Insulin secretion and sensitivity in Bangladeshi prediabetic subjects

There are still considerable controversies regarding the basic pathophysiological mechanisms of impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). The present study was undertaken to explore the beta-cell function and insulin sensitivity in a Bangladeshi prediabetic population.

Twenty-four IFG and 112 IGT subjects, along with 40 healthy controls, were selected purposively following 2003 ADA cut-off values and 2006 WHO/IDF grouping. IGT subjects were subcategorized into 53 isolated IGT (I-IGT) and 59 combined IFG-IGT subjects. Plasma glucose and insulin (by chemiluminescent immunoassay) were measured at fasting and 2 h after 75 g of oral glucose load. Insulin sensitivity was assessed by homeostasis model assessment (HOMA-S%) and insulin sensitivity index for glycemia (ISI(gly)) and insulin secretion by HOMA-B%.

Compared to control, fasting and 2-h plasma insulin were higher in I-IGT and IFG-IGT subjects; similarly, HOMA-S% [median (range)] was lower in I-IGT and IFG-IGT subjects [116 (54-227) vs. 93 (23-187) and 79 (32-197)%, P<.05 and P<.001]; ISI(gly) was also lower in I-IGT and IFG-IGT subjects [0.95 (0.54-1.64) vs. 0.64 (0.26-1.24) and 0.65 (0.29-1.20), P<.001]. But HOMA-B% was compromised in IFG and IFG-IGT groups [88 (59-182) vs. 68 (37-107) and 74 (36-141)%, P<.001 and P<.05]. The IGT group (combination of I-IGT and IFG-IGT) showed higher fasting and 2-h insulin, and lower HOMA-S% as well as ISI(gly), but compromised HOMA-B% was not evident.

The pathophysiological mechanisms differ in IFG (having B-cell dysfunction) and I-IGT (an insulin-resistant condition). The pathophysiology of IFG-IGT (having both B-cell dysfunction and insulin resistance) indicates that it may be a different entity and not be included in IGT.