptimal levels of dietary nicotinic acid.

Aged↗

PubMed1981

Renal acid, urinary cyclic AMP, and hydroxyproline excretion as affected by level of protein, sulfur amino acid, and phosphorus intake.

Two 51-day human studies were conducted to investigate the effects of level of protein and phosphorus intake on the various components of renal acid excretion and on urinary sulfate, cyclic AMP and hydroxyproline; the role of the sulfur amino acids (Saa) of the protein was also evaluated. Dietary treatments included: 1) a 50 g protein diet; 2) a 150 g protein diet; and 3) a 50 g protein diet plus Saa to equal that of the 150 g protein diet, each given at 2 levels of phosphorus (1010 and 2525 mg). Calcium intake was 500 mg. Subjects were 16 young adult males. The results are discussed in relationship to calcium data previously reported (1, 2). Changes in renal acid and calcium excretion are not directly related for these reasons: a) the Saa accounted for all of the protein-induced increase in urinary sulfate and acid but for only 43% of the increase in urinary calcium and b) the acid phosphate supplement decreased urinary calcium but increased total acid excretion. The phosphorus supplement increased cyclic AMP but not hydroxyproline excretion. In fact, protein and Saa caused increases in hydroxyproline that were greatly reduced by the phosphorus supplement. Increases in urinary hydroxyproline and calcium were well correlated indicating that, at low calcium intakes, protein or Saa-induced increases in urinary calcium result in increased bone resorption which is reduced by the administration of phosphorus.

Acids↗

PubMed1981

Calcium metabolism in the young adult male as affected by level and form of phosphorus intake and level of calcium intake.

A 60-day human metabolic study was conducted to measure polyphosphate hydrolysis and to compare the effects of supplements of phosphorus from ortho- and polyphosphates as well as supplements of both calcium and orthophosphates on calcium metabolism. The experiment was arranged in a 4 x 4 latin square design with eight subjects and four 15-day dietary periods. During its passage through the digestive tract, the polyphosphate supplement was 80.5 +/- 5% hydrolyzed to orthophosphate. Calcium absorption was significantly lower when the polyphosphate supplement was given than when the orthophosphate supplement was given. Both forms of phosphate caused a reduction in fractional renal tubular reabsorption of calcium, but only the orthophosphate supplement improved calcium balance. Calcium equilibrium was achieved, however, only when supplements of both calcium and orthophosphate were given. Both phosphorus supplements caused an increase in urinary cyclic AMP, indicating an increase in parathyroid hormone (PTH) secretion, but bone resorption as measured by urinary hydroxyproline was not affected by either phosphate supplement. The combined supplement of calcium and orthophosphate, however, caused decreases in the excretion of both cyclic AMP and hydroxyproline, suggesting a decrease in PTH-mediated bone resorption.

Adolescent↗

PubMed1981

Role of the sulfur-containing amino acids in protein-induced hypercalciuria in men.

A human metabolic study was conducted to determine what part sulfur-containing amino acids play in protein-induced hypercalciuria. The effects on the renal handling of calcium of increasing dietary protein from 50 to 150 g protein were compared with those of increasing the sulfur amino acids to simulate the amounts present in the 150 g protein diet; we also evaluated the effects of adding a 1.5 g supplement of phosphorus to the 50 g protein diet containing the sulfur amino acids. An increase in protein intake caused urinary calcium to double, increased glomerular filtration rate and decreased fractional renal tubular reabsorption of calcium and urinary sodium. Sulfur amino acids added to the low protein diet also caused urinary calcium to increase and fractional tubular reabsorption of calcium and urinary sodium to decrease, but the changes were only 43, 44 and 66%, respectively, those caused by the increase in protein. The phosphorus supplement effectively prevented the hypercalciuria caused by adding the sulfur amino acids to the low protein diet.

Absorption↗

PubMed1981

Urinary calcium and calcium balance in young men as affected by level of protein and phosphorus intake.

Eight young adult males were subjects in a 51-day metabolic study conducted to examine the effects of level of protein and of phosphorus intake on urinary calcium and calcium balance. Two levels of protein (50-150 g) were given at each of two levels of phosphorus intake (1,010 and 2,525 mg). Dietary calcium and magnesium were maintained at 500 and 350 mg, respectively. Raising the protein intake from 50 to 150 g caused a calciuresis at both phosphorus intakes, but the actual increase in urinary calcium was 71 mg/day greater at the low than at the high phosphorus intake and calcium balance was changed from 24 to -116 mg/day at the low phosphorus intake and from 8 to -25 mg/day at the high. When the phosphorus intake was raised, urinary calcium decreased from 156 to 93 mg/day at the low protein intake and from 334 to 200 mg/day at the high protein intake and the markedly negative calcium balance found at the high protein intake was greatly improved. Simultaneous increases in protein and phosphorus intakes caused a 28% increase in urinary calcium whereas the increase in protein intake alone caused a 115% increase.

Absorption↗

PubMed1981

Protein-induced hypercalciuria.

Under controlled dietary conditions the level of dietary protein has a profound and sustained effect on urinary calcium and calcium retention of man. Young adults achieve calcium balance at low intakes of 500 mg calcium and 700 to 1,000 mg phosphorus when protein intake is 50 g. Large calcium losses occur at the same calcium and phosphorus intakes when the protein intake is increased approximately threefold. The protein-induced hypercalciuria is due mainly to a decrease in fractional renal tubular reabsorption of calcium, although an increase in glomerular filtration rate is also involved. The changes in kidney function appear to result from the catabolism of excess dietary sulfur amino acids to sulfate and the subsequent excretion of sulfate in the urine. An increase in both protein and phosphorus intakes has a much less dramatic effect on urinary calcium and calcium retention than an increase in protein intake alone. An increase in dietary phosphorus greatly reduces urinary calcium by increasing the fractional renal tubular reabsorption of calcium. It appears therefore that high protein intakes may increase the requirements for both calcium and phosphorus.

Calcium↗

PubMed1980

Studies on the mechanism of protein-induced hypercalciuria in older men and women.

A human metabolic study was conducted to observe the effect of level of protein intake on urinary calcium, calcium absorption and calcium balance in older adults and to further study the mechanisms of protein-induced hypercalciuria. An increase in protein intake from about 47 to 112 g while maintaining calcium, magnesium and phosphorus intakes constant caused an increase in urinary calcium and a decrease in calcium retention. Glomerular filtration rate was increased and fractional renal tubular reabsorption was decreased by the increase in protein intake; total renal acid, ammonium and sulfate excretions more than doubled, whereas urinary sodium decreased by 38%. The changes in urinary calcium were positively correlated with the increase in total renal acid and sulfate excretion as well as with the decrease in fractional renal tubular reabsorption of calcium. Thus, the data indicate that protein-induced hypercalciuria is due to an increase in glomerular filtration rate and a decrease in fractional renal tubular reabsorption of calcium, the latter of which may be caused by the increased acid load on the renal tubular cells.

Adult↗