In 707 non-obese female adults with unimpaired glucose tolerance, the fasting blood glucose levels of those in the fourth, fifth and sixth decades of life exceeded the levels found in those of the third decade (20-29 years), but there was no evidence of a progressive increase in successive age decades. The slightly greater fasting glycemia in the later age decades was accompanied by higher increments in blood glucose in the first half hour of the glucose tolerance test. These higher levels of glucose during the fasting state and in the first half hour after oral administration of glucose were not associated with increments in serum insulin greater than those recorded for the third age decade. This age-related increase in fasting and post-glucose blood sugar levels without an increase in serum insulin could result from the age-related increase in the thickness of capillary basement membranes. The higher levels of glucose could then serve to restore glucose transport and cell glucose metabolites to normal without evoking a rise in serum insulin.In 479 obese women with unimpaired glucose tolerance, there was no evidence of the age-related increase in fasting blood glucose nor the slightly exaggerated hyperglycemia found early in the test in non-obese subjects with normal glucose tolerance. The relative fasting hyperinsulinemia and the increased insulin responses to induced hyperglycemia known to characterize obese persons were present in all age decades but the hyperinsulinemia was less marked in subjects older than 30. In these obese subjects with unimpaired glucose tolerance, there was no evidence of any delay in the insulin response to the induced hyperglycemia.In a previous study (1), we observed that in older non-obese females with unimpaired glucose tolerance there was a slightly higher concentration of fasting blood glucose and a slightly greater blood glucose response without 1na a concomitant increase in the serum insulin level. In the studies reported here, we characterize the glucose and insulin patterns for successive age decades in both non-obese and obese women. Detailed analyses of the data indicate that, within the range of normal glucose tolerance, only minor age-related differences are evident in the blood sugar and insulin responses to orally administered carbohydrate. However, the many incompletely defined aspects of aging and of obesity warrant citation of even slight differences which are lost when such data are pooled solely on the basi~of age or body weight.

Hyperinsulinemic patterns are a well recognized feature of equivocal glucose tolerances of the chemical diabetes type, i.e. those that are neither definitely nondiabetic nor clearly diabetic. A more complete characterization of such insulin responses is obtained when the data are expressed in terms of increments in insulin from the zero time point.Thus, two patterns of insulin increments after oral glucose become evident when the equivocal zone of glucose tolerance is divided into lower and upper segments. Tests in the lower segment show normal increments at the halfhour point of the test; at one hour these tests show excessive increments which persist throughout the five hours of observation. On the other hand, tests in the upper zone show delays in the serum insulin rise at the half-hour point, followed by normal increments at one hour and excessive increments thereafter. The pattern is the same whether or not obesity is present. It is suggested that tests in the equivocal zone of Glucose Tolerance Sum values be taken to be indicative of chemical diabetes. Tests with the Sum in the lower half of the equivocal zone could then represent chemical diabetes with mild intolerance stemming from insulin ineffectiveness, since insulin increments in this group are at or above the mean values recorded in nondiabetic controls. On the other hand, chemical diabetes with moderate glucose intolerance and Glucose Tolerance Sums in the upper half of the equivocal zone would be understood to result from a combination of an initial delay in the serum insulin rise followed by normal and then excessive increments in serum insulin with the latter two indicative of insulin ineffectiveness. However, insulin ineffectiveness may also be present at the time of the insulin delay.High glucose:insulin ratios in tests indicative of chemical diabetes are almost always attributable to higher glucose increments with insulin increments normal or excessive compared to normal glucose tolerances. Deficient insulin increments contribute to the high ratios only at the half-hour point in tests with Glucose Tolerance Sums in the upper zone of equivocal glucose tolerances. DIABETES 22:808-12, November, 1973.

In non-obese women with unimpaired glucose tolerance (1,185 oral glucose tolerance tests) the serum level of growth hormone (GH) in the fifth and sixth age decades was below that in the third and fourth decades. Although obesity was associated with serum GH levels below those characteristic of non-obese women, there was no evidence of a further age-related decrease of the type observed in the non-obese subjects. The lower serum GH level in women of the later age decades may well be related to the menopause with its decrease in the serum level of estrogen. Since there is no further age-related decline in GH in obesity, it would appear that in obese premenopausal females, estrogen does not exert its usual GH-enhancing effects.