The fact that basal insulin, regardless of NPH or glargine, decreases A1C more in obese than in nonobese patients with type 2 diabetes (independent of baseline A1C) might be explained by greater endogenous insulin secretion, which is reported in the former as compared with latter patients.[20] It is likely that the lower A1C in the obese patients was explained by less postprandial hyperglycemia as a consequence of more preserved insulin secretion in this group. Here, INS is linked to Hyperglycemia.