OBJECTIVES: Glycosylated haemoglobin (HbA1c), leptin, leptin soluble receptors (sOB-R) and free leptin index (FLI) may all be influenced by diabetes, but their associations remain unclear. Therefore, we put forward a hypothesis that serum leptin, sOBR and FLI might be parallel to Hb1c, as they all reflect the metabolic status.
DESIGN AND SETTING: We measured leptin and sOB-R concentrations in 97 obese non-diabetic (47 women and 50 men), and 65 obese diabetic (32 women and 33 men) humans, and examined whether they were related to HbA1c. Under the condition, the presence of diabetes was the only differentiating factor between two groups of frankly obese humans.
RESULTS: Non-diabetic vs. diabetic, median and interquartile range, respectively: Leptin (ng/ml), 30.83, 37.27 vs. 28.24, 23.34; p>0.05; sOB-R (ng/ml), 17.62, 17.05 vs. 21.81, 16.61, p<0.05; FLI, 231.23, 310.00 vs. 131.76, 157.68, p<0.05. To investigate the influence of HbA1c on leptin and sOB-R, both groups were divided into tertiles based on HbA1c. In diabetics, leptin did not differ between the high, intermediate, and low HbA1c levels subgroups, p>0.05, and leptin was not influenced by HbA1c levels: r=0.086; p>0.05. For sOB-R, respectively: p>0.05; r=0.080; p>0.05. In non-diabetics, respectively: p<0.05; r=0.2923; p<0.05 for leptin; and p<0.0001, r=0.5103; p<0.0001, for s-OB-R.
CONCLUSIONS: Not leptin alone but serum sOB-R and FLI are the markers of leptin action impairment in type 2 diabetes. Further, HbA1c is not associated with metabolic status of leptin in obese diabetic patients, whereas this association is found in obese non-diabetic humans.