Adipocyte Insulin Binding and Action in Moderately Obese NIDDM Patients After Dietary Control of Plasma Glucose: Reversal of Postbinding Abnormalities

Abstract

Studies of fat cells from patients with newly diagnosed, untreated non-insulin-dependent diabetes mellitus (NIDDM) have revealed severe abnormalities in insulin action on glucose transport and metabolism. To determine whether these defects can be reversed if good glycemic control is reached by dietary treatment, eight moderately obese NIDDM subjects were studied at diagnosis and again when the patients had been in good glycemic control induced by low-energy dieting for at least 2 mo (absence of glycosuria and fasting plasma glucose P < .05). Fasting plasma glucose decreased from 11.5 ± 1.2 to 6.9 ± 0.9 mM, whereas fasting serum insulin concentrations were unchanged. Adipocyte insulin binding at tracer concentration (15 pM, 37°C) was not changed significantly (1.94 ± 0.52 to 2.05 ± 0.62% per 30 cm² surface area/ml). The basal (noninsulin-stimulated) glucose transport (tracer glucose concentration 5 μM) increased from 25 ± 12 to 44 ± 14 pmol · 90 min⁻¹ · 10 cm⁻² surface area (P < .02). The maximally insulin-stimulated glucose transport rate increased from 35 ± 20 to 78 ± 26 pmol/90 min (P < .01). The percentage insulin response above basal levels increased from 31 ± 40 to 89 ± 58% (P < .01). The insulin sensitivity (half-maximally stimulating insulin concentrations) was also improved (P < .05). Glucose conversion rates to total lipids increased 34 ± 62 and 65 ± 80% in basal cells and maximally insulin-stimulated cells, respectively (.2 > P > .1 , .1 > P > .05). The percentage insulin response above basal level increased from 30 ± 24 to 67 ± 52% (P < .05). The percentage insulin response above basal level of glucose conversion to CO₂ also increased (P < .05). The results after diet treatment were not different from those of normal controls. We conclude that dietary treatment of moderately obese NIDDM patients that leads to good glycemic control results in reversal of the abnormalities observed in adipocytes of untreated NIDDM subjects.