1. ^*Department of Chemical Pathology, South African Institute for Medical Research, University of the Witwatersrand Faculty of Health Sciences, Parktown 2193, South Africa
2. ^†Department of Endocrinology, University of the Witwatersrand Faculty of Health Sciences, Parktown 2193, South Africa
3. ^‡Department of Internal Medicine, University of Göteborg, Sahlgren's Hospital S-41345, Göteborg, Sweden

Correspondence: Dr. N. J. Crowther Department of Chemical Pathology, South African Institute for Medical Research, University of the Witwatersrand Faculty of Health Sciences, 7 York Road, Parktown 2193, Johannesburg, South Africa. E-mail: 158njcro@chiron.wits.ac.za

Received 23 February 1999; Accepted 3 August 1999.

Abstract

Objective: The goal of this study was to quantify differences in lipid metabolism and insulin sensitivity in black and white subjects to explain ethnic clinicopathological differences in type 2 diabetes.

Research Methods and Procedures: The in vitro lipolytic activity of adipocytes isolated from obese black and white women was measured in the presence of insulin and isoproterenol. Insulin resistance was assessed in vivo using the euglycemic hyperinsulinemic clamp technique.

Results: Fasting plasma levels of insulin and nonesterified fatty acid (NEFA) in black and white women were 67 5 pM vs. 152 20 pM (p < 0.01) and 863 93 M vs. 412 34 M (p < 0.01), respectively. Euglycemic hyperinsulinemic clamp studies showed that obese black subjects were more insulin-resistant than their white counterparts (glucose infusion rates: 1.3 0.2 vs. 2.2 0.3 mg/kg per min; p < 0.05). Isolated adipocytes from white women were more responsive to insulin than those from black women with 0.7 nM insulin causing a 55 4% inhibition of isoproterenol-stimulated lipolysis compared with 27 10% in black women (p < 0.05).

Discussion: The low responsiveness of adipocyte lipolytic activity to insulin in black women in the presence of a relative insulinopenia may account for the high plasma NEFA levels seen in these women, which may, in turn, account for their higher in vivo insulin resistance. High NEFA levels may also contribute to the low insulin secretory activity observed in the obese black females. These data suggest that the pathogenesis of insulin resistance and type 2 diabetes within the black obese community is strongly influenced by their adipocyte metabolism.