Abstract

Diabetes mellitus is classified into two categories, type 1 and type 2. Type 1 diabetes mellitus (T1D or IDDM; Insulin Dependent Diabetes Mellitus) is characterized by a loss of insulin secretion due to pancreatic β-cell degeneration, leading to autoimmune attack. Type 2 diabetes mellitus (T2D or NIDDM; Non Insulin Dependent Diabetes Mellitus) is metabolic disorder that is caused by insufficient insulin secretion and/or insulin resistance in peripheral and liver tissues. It is known that 90-95% of diabetes is diagnosed as T2D [2]. Development of T2D is usually caused by several factors, which are combined with lifestyle, genetic defects, virus infection, and drugs [3, 4]. Sustained hyperglycemia causes severe diabetic microvascular complications, such as retinopathy, peripheral neuropathy, and nephropathy. In the diabetic states, multiple mechanisms have been implicated in glucosemediated vascular damage and contribute to diabetic microvascular complications. In addition, postprandial state is also an important factor in the development of macroangiopathy. In diabetes, the postprandial phase is characterized by an exaggerated rise in blood glucose levels. It has recently been shown that postprandial hyperglycemia is relevant to onset of cardiovascular complications. From this evidence, treatment of diabetes has become a part of the strategies for the prevention of diabetic vascular complications.

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