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Biomedical subjects

A R Glass

Publications and source records attributed to A R Glass.

At least 55 records · Page 3Linked to original sources
PubMed1981

Changes in maternal serum total and free androgen levels in early pregnancy: lack of correlation with fetal sex.

The fetal testis actively produces androgens during early gestation. To determine whether this fetal production of androgens might be reflected by levels of androgens in maternal serum, which might then be a useful test for antenatal fetal sex determination, we measured serum testosterone (total and free) and serum dihydrotestosterone in 83 pregnant women whose fetuses ranged from 4 to 20 weeks in age. For no maternal serum androgen measured was there a significant difference between women carrying a male fetus and those carrying a female fetus, even when this comparison was limited to various 4-week subintervals or fetal age. Total serum testosterone correlated directly with fetal age (r = 0.341, p less than 0.005), but serum dihydrotestosterone did not (r = 0.146, p = NS). Inverse correlations with fetal age were observed for percentage free testosterone (r = -0.531, p less than 0.001) as well as absolute serum free testosterone (r = -0.349, p less than 0.005). We conclude that maternal serum androgen levels are not useful for antenatal fetal sex determination in early pregnancy. The reason for the progressive fall in serum free testosterone, and presumably androgen production, during early gestation remains obscure.

Dihydrotestosterone↗
PubMed1981

Normal valine disposal in obese subjects with impaired glucose disposal: evidence for selective insulin resistance.

Insulin has major effects on both glucose and branched chain amino acid metabolism. To determine whether the insulin resistance of obesity equally affects both glucose and branched chain amino acid metabolism, we measured the ability of obese and normal subjects to dispose of intravenous bolus dose of glucose (25 g) or L-valine (4 g). Basal plasma glucose levels were the same in the 18 normal and 17 obese (163 plus or minus 8% of ideal body weight) subjects, but basal plasma insulin levels were higher in the obese group (15 plus or minus 2 vs 6 plus or minus 1 microU/ml; p less than 0.001). The obese group had a slower glucose disappearance rate after glucose challenge (0.84 plus or minus 0.06 vs. 1.11 plus or minus 0.07 hr(-1); p less than 0.01) despite having a greater serum insulin response to the glucose load (26 plus or minus 4 vs 11 plus or minus 1 insulin area units; p less than 0.01), confirming insulin resistance. In contrast, disposal of a valine load was the same in normal and obese subjects, as assessed by initial and second phase exponential disappearance rates, metabolic clearance rates of valine, and volumes of distribution. In normal men, disposal rates of glucose and valine after simultaneous administration of both substances were slower than corresponding disposal rates determined when each substance was given alone. We conclude that obese subjects with impaired glucose disposal have normal valine disposal, suggesting that the insulin resistance of obesity can be selective in its effect on different metabolic systems. Glucose and valine also appear to mutually antagonize each other's disposal.

Blood Glucose↗
PubMed1981

Effects of delta 1-testolactone on the pituitary-testicular axis in oligospermic men.

Ten men with idiopathic oligospermia were treated with delta 1-testolactone (Teslac), a potent inhibitor of conversion of androgens to estrogens. Teslac therapy caused a fall in serum estradiol and estrone levels of 34% (P less than 0.01) and 41% (P less than 0.01), respectively, and a rise in serum testosterone and androstenedione of 47% (P less than 0.02) and 70% (P less than 0.01), respectively. The testosterone-estradiol ratio increased by 126% (23.5 +/- 2.5 x 10(-1) to 45.2 +/- 5.0 x 10(-1); P less than 0.01) and the androstenedione:estrone ratio increased 231% (4.7 +/- 0.6 x 10(-1) to 12.9 +/- 2.0 x 10(-1); P less than 0.01). Basal and LRH-stimulated serum gonadotropin levels were unaffected by these changes. Sperm density rose from 10.8 +/- 2.5 to 19.8 +/- 4.7 x 10(6)/ml (P less than 0.01) and total sperm count from 26.8 +/- 6.5 to 60.6 +/- 14.3 x 10(6) (P less than 0.001). There was no significant change in motility or semen volume. Three of the wives became pregnant. There were no adverse effects of Teslac administration. These data suggest that Teslac may be an effective treatment for men with idiopathic oligospermia. Though the data do not clearly elucidate the mechanism of this effect, they are consistent with the possibility that Teslac's lowering of estrogen levels may have been responsible for the improvement in spermatogenesis. The findings also suggest that moderate increases in the circulating androgen-estrogen ratio do not affect gonadotropin output in men.

Adult↗
PubMed1980

Nutritional influences on sexual maturation in the rat.

The effect of altered nutrition on sexual maturation may depend in part on the nature and timing of the dietary change. The data are conflicting as to whether rats undernourished before weaning but normally fed after weaning have delayed puberty, but such undernourished rats clearly weigh less at vaginal opening than do normally fed animals. Altered nutrition after weaning can change the timing of puberty, and in such cases the body weight at puberty of the animals given the modified diet is frequently abnormal. The factors regulating the age and weight at puberty of rats fed altered diets seem to include the degree of underfeeding, as reflected in the growth rate, and the composition of the diet. Undernourished immature male rats have low serum testosterone secondary to gonadotropin deficiency. Basal luteinizing hormone (LH) in these animals is either low or "inappropriately normal" relative to their hypoandrogenic state (low serum testosterone and sexual accessory gland weights), and serum LH increases after luteinizing hormone-releasing hormone (LHRH) or castration are normal or minimally reduced. Serum follicle-stimulating hormone (FSH) in undernourished rats is subnormal basally and after administration of LHRH, but not after castration, which suggests that the low basal serum FSH is due to inhibition of FSH output by a testicular factor. Spermatogenesis may be unaltered by dietary changes severe enough to cause hypoandrogenism, although very severe under-nutrition will impair sperm production.

Animals↗
PubMed1980

Leydig cell function in idiopathic oligospermia.

To assess Leydig cell function in men with idiopathic oligospermia, serum levels of testosterone and 17-hydroxyprogesterone were measured before and after the administration of human chorionic gonadotopin (hCG) to men with oligospermia (< 20 x 10(6) sperm/ml). Serum testosterone and 17-hydroxyprogesterone levels, both basally and after 2 or 72 hours of hCG stimulation of Leydig cell output, were the same in the oligospermic and control groups, although basal serum testosterone levels correlated directly with sperm density (r = 0.34; P < 0.05). The basal serum level of luteinizing hormone (LH) was slightly but significantly higher in the oligospermic group than in the control group (12.0 +/- 1.0 [SE] mIU/ml versus 9.5 +/- 0.5; P < 0.05), as was the LH:testosterone ratio (2.45 +/- 0.20 versus 1.74 +/- 0.20; P < 0.02). The combination of slightly elevated serum LH levels with unchanged basal serum levels of gonadal steroids suggests that men with idiopathic oligospermia have a mild, compensated Leydig cell defect. The mildness of this defect is reflected by the ability of maximal gonadotropic stimulation to increase androgen output.

Adult↗
PubMed1979

Stress-induced cortisol release in hypothalamic hypoadrenalism.

A 52-year-old woman experienced hypoadrenalism (mean 8 AM plasma cortisol level, 3.7 microgram/dL) after hypothalamic surgery and radiotherapy for craniopharyngioma. Despite low plasma adrenocorticotropic hormone levels (less than 25 pg/mL), absent diurnal variation of the plasma cortisol level, and subnormal urinary 17-hydroxycorticosteroid response to metyrapone, she had normal plasma cortisol responses to insulin-induced hypoglycemia and to administration of vasopressin or synthetic adrenocorticotropic hormone. Stress-induced cortical release may be preserved despite notable abnormalities in regulation of cortisol secretion by diurnal and feedback-mediated mechanisms.

17-Hydroxycorticosteroids↗
PubMed1979

Body fat at puberty in rats: alteration by changes in diet.

The body composition (percent body fat) at vaginal opening of groups of rats fed different diets was determined. Serial changes in body composition prior to vaginal opening were also measured to assess the temporal relationship between first achievement of the body composition subsequently found at puberty and the actual onset of puberty (vaginal opening). The body weight at vaginal opening and the total carcass fat at vaginal opening were significantly different among the three dietary groups (F = 43.06 and 44.60, respectively; P less than 0.001). In addition, the percent body fat at vaginal opening was also significantly different among the three dietary groups (F = 30.30; P less than 0.001). In one group, the percent body fat was the same at the age of 31 days as it was at vaginal opening (mean age 41 days). In a group where food intake was restricted, the percent body fat prior to and at vaginal opening remained lower than that seen at vaginal opening in a group fed the same diet ad libitum. Thus, attainment of a critical level of body weight, total body fat stores, or percent body fat does not trigger puberty in rats.

Adipose Tissue↗
PubMed1979

Hypoandrogenism and abnormal regulation of gonadotropin secretion in rats fed a low protein diet.

The function of the hypothalamic-pituitary-testicular axis was evaluated in rats fed a low protein diet for 4 weeks beginning at 21 days of age. Compared to control, the low protein group had decreased seminal vesicle and prostate weights as well as decreased testicular testosterone output in vitro, although serum testosterone was not different. The low protein group showed no consistent alterations in serum LH (basal, post-LHRH, and postcastration) compared to control although serum FSH (basal and post-LHRH) was lower in the low protein group. Despite this lower basal FSH, the low protein group had supranormal serum FSH after castration. Seminiferous tubule diameter and testicular histology were normal in the low protein group although testicular androgen-binding protein was absent. Testicular androgen-binding protein was also undetectable in a modestly food-restricted control group which had normal testicular size, testicular histology, androgen output, and serum FSH. This finding suggests that loss of testicular androgen-binding protein may be a sensitive sign of undernutrition. We conclude that rats fed a low protein diet have hypoandrogenism, normal testicular histology, and supranormal FSH after castration despite subnormal basal FSH. The latter combination suggests overproduction of an FSH inhibitor of testicular origin.

Androgens↗
PubMed1979

Absent growth hormone response to L-tryptophan in acromegaly.

In acromegaly, regulation of GH secretion by dopamine pathways appears to be qualitatively abnormal. To determine whether regulation of GH secretion by serotonin pathways is also abnormal in acromegaly, we administered L-tryptophan (5 g orally), the initial precursor of serotonin, to 10 patients with active acromegaly (9 treated and 1 untreated), 3 patients with cured acromegaly, and 8 normal subjects. The normal group showed a significant (P less than 0.05) increase in serum GH after L-tryptophan [peak value, 12.3 +/- 4.0 (se) ng/ml], though the magnitude of the response was highly variable. In contrast, subjects with active acromegaly did not show an increase in serum GH after L-tryptophan [mean integrated percentage change in serum GH, -25 +/- 25% (SE); P = NS]. One patient whose acromegaly had been surgically cured did show a GH rise after L-tryptophan. In acromegaly, the GH response to L-tryptophan is absent, suggesting that regulation of GH secretion by serotonin pathways might be qualitatively abnormal.

Acromegaly↗