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Plasma 25-hydroxyvitamin D concentrations and bone histomorphometry were investigated in 24 grossly obese subjects. The mean plasma 25OHD concentration was significantly lower in the obese group than in age-matched, healthy controls. Subnormal values were found in four obese subjects and in a further two subjects, who were investigated at the end of the summer, plasma 25-hydroxyvitamin D levels were at the lower end of the normal winter range. Bone histology was abnormal in two patients. In one, mild osteomalacia and secondary hyperparathyroidism were present while in the other patient the appearance suggested increased bone turnover, possibly as a result of healing osteomalacia. We conclude that gross obesity is associated with an increased risk of vitamin D deficiency, probably because of reduced exposure to uv radiation. Histological evidence of metabolic bone disease may also occur. Preoperative vitamin D deficiency may contribute in some patients to the development of metabolic bone disease after intestinal bypass.

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Total forearm glucose utilization (FGU) was determined during 100 gm. oral glucose tolerance tests (GTT) in twenty-five normal volunteers. In addition, the concomitant balance of insulin, growth hormone, and lactate across the forearm was studied in thirteen subjects. The increment in FGU during the three hours following glucose ingestion amounted to 74 mg./100 ml. forearm; it may be calculated that increased peripheral glucose utilization accounted for the disposal of 42 per cent of the 100 gm. load and that during the GTT some 58 gm. of extra glucose reached the peripheral circulation. Serum insulin concentrations in mixed venous (MY) blood rose steeply after glucose loading, while growth hormone levels were reduced. Additional observations in thirteen subjects showed that MV insulin levels remained significantly lower than corresponding arterialized venous (AV) concentrations between thirty and 150 minutes, suggesting that insulin was being continually removed bythe forearm tissues during this time. Significant AV-MV differences were not detected in growth hormone levels. Plasma lactate concentrations rose immediately after glucose loading, reaching a peak at sixty minutes and declining thereafter. The initial elevation was associated with lactate uptake by the forearm and the subsequent fall with lactate release, suggesting that peripheral lactate metabolism has little or no influence on the shape of the lactate response curve. It is suggested thatthis early rise in lactate concentrations is the result of increased hepatic lactate production and that the timing and height of the lactate peak reflect the pattern of enhanced hepatic glucoseutilization after oral glucose loading. Our results suggest that the disposition of a 100 gm. oral glucose load is accounted for mainly by hepatic glucose conservation rather than peripheral uptake and, therefore, that the former is the major determinant of the shape of the oral glucose tolerance curve.

We have measured the plasma concentrations of sex steroids and sex hormone-binding globulin (SHBG) in twenty-three massively obese women and ten age-matched lean female volunteers. In the obese women increased plasma testosterone (obese 3.2 +/- 0.5 nmol/l controls 1.7 +/- 0.5 nmol/l, P less than 0.3) and androstenedione concentrations (obese 9.7 +/- 1.2 nmol/l, controls 4.4 +/- 0.6 nmol/l, P = less than 0.01) an increased ratio of oestrone:oestradiol (obese 2.4 +/- 0.4, controls 1.0 +/- 0.1, P = less than 0.1) and decreased SHBG levels (obese 30 +/- 4 nmol/l, controls 60 +/- 8 nmol/l, P = less than 0.001) were found. Obesity differed from the polycystic ovary syndrome (in which a similar pattern of changes of sex steroid concentrations and binding are seen) in that it was associated with normal increases in serum luteinizing hormone (LH) follicle stimulating hormone (FSH) levels in response to the administration of LHRH. We conclude that the common occurrence of menstrual abnormalities in obesity results from abnormal secretion and binding of sex steroids. In addition, the unaltered secretion of LH and FSH in the presence of such changes is evidence for a disorder of hypothalamic function.