Israt Ara Hossain, Mijanur Rahman Shah, Fatema Jebunnesa and Liaquat Ali
Background: Accumulating evidence indicates that various adipokines released from adipose tissue have been involved in abnormal insulin signalling in obesity and type 2 diabetes. However, it is not entirely clear whether these alterations in serum adipocyte concentrations are already present in the pre-diabetic state. The present study was designed to test the hypothesis that elevated levels of serum lepin an index of insulin sensitivity is independently associated with insulinemic indices among different subgroups of prediabetes.
Materials: Under an observational cross-sectional design a total of 116 Control subjects (M/F, 58/58) and 99 prediabetic subjects (55/44) consisting of 49 Impaired Fasting Glucose (IFG) and 50 Impaired Glucose Tolerance (IGT) were investigated. Serum glucose was measured by glucose-oxidase method. Serum insulin and leptin were measured by ELISA techniques. Insulin secretory function (HOMA%B), insulin sensitivity (HOMA%S) and Homeostasis Model Assessment-insulin resistance (HOMA-IR) were calculated from Homeostasis Model Assessment (HOMA).
Results: Compared to the Control, IFG and IGT subjects had significantly higher levels of serum leptin (ng/mL) (p<0.001) and HOMA-IR (p=0.001) respectively. However, compared to their Control counterparts, IFG and IGT subjects had significantly lower levels of HOMA%B (p=0.001) and HOMA%S (p=0.010). On binary logistic regression analysis, serum leptin (OR (95% CI): 1.074 (1.019-1.131), p=0.007) and reduced HOMA%S (OR (95% CI): 0.972 (0.950-0.995), p=0.015) were found to be significant determinants of IGT group after adjusting the effects of WC and TG. In the same analysis, serum leptin (1.109 (1.054-1.167), p<0.001) and reduced HOMA%B (0.966 (0.951-0.981), p<0.001) were found to be significant predictors of IFG group after adjusting the effects of WC and TG.
Conclusion: Elevated levels of serum leptin may have an association with the state of IFG and IGT of prediabetes and this association, in turn, is mediated by insulin secretory dysfunction and reduced insulin sensitivity during this disorder.