The acute effects of hyperinsulinemia on plasma leptin levels were determined in body fat matched 8 controls, 7 IGT subjects, 6 NIDDM patients and 10 PCO subjects, using the glucose clamp technique.
The plasma leptin levels changed little from basal during hyperglycemic hyperinsulinemic(89.0±2.1uU/mL)-euglycemic(89.5±0.8mg/dL) clamp studies in either controls, IGT, NIDDM or PCO subjects(Basal Vs After; 4.7 ±2.1 Vs. 5.6± 2.2, 6.1±1.0 Vs. 4.9±1.0, 7.4±2.9 Vs. 7.1±2.5, 11.6±0.8 Vs. 11.5±0.9ng/mL). Basal leptin levels were higher in PCO, NIDDM, IGT than controls(11.6±0.8, 7.4 ±2.9, 6.1±1.0 Vs. 4.7 ±2.ing/mL, P<0.05 ), and insulin sensitivity index were lower in PCO, NIDDM, IGT than controls (3.6 ±0.3, 5.2±0.6, 6.6-1-0.7 Vs. 9.6=1=1.3 ml/kg/ min/U/mL X 104 , P<0.05). A strong correlation between plasma leptin levels and percent body fat, fasting insulin level and insulin sensitivity index were present. In a multivariate regression analysis, plasma leptin was associated with percent body fat(B=0.380, P=0.011) and insulin sensitivity index(B=0.380, P=0.011).
Above results demonstrate that insulin resistance, independent of adiposity, is associated with elevated plasma leptin levels. Although we found insulin did not regulatre leptin production acutely, it is possible that chronically elevated plasma insulin concentrations stimulate OB gene expression.