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Quantitation of Forearm Glucose and Free Fatty Acid (FFA) Disposal in Normal Subjects and Type II Diabetic Patients: Evidence Against an Essential Role for FFA in the Pathogenesis of Insulin Resistance^*

Department of Internal Medicine, II School of Medicine, University of Naples Naples, Italy

Address all correspondence and requests for reprints to: Luigi Sacca’, M.D., Institute of Internal Medicine, Via Pansini 5, 80131 Naples, Italy.

This study was designed to quantitate glucose and FFA disposal by muscle tissue in patients with type II diabetes and to investigate the relationship between FFA metabolism and insulin resistance. The forearm perfusion technique was used in six normal subjects and two groups of normal weight diabetic patients, i.e. untreated (n = 8) and insulin-treated (n = 6). The latter received 2 weeks of intensive insulin therapy before the study. Plasma insulin levels were raised acutely [950–1110 pmol/L) (130–150 µU/mL)], while the blood glucose concentration was clamped at its basal value [4.9 ± 0.1 (±SE) mmol/L in the normal subjects, 5.7 ± 0.5 in the insulin-treated diabetic patients, and 5.5 ± 0.3 in the untreated diabetic patients] by a variable glucose infusion. During the control period, arterial FFA concentrations were similar in the three groups, and they decreased to a comparable extent (<0.1 mmol/L) in response to insulin infusion. During the control period, the mean forearm FFA uptake was 2.5 ± 0.5 µmol/L·min in the normal subjects, 2.9 ± 0.5 in the insulin-treated patients, and 2.1 ± 0.5 in the untreated diabetic patients. During the insulin infusion, FFA uptake was profoundly suppressed to similar levels in the normal subjects (0.9 ± 0.1 µmol/L·min), the insulin-treated diabetic patients (1.1 ± 0.3), and the untreated diabetic patients (0.9 ± 0.1; P < 0.001). Forearm glucose uptake was similar in the three groups during the control period. It increased during the insulin infusion, but the response in both diabetic groups was less than that in the normal subjects. The total amounts of glucose taken up by the forearm during the study period were 5.2 ± 0.7, 2.6 ± 0.5, and 2.1 ± 0.6 mmol/L-min in the normal subjects, the insulin-treated diabetic patients, and the untreated diabeticpatients, respectively (P < 0.01). We conclude that 1) insulinmediated glucose uptake by forearm skeletal muscle is markedly impaired in type II diabetes and improves only marginally after 2 weeks of intensive insulin therapy; 2) in contrast, no appreciable abnormality in forearm FFA metabolism is demonstrable in insulin-treated type II diabetic patients; and 3) FFA do not contribute to the insulin-treated skeletal muscle insulin resistance that occurs in patients with type II diabetes mellitus.

^* This work was supported in part by a grant from Consiglio Nazionale delle Richerche, Italy (Contract 870043756), and Novo Farmaceutici Italia.

Received February 1, 1988.

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