Effects of Obesity and Diabetes on Beta-Cell Mass in Japanese

Jun Inaishi, Yoshifumi Saisho* and Hiroshi Itoh

Effects of Obesity and Diabetes on Beta-Cell Mass in Japanese.

The prevalence of type 2 diabetes mellitus continues to increase all over the world. T2DM is characterized
by insulin resistance and β-cell dysfunction. Recent studies have shown that β-cell dysfunction, but not
insulin resistance, is critical
for the development of T2DM.

Since Butler et al and other groups have reported reduced β-cell mass in both lean and obese
individuals with T2DM, it is now widely recognized that β-cell deficit is a core feature of T2DM. In
adult humans, we and others have shown that BCM is increased by approximately 20-50% in obese
non-diabetic individuals in the Caucasian population.

Increased workload of beta-cells may result in beta-cell death through various
mechanisms such as hyperglycemia, dyslipidemia, oxidative stress, endoplasmic reticulum
stress, inflammatory cytokines, and amyloid deposition. Recent rodent studies have suggested
that dedifferentiation of β-cells to α-cells is another cause of the reduction of BCM in T2DM.
However, the change in α-cell mass in patients with diabetes is controversial.

ACM has been reported to increase or decrease in patients with T2DM, while
we and another Japanese
study observed no significant increase in BCM in obese
non-diabetic adults in the Japanese population.

Considering the similar incidence of T2DM despite the lower degree of obesity in Japanese compared with
Caucasians these findings suggest that β-cell regenerative capacity may differ between Japanese and Caucasians.

Pancreas Open J. 2016; 1(2): e11-e13. doi: 10.17140/POJ-1-e004

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