Basal and Stimulated Plasma Leptin in Diabetic Subjects

LIU, JIANMEI, HASAN ASKARI, AND SAMUEL DAGOGO‐JACK. Basal and stimulated plasma leptin in diabetic subjects. Obes Res . Objective : To determine whether leptin secretion is impaired in diabetes, we compared basal and stimulated plasma leptin levels in diabetic subjects and healthy controls. Research Methods and Procedures : Blood samples for assay of leptin and other hormones were obtained at baseline in 54 diabetic patients and 65 controls, and 8 hours, 16 hours, and 40 hours following ingestion of dexamethasone (4 mg) in 6 healthy and 12 controls. C‐peptide status was defined as “negative” if ≤0.1 ng/mL or “positive” if ≥0.3 ng/mL, in fasting plasma. Results : Basal plasma leptin levels were 19. 7±2. 2 ng/mL in nondiabetic subjects, 13. 4±1. 5 ng/ml in C‐peptide negative ( n = 28) and 26. 1±23. 7 ng/mL in C‐peptide positive ( n = 26, p = 0. 001) diabetic patients. Dexamethasone increased leptin levels of controls ( n = 6) to 145±17% of baseline values at 8 hours ( p = O. O3), 224±18% at 16 hours ( p = 0. 01), and 134218% at 40 hours ( p = 0. 05). The corresponding changes were 108±13%, 126±23%, and 98±16% in C‐peptide negative ( n = 6), and 121±10%, 144±16% ( p = 0. 03), and 147±23% ( p = 0. 11) in C‐peptide positive ( n = 6) diabetic patients, respectively. The peak stimulated leptin levels were lower in the diabetic patients, compared with controls. Plasma insulin increased ( p = 0. 02) in controls, but not in the diabetic patients, following dexamethasone. Discussion : Although diabetic patients have normal plasma leptin levels under basal conditions, their leptin responses to glucocorticoid are impaired, probably because of the concomitant insulin secretory defect. A subnormal leptin secretory response could worsen obesity and insulin resistance in diabetes.