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Biomedical subjects

H M Linkswiler

Publications and source records attributed to H M Linkswiler.

At least 19 recordsLinked to original sources
PubMed1982

Effects on Ca and P metabolism in humans by adding meat, meat plus milk, or purified proteins plus Ca and P to a low protein diet.

The effects on calcium and phosphorus metabolism of adult man by adding meat or meat plus dairy products to a diet low in protein (55 g), calcium (590 mg), and phosphorus (890 mg) were determined. When the low protein diet was consumed, the subjects retained a mean of 20 mg calcium daily but lost 106 mg phosphorus. The addition of meat which increased protein and phosphorus to 146 g and 1660 mg, respectively, caused calcium retention to decrease from 19 to -17 mg but phosphorus retention to increase from 106 to 55 mg. When the meat plus dairy diet high in protein (146 g), calcium (1370 mg), and phosphorus (2060 mg) was consumed the subjects retained substantial amounts of calcium (101 mg) and phosphorus (177 mg). The simulated diets high in purified proteins and supplemented with calcium and phosphorus affected calcium retention in a manner similar to the meat and meat plus dairy diets, but they had a marked negative effect on phosphorus retention; this indicates that supplements of calcium gluconate were well utilized but that those of monopotassium phosphate were not. The results obtained on urinary sulfate, acid, cyclic AMP and hydroxyproline support the conclusions made from the calcium and phosphorus data.

Absorption↗
PubMed1981

Calcium metabolism in postmenopausal and osteoporotic women consuming two levels of dietary protein.

Eight postmenopausal women, four with osteoporosis diagnosed by their physician and four without, participated in a metabolic study to investigate the effects of level of protein intake on calcium metabolism; renal acid excretion; plasma total and ultrafiltrable calcium; 1,25-dihydroxyvitamin D; and serum immunoreactive parathyroid hormone. Radial bone mineral content was evaluated. Protein intake was 50 g/day during the 1st 15-day experimental period and 110 g during the 2nd period. Calcium, magnesium, and phosphorus intakes were held constant at 713, 323, and 1078 mg/day. The increase in protein intake significantly increased net calcium absorption and urinary calcium. A calcium intake of 713 mg was not sufficient for calcium balance for most of the women studied. The calciuretic effect of increased protein intake was associated with increased renal acid excretion. None of the plasma and serum measurements mentioned above was significantly affected by the level of protein intake except for a slight increase in plasma total calcium. No significant differences in radial bone mineral content or in any of the other measurements were observed between the osteoporotic and the normal group of women.

Absorption↗
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

Long-term effects of level of protein intake on calcium metabolism in young adult women.

The long-term effect of level of protein intake on calcium metabolism, renal function and renal acid excretion was determined during a 75-day metabolic study. Six women consumed a diet containing either 46 or 123 g protein for 60 days; they then consumed the alternate diet for 15 days. Calcium, phosphorus and magnesium intakes were maintained constant at 500, 900 and 350 mg, respectively, throughout the 75-day study. Urinary calcium was remarkably constant with time at both levels of protein intake but was approximately twice as high when the 123 g protein diet was consumed. Level of protein intake had no effect on calcium absorption; the increase in urinary calcium found when the high protein diet was given, therefore, caused a markedly negative calcium balance. Glomerular filtration rate (GFR) and renal acid excretion were higher and fractional renal tubular reabsorption of calcium was lower when the high protein diet was given. The hypercalciuria caused by the high protein intake was due primarily to the decrease in fractional tubular reabsorption of calcium and, to a lesser extent, to the increase in GFR. Neither GFR, fractional renal tubular reabsorption of calcium nor any of the components of renal acid excretion exhibited any tendency to change with time over the 60-day experimental period.

Absorption↗
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↗
PubMed1979

Effect of level of protein intake on calcium metabolism and on parathyroid and renal function in the adult human male.

Mechanisms involved in the hypercalciuria caused by high levels of protein intake were investigated. Six healthy males participated in a 20-day metabolic study. During the first 10-day period, all subjects were given a 47 g protein diet and during the second 10-day period, a 142 g protein diet. Calcium, magnesium and phosphorus intakes were kept constant at 515, 320 and 1,110 mg daily, respectively. Urinary calcium was elevated significantly when the protein intake was increased. Glomerular filtration rate and calcium clearance were increased significantly when the high protein diet was fed; the fractional tubular reabsorption of calcium was decreased from 98.4 to 97.4%. Thus, the increase in urinary calcium caused by the high protein diet appears to be due in part to an increase in the filtered load of calcium by the glomeruli and in part to a decrease in calcium reabsorption by the renal tubules. The level of protein intake had no effect on the fasting serum concentrations of parathyroid hormone, total calcium, magnesium or inorganic phosphorus or plasma ultrafiltrable calcium.

Adult↗
PubMed1977

Metabolism of methionine in oral contraceptive users and control women receiving controlled intakes of vitamin B6.

The metabolism of methionine was studied in 10 control and in 14 women using estrogen-containing oral contraceptives during 28 days of vitamin B6 deficiency and then for another 28 days while ingesting the same diet with daily supplements of 0.8, 2.0, or 20.0 mg of pyridoxine hydrochloride. Urinary cystathionine excretion after a 3-g load of L-methionine increased promptly in both groups and continued to increase throughout the 28 days of vitamin B6 depletion; there was no significant difference in the amount excreted by controls and oral contraceptive users. Two milligrams of pyridoxine-HCl restored the cystathionine excretion to predepletion levels within three to four weeks for both control and oral contraceptive users. Daily supplements of 0.8 mg of pyridoxine-HCl for as long as four weeks failed to restore cystathionine excretion to normal levels for either controls or contraceptive users; supplements of 2.0 mg met the vitamin B6 requirements for both groups. Urinary methionine, cysteine sulfinic acid, and taurine excretion did not differ significantly between the two groups at any time. The data indicate that oral contraceptive users are not generally different from non-users with respect to vitamin B6 requirements as evidenced by methionine metabolism.

Adult↗
PubMed1975

Vitamin B6 requirements of women using oral contraceptives.

Fifteen women who used combined estrogen-progestogen oral contraceptives and nine control women were given a vitamin B6-deficient diet for 4 weeks and the same diet supplemented with 0.8, 2.0, or 20.0 mg of pyridoxine hydrochloride for an additional 4 weeks. At weekly intervals a variety of indices of vitamin B6 nutrition were measured to determine rates of depletion and repletion. The tryptophan load test (2.0 g) was significantly different in the contraceptive users. However, other indices, including urinary cystathionine (3.0 g L-methionine load), urinary 4-pyridoxic acid, plasma phosphate, and erythrocyte alanine and aspartate aminotransferases, were not significantly different. Since altered tryptophan metabolism persisted in contraceptive users even when other indices of vitamin B6 nutrition were normal, we suggest that the use of oral contraceptives specifically affects tryptophan metabolism by some means other than through a vitamin B6 deficiency.

Adult↗
PubMed1975

Effect of oral contraceptives and vitamin B6 deficiency on carbohydrate metabolism.

Oral glucose tolerance, urinary xanthurenic acid excretion, and plasma pyridoxal phosphate concentrations were determined in nine women taking oral contraceptives and in four controls. The tests were repeated after 4 weeks ingestion of a vitamin B6-deficient diet, and again after pyridoxine supplementation. Vitamin B6 deficiency, as judged by an increased xanthurenic acid excretion and reduced plasma pyridoxal phosphate, was associated with a deterioration in the glucose tolerance of the contraceptive steroid-treated group despite normal or elevated plasma insulin levels. This abnormality was reversed by pyridoxine. There was no change in the glucose tolerance of the vitamin B6-deficient controls. The observed pyridoxine-responsive alteration in carbohydrate metabolism may involve the complexing of insulin with xanthurenic acid with a consequent loss of biological activity. In addition, oral contraceptives may enhance gluconeogensis.

Adult↗
PubMed1975

Effects of oral contraceptives on tryptophan metabolism and vitamin B6 requirements in women.

To evaluate the effect of oral contraceptive usage on the nutritional requirement for vitamin B6, control women and oral contraceptive users were depleted of vitamin B6 for 1 month followed by a month of repletion with 0.8, 2.0, or 20.0 mg of pyridoxine hydrochloride per day. At weekly intervals a number of indices of vitamin B6 nutrition were measured. Marked elevation in excretion of tryptophan metabolites occurred in oral contraceptive users after tryptophan loads. However, other indices of vitamin B6 nutritional state, including urinary 4-pyridoxic acid excretion, urinary cystathionine excretion, plasma pyridoxal phosphate concentrations, and erythrocyte aspartate and alanine aminotransferases were not different between controls and oral contraceptive users. The excretion of metabolites after oral loading doses of L-kynurenine (which bypasses tryptophan oxygenase) was elevated in oral contraceptive users indicating that abnormal metabolism of tryptophan was not due only to induced tryptophan oxygenase. The data indicate that use of oral contraceptives does not generally change the requirement for vitamin B6 but rather produces a specific change in activity of enzymes beyond kynurenine in the pathway of tryptophan metabolism.

Adult↗