Can Inhibitors of Luminal Carbohydrate Digestion Decrease Insulin Resistance in Obesity and T2DM?

Abstract

Premature dysregulation of gastric emptying in concert with hyperinsulinemia are a common observation in early stages of Type 2 Diabetes (T2DM) and contributes to the magnitude of the typical glycemic excursions and insulinogenic responses following carbohydrate-laden meals. In contrast, in later stages of the disorder gastroparesis may occur secondary to diabetic neuropathy. While dietary measures are often a first line approach, inhibitors of luminal starch digestion have been demonstrated to slow the rate of α-glucosidase and sucrase activity following a carbohydrate meal in man and animals, thereby attenuating the immediate glycemic and insulinogenic responses. The improved glycemic and insulinogenic responses if maintained over the course of weeks or months result in improvements in glycated hemoglobin, insulin sensitivity and glucose disposal in peripheral tissues, with secondary improvements in lipogenesis, plasma lipid profiles including plasma triglycerides and LDL cholesterol fractions. Thus, incorporation of inhibitors of α-glucosidase and sucrase activity posit to become useful adjuncts as monotherapy or in combination with other therapeutic agents including GLP-1 incretin mimetics, phototherapeutics, phyto therapeutics and other obesity and diabetic therapeutic agents in the clinical management of hyperinsulinemia, obesity, prediabetes, T2DM and insulin resistant states as they occur in man and animals.