Serum adiponectin concentrations during a 72-hour fast in over- and normal-weight humans

OBJECTIVE: Adiponectin is currently considered an important link between obesity and insulin resistance, since circulating levels of this insulin sensitizing hormone have consistently been found to be reduced in obese subjects. However, until now it is not known how the secretion of adiponectin is regulated in response to acute metabolic changes. Here, we assessed the influence of complete fasting for 72 h on serum adiponectin levels. DESIGN: Between group comparison of repeated measurements. SUBJECTS: In total, 18 normal-weight (mean ± s.e.m. BMI: 22.2 ± 0.4 kg/m²; age: 39.2 ± 4.4 y) and nine over-weight (BMI: 33.2 ± 1.8 kg/m ²; age: 36.9 ± 4.5 y) subjects. MEASUREMENTS: Serum adiponectin levels were measured every 4 h during a 72-h fasting period. Additionally, concentrations of plasma glucose and serum insulin and leptin were assessed at the beginning and in the end of the fasting experiment. Insulin resistance was estimated using the homeostasis model assessment (HOMA). RESULTS: While concentrations of glucose, insulin, and leptin decreased across the fasting period by 31.0, 33.1 and 60.0%, respectively (all P < 0.005), adiponectin levels remained unchanged (P = 0.817). Overall, over-weight subjects exhibited slightly lower adiponectin levels than normal-weight subjects (P = 0.092), but there was no difference in the time course of adiponectin levels during fasting between these two groups (P = 0.970). Although, averaged adiponectin levels before and after fasting did not systematically differ, individual changes in adiponectin levels across fasting displayed a slight but significant inverse correlation with changes in plasma glucose concentration (r = -0.42, P = 0.03). DISCUSSION: The data show that serum adiponectin concentrations remain remarkably stable during 72 h of fasting in normal- and over-weight subjects. Thus, adiponectin appears to reflect primarily long-term changes in body weight with little evidence for a dependence on short-term regulatory influences.