Body composition, adipocyte size, free fatty acid concentration, and glucose tolerance in children of diabetic pregnancies.

Previous studies show that children of women who are diabetic during pregnancy are more obese and have a higher prevalence of non-insulin-dependent diabetes mellitus (NIDDM) than children of women who first developed NIDDM greater than 1 yr after the pregnancy (prediabetic mothers) and children of women who have never developed diabetes (nondiabetic mothers). To determine whether lean and obese children of glucose-intolerant pregnancies can be distinguished from similar children of glucose-tolerant pregnancies, we measured body composition, abdominal and gluteal adipocyte size, fasting free fatty acid (FFA), and fasting and stimulated glucose and insulin concentrations during an oral glucose tolerance test in prepubertal children of glucose-intolerant and prediabetic mothers. Each group ranged in adipocity from 6 to 40% body fat.

Insulin and atherogenesis: clinical trials.

The possible role of hyperinsulinism in the generation and perpetuation of atherosclerosis is discussed. Although the hypothesis is an important one that merits intensive study, it is premature to approach the question through a clinical trial. Rather, a concerted effort should be made to gain more information through basic research in laboratory animals and clinical investigations in man.

Insulin-induced translocation of intracellular glucose transporters in the isolated rat adipose cell.

Three techniques have now been used to demonstrate that insulin stimulates glucose transport in isolated rat adipose cells through the translocation of glucose transporters from a large intracellular pool to the plasma membrane. By using a specific D-glucose-inhibitable cytochalasin B-binding assay, most of the basal cell's transporters are found associated with a low-density microsomal membrane fraction. However, although Golgi marker enzyme activities are also enriched in this fraction, their distributions over all fractions do not parallel that of the transporters.

Insulin-stimulated translocation of glucose transporters in the isolated rat adipose cells: characterization of subcellular fractions.

Insulin stimulates glucose transport in rat adipose cells through the translocation of glucose transporters from an intracellular pool to the plasma membrane. A detailed characterization of the morphology, protein composition and marker enzyme content of subcellular fractions of these cells, prepared by differential ultracentrifugation, and of the distribution of glucose transporters among these fractions is now described. Glucose transporters were measured using specific D-glucose-inhibitable [3H]cytochalasin B binding.

Mechanism of insulin-resistant glucose transport activity in the enlarged adipose cell of the aged, obese rat.

The effects of increasing cell size on glucose transport activity and metabolism and on the concentrations of glucose transport systems in both the plasma and low density microsomal membranes in isolated adipose cells from the aging rat model of obesity have been examined. Glucose transport activity was assessed by measuring l-arabinose transport and the concentration of glucose transport systems estimated by measuring specific d-glucose-inhibitable cytochalasin B-binding. Basal glucose transport activity increases from 0.

Adipose tissue cellularity in woodchucks: effects of season and captivity at an early age.

The objectives of this study were to determine the roles of adipocyte hypertrophy and hyperplasia in the prehibernatory weight gain of adult woodchucks and in the increased body weight of woodchucks born in captivity. The seasonal increase in weight in wild adult woodchucks was associated with an increase approaching tenfold in both body fat and in subcutaneous and retroperitoneal adipocyte size. There was no increase in total adipocyte number.

A possible mechanism of insulin resistance in the rat adipose cell with high-fat/low-carbohydrate feeding. Depletion of intracellular glucose transport systems.

The effects of high-fat/low-carbohydrate feeding on glucose transport activity and on the concentrations of glucose transport systems in the plasma and low-density microsomal membranes in isolated rat adipose cells have been examined. Glucose transport activity was assessed by measuring 3-O-methylglucose transport and the concentration of glucose transport systems estimated by measuring specific D-glucose-inhibitable cytochalasin B-binding. Basal glucose transport activity is not significantly influenced by high-fat/low-carbohydrate relative to low-fat/high-carbohydrate feeding and is accompanied by a constant 10 pmol of glucose transport systems/mg of membrane protein in the plasma membrane fraction.

A possible mechanism of insulin resistance in the rat adipose cell in streptozotocin-induced diabetes mellitus. Depletion of intracellular glucose transport systems.

The effects of insulin-dependent diabetes mellitus on glucose transport activity and on the concentrations of glucose transport systems in the plasma and low density microsomal membranes in adipose cells isolated from streptozotocin-induced diabetic rats have been examined. Glucose transport activity was assessed by measuring 3-O-methylglucose transport and the concentration of glucose transport systems estimated by measuring specific D-glucose-inhibitable cytochalasin B-binding. Basal glucose transport activity decreases from 0.

Effects of dietary composition on glucose metabolism in rat adipose cells.

The effect of altered dietary carbohydrate and fat content on equilibrium insulin binding to, and glucose transport activity and metabolism in, isolated rat epididymal adipose cells has been studied. Alterations in basal and insulin-stimulated total glucose utilization induced by changes in the ratio of dietary carbohydrate to fat are accounted for by specific effects of dietary composition at two levels of cellular function: 1) glucose transport across the cell's plasma membrane, specifically, the number of functional glucose transport systems, and 2) the cell's maximal capacity for glucose metabolism. These effects occur without alterations in insulin binding or the cell's sensitivity to insulin.

Adipose cell size-function relationships: insulin binding and degradation.

125I-insulin binding and degradation have been studied in isolated rat adipose cells of increasing size. Binding at 24 degrees C reaches a steady state by 40-60 min in the absence of significant degradation. At 37 degrees C, binding reaches only a transient maximum by 10-15 min because insulin is rapidly degraded.

Intracellular glucose concentration in small and large rat adipose cells.

Intracellular free glucose concentrations have been estimated in small and large isolated epididymal adipose cells prepared from young lean and older obese rats using glucose-induced steady-state tracer 3-O-methylglucose countertransport. Steady-state 3-O-methylglucose uptake was measured in the presence of 2--50 mM glucose or sucrose in the absence or presence of 100 microU insulin/ml. The ratio of the uptake of 3-O-methylglucose in the presence of glucose to that in the presence of sucrose at each sugar concentration was then utilized to estimate the corresponding intracellular glucose concentration.

Determinations of adipose cell size and number in suspensions of isolated rat and human adipose cells.

The osmic acid fixation-Coulter electronic counter method described for determining adipose cell size and number in intact adipose tissue fragments has been modified for use with suspensions of isolated rat and human adipose cells. Mean cell sizes in tissue fragments and isolated cell suspensions prepared from the same tissue are virtually identical in rats of various weights. No statistically significant difference in mean adipose cell size between tissue and isolated cell suspension was observed in human adipose tissue although the variability was much greater than in rat tissue.

Glucose transport in isolated rat adipocytes with measurements of L-arabinose uptake.

Data is presented suggesting that rates of L-arabinose transport, calculated from L-[1-14C]arabinose uptake measurements, can be used as indicators of changes in the rates of glucose transport in isolated rat adipocytes. L-[1-14C]arabinose, at 37 degrees C, was found to be nonmetabolizable and taken up by adipocytes exponentially with time reaching 95% of equilibrium in 30 min. When L-arabinose is corrected for background, the corrected uptake values conform to the time-dependent monoexponential uptake relationshiop predicted for a facilitated transport system and are not significantly different from 0 in the presence of 70 micron cytochalasin B.

Glucose metabolism and the response to insulin by human adipose tissue in spontaneous and experimental obesity. Effects of dietary composition and adipose cell size.

[1-(14)C]glucose oxidation to CO(2) and conversion into glyceride by adipose tissue from nonobese and obese subjects has been studied in vitro in the presence of varying medium glucose and insulin concentrations as functions of adipose cell size, the composition of the diet, and antecedent weight gain or loss. Increasing medium glucose concentrations enhance the incorporation of glucose carbons by human adipose tissue into CO(2) and glyceride-glycerol. Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol.