Author(s): Kou K, Saisho Y, Satoh S, Yamada T, Itoh H, Kou K, Saisho Y, Satoh S, Yamada T, Itoh H, Kou K, Saisho Y, Satoh S, Yamada T, Itoh H, Kou K, Saisho Y, Satoh S, Yamada T, Itoh H
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Abstract AIM: The aim of this study was to clarify the change in β-cell mass in Japanese obese individuals. METHODS: We obtained the pancreas at autopsy from 39 lean and 33 obese Japanese nondiabetic individuals (aged 47 ± 13 vs 47 ± 12 y, P = .83, body mass index 20.4 ± 1.6 vs 28.5 ± 3.9 kg/m(2), P < .01). Pancreatic sections were stained for insulin, and β-cell area (\%BCA) was measured as the fraction of the β-cell area to the total pancreas area. β-Cell mass was then calculated as the product of \%BCA and estimated pancreas weight. β-Cell replication and apoptosis were assessed by double staining for insulin and Ki67 and insulin and single-stranded DNA, respectively. The frequencies of insulin-positive duct cells and scattered β-cells were assessed as the surrogate markers of β-cell neogenesis. The α-cell area (\%ACA) was also measured, and the \%ACA to \%BCA ratio was determined. RESULTS: There was no increase in β-cell mass in obese individuals compared with lean individuals (0.6 ± 0.4 vs 0.7 ± 0.4 g, P = .12). β-Cell replication, β-cell neogenesis, and β-cell apoptosis were not significantly increased in the presence of obesity. There was no significant difference in \%ACA to \%BCA ratio between obese and lean individuals (0.91 ± 1.09 vs 0.75 ± 0.51, P = .47). CONCLUSION: There was no increase in β-cell mass and no detectable change in β-cell turnover in Japanese obese individuals.
This article was published in J Clin Endocrinol Metab
and referenced in Diabetes Case Reports