An unfavorable body fat distribution is associated with many metabolic abnormalities including a high prevalence and incidence of noninsulin dependent diabetes mellitus and decreased high density lipoprotein cholesterol and increased triglyceride levels. One mechanism for the effect of body fat distribution on metabolic variables may be through sex hormones. We examined the relationship of body mass index (BMI), ratio of subscapular-to-triceps skinfold ratio (centrality index) and ratio of waist-to-hip ratio (WHR) to sex hormone binding globulin (SHBG) (an in vivo measure of androgenicity) in 101 postmenopausal Mexican-American and non-Hispanic white women from the San Antonio Heart Study,a population based study of diabetes and cardiovascular disease. SHBG was significantly correlated with BMI (r = -0.440,P < 0.001), WHR (r = -0.255, P < 0.01) and centrality index (r = -0.210,P < 0.05). In a multiple linear regression analysis, SHBG remained significantly associated with BMI (P < 0.001) and WHR (P < 0.05) but not with age, ethnicity or centrality index. This work suggests that in postmenopausal women overall adiposity and an unfavorable body fat distribution are associated with increased androgenicity as measured by a lower SHBG concentration. Our finding may help to explain the association of body fat distribution with diabetes and cardiovascular risk factors in older women.

The rat Leydig cell tumor is a well characterized model of the humoral hypercalcemia of malignancy. The studies reported here were provoked by the observation that tumor-bearing rats become extremely cachectic and develop hypertriglyceridemia as they become hypercalcemic. Since the bone resorbing cytokine tumor necrosis factor (TNF)/cachectin is associated with cachexia and hypertriglyceridemia, we examined hypercalcemic tumor-bearing rats for evidence of increased TNF production using a TNF radioimmunoassay. We found that immunoreactive TNF was increased in the plasma of tumor-bearing rats. The increase in plasma TNF was comparable to that previously shown in hypercalcemic nude mice bearing Chinese hamster ovarian cell tumors transfected with the human TNF gene. There was no detectable TNF activity in tumor culture media which suggested that the tumor itself was not the source of excess TNF production. However, we found that tumor cell conditioned media enhanced the production of TNF activity by normal macrophages in vitro, indicating that increased TNF production in vivo may result from a tumor factor(s) which stimulates TNF production by normal immune cells. When TNF was added together with tumor products to organ cultures of fetal rat long bones, osteoclastic bone resorption was potentiated. These data are consistent with the concept that in this model of the humoral hypercalcemia of malignancy, increased TNF production by normal immune cells is increased, has systemic effects as suggested by cachexia and hypertriglyceridemia, and may work in concert with factors produced directly by tumor cells to overwhelm normal calcium homeostasis.

Studies were performed to investigate vitamin D metabolism in Mexican-Americans. Groups of 15 whites and 16 Mexican-Americans ranging in age from 18 to 41 years were evaluated. All of them were within 25% of their ideal body weight. Each of them was admitted to the Clinical Research Center of the University of Texas Health Science Center and placed on a daily diet estimated to contain 400 mg calcium and 900 mg phosphate. It was found that whereas serum vitamin D (1.8 +/- 0.5 versus 7.6 +/- 1.3 ng/ml, P less than 0.001) and serum 25-hydroxyvitamin D (9 +/- 1 versus 17 +/- 2 ng/ml, P less than 0.01) were significantly lower and serum 1,25-dihydroxyvitamin D (37 +/- 2 versus 28 +/- 2 pg/ml, P less than 0.001) was significantly higher in the Mexican-Americans than in the whites, serum calcium (9.1 +/- 0.1 versus 9.2 +/- 0.1 mg/dl), magnesium (1.84 +/- 0.07 versus 1.80 +/- 0.07 mEq/liter), and Gla protein (19 +/- 3 versus 21 +/- 2 ng/ml) were not different in the two groups. Urinary calcium (144 +/- 14 versus 124 +/- 16 mg/day), phosphate (672 +/- 51 versus 683 +/- 44 mg/day), sodium (110 +/- 8 versus 99 +/- 9 mEq/day), potassium (43 +/- 4 versus 49 +/- 3 mEq/day), and magnesium (7.3 +/- 0.7 versus 7.7 +/- 0.5 mEq/day) and creatinine clearance (173 +/- 14 versus 154 +/- 7 liters/day) were not different in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Mexican-Americans, a high-risk population for non-insulin-dependent diabetes mellitus (NIDDM), have been previously reported to have decreased levels of sex-hormone-binding globulin (SHBG). We measured total testosterone, total estradiol and SHBG, glucose and insulin in premenopausal women (58 Mexican-Americans and 38 non-Hispanic whites) as part of the San Antonio Heart Study, a population-based study of cardiovascular risk factors. Although total estradiol and total testosterone were, in general, not correlated with metabolic variables, SHBG was negatively correlated with glucose and insulin. After adjustment for body mass index (BMI), ratio of waist-to-hip circumference (WHR) and ratio of subscapular-to-triceps skinfold (Centrality Index), SHBG was still significantly correlated with insulin concentrations (P < .001). Since Mexican-Americans were previously reported to be more hyperinsulinemic than non-Hispanic whites, we examined the effect of adjusting for SHBG on insulin levels in this small population. While unadjusted insulin concentrations in Mexican-Americans were higher than in non-Hispanic whites (354 μU/mL v 236 μU/mL, respectively, P = .009), adjustment for BMI, WHR, and centrality index reduced the ethnic difference in insulin levels considerably (P = .014). However, only after adjusting for SHBG as well, did the ethnic difference in insulin levels became nonsignificant. Our data suggest that alterations in sex hormones and SHBG in particular may be related to the hyperinsulinemia and the high rates of NIDDM in Mexican-Americans.

Twenty-five women fulfilling the criteria for female alopecia, of either the male pattern baldness type or female pattern baldness type, were evaluated for hormone markers to delineate the clinical baldness patterns. Women with a marked increase in the 3 alpha,17 beta-androstanediol glucuronide/sex hormone binding globulin ratio and low serum sex hormone binding globulin were noted to have female pattern baldness. This pattern of baldness may represent hair loss from the influence of minimal androgen excess on genetically sensitive hair bulbs in the absence of other signs of maximal androgen excess, including hirsutism, acne, or virilism.