Abstract
Type 2 diabetes (T2DM) is characterized by insulin resistance and beta cell dysfunction. Although both factors are hallmarks of T2DM, evidence from recent studies has emerged showing that impaired beta cell function is always present in humans with T2DM, suggesting that beta cell dysfunction is a core factor in the pathogenesis of T2DM. Deficit of beta cell mass in humans with T2DM has also been reported, probably through an increase in beta cell apoptosis. Whether deficit of function or mass of beta cells is more important in beta cell dysfunction in T2DM remains unclear; however, collectively, functional beta cell mass is decreased in humans with T2DM. Beta cell dysfunction is not only present in T2DM but also progressively worsens with duration of the disease. Recent studies have also revealed that the functional beta cell mass is already impaired before the onset of T2DM, implying that beta cell dysfunction is essential in the development of T2DM. Finally, ethnic difference in beta cell function has also been proposed. Recent studies suggest that Asians have less beta cell functional capacity compared with Caucasians. Therefore, preservation or recovery of functional beta cell mass is an important therapeutic strategy to prevent, treat and even cure T2DM, and this seems to be further emphasized for Asians.
Highlights
The number of patients with type 2 diabetes (T2DM) is continuously increasing throughout the world
Since a rather higher plasma insulin level was found in patients with Type 2 Diabetes (T2DM) following the development of a radioimmunoassay for insulin, insulin resistance has been emphasized as a cause of T2DM in contrast to type 1 diabetes, and it has been often assumed that T2DM is a disease of “insulin resistance” over the last several decades
Recent studies have consistently shown that people with T2DM have reduced beta cell function and even beta cell mass, indicating that beta cell failure is central in the pathogenesis of T2DM [2,3,4]
Summary
The number of patients with type 2 diabetes (T2DM) is continuously increasing throughout the world. If insulin sensitivity is decreased, insulin secretion increases to maintain normoglycemia. This relationship between insulin secretion and insulin sensitivity is expressed as a hyperbola (Figure 1). In patients with T2DM, a higher plasma insulin concentration is often found Based on this relationship, higher plasma insulin reflects greater insulin demand due to decreased insulin sensitivity. True beta cell function needs to be assessed with adjustment for concomitant insulin sensitivity, the socalled disposition index developed by Bergman et al [7,8]. Since the insulin secretion-insulin sensitivity relationship is hyperbolic, the disposition index, i.e., the product of insulin secretion and insulin sensitivity, is constant as long as normoglycemia is maintained. The disposition index decreases (Figure 1) [9,10]
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