Postprandial hyperglycemia and postprandial hypertriglyceridemia in type 2 diabetes

Abstract

Postprandial glucose level is an independent risk factor for cardiovascular disease that exerts effects greater than glucose levels at fasting state, whereas increase in serum triglyceride level, under both fasting and postprandial conditions, contributes to the development of arteriosclerosis. Insulin resistance is a prevailing cause of abnormalities in postabsorptive excursion of blood glucose and postprandial lipid profile. Excess fat deposition renders a vicious cycle of hyperglycemia and hypertriglyceridemia in the postprandial state, and both of which are contributors to atherosclerotic change of vessels especially in patients with type 2 diabetes mellitus. Several therapeutic approaches for ameliorating each of these abnormalities have been attempted, including various antidiabetic agents or new compounds targeting lipid metabolism.

Fig.1

Blood glucose and lipid regulation. pancreas, liver and blood vessels. After meal, pancreatic beta cells release insulin to inhibit hepatic gluconeogenesis and glycogenolysis. Insulin also acts at peripheral tissues to increase glucose uptake (muscle), contributing to decreased blood glucose level. GLP-1 and GIP are incretin hormones which secreted by the gut. Incretin hormones can stimulate pancreatic beta cells to secrete insulin. GLP-1 suppressed inappropriate glucagon secretion from pancreatic alpha cells. Nutrient from the gastrointestinal tract, muscle and adipose tissue such as glucose, amino acids and glycerol which are energy resource of the body introduce into the liver. In insulin resistance state, overproduction of TRL associated with hepatic VLDL production. Increasing TRL is strongly contribute hypertryglyceridemia which is related indirectly to atherosclerotic progression through increase in sdLDL and lowered HDL. Interaction between enlarged fat cell and macrophages in adipose tissue evokes chronic inflammatory response, resulting in overproduction of FFA.

Fig.2

Vascular injury due to glucose spike in T2D. The rapid fluctuation in blood glucose level repeated every meal is called "glucose spike", which damages blood vessels and causes progression of atherosclerosis. In this condition, increasing lipid peroxydation, platelet coagulation and synthesis of ROS. Arteriosclerosis starts from the early stage of postprandial hyperglycemia of diabetes, or the stage of IGT earlier than that.