Prolonged oral glucose tolerance test combined with indirect calorimetry and estimation of several substrates and hormones in obese subjects.

Abstract

OGTT prolonged to 4 hours was performed in untreated 50 obese outpatients (mean age 37.9 years and BMI 37.2). Parallel to glucose, insulin, growth hormone (GH), cortisol, beta-hydroxybutyrate (BOHB), nonesterified fatty acids (NEFA) and indirect calorimetry (RQ) were estimated at hourly intervals. Basal values of thyroxine (T4), triiodothyronine (T3), total cholesterol and triacylglycerols were also obtained. Mean glycemia after overnight fasting as well as after 75 g glucose reached upper limits of the normal range. The subsequent decrease was slower. Insulinemia followed a similar trend. The initial drop of GH after the glucose load reverted to an increase above the basal value. A similar pattern was observed with cortisolemia, but the decrease and increase were less important. The basal value of RQ was rather low and glucose ingestion produced only a small increase, followed by a greater decrease. Serum levels of NEFA and BOHB sharply decreased one hour after glucose intake and afterwards regained the initial values. The mean basal values of T4 and T3 were within the normal range--the low T3 syndrome was not involved in the large majority of cases. Cholesterol and triacylglycerols approached the upper normal limit. The correlations brought additional information. Insulinemia increased parallel with the amount of body fat. The basal level was decisive for most hormones and substrates--the high or low set level could be followed in the course of the whole test. Increased insulinemia and increased glycemia suggested the presence of a mild insulin resistance with the participation of GH and cortisol. Increased levels of fasting insulinemia and glycemia were present also in obese subjects with a normal OGTT. The correlations permitted to disclose insulin-like effects of GH on basal conditions. Increased BOHB was responsible for a high cholesterol. It is suggested that even small fluctuations of glycemia related to food intake may produce a substantial modification of the hormonal status in obese subjects and initiate or support the metabolic disorders in obesity. In this respect a greater role is ascribed to the phase of decreasing glycemia in comparison to the increasing phase. Lipids are the prevailing source of energy in insulin resistant subjects. The rather stable values of indirect calorimetry indicate that energy metabolism of obese subject works on a low, pre-set level-independently on the supply of some relevant hormones and substrates.