期刊
ISLETS
卷 2, 期 6, 页码 353-356出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/isl.2.6.13619
关键词
beta cell mass; insulin resistance; islet adaptation; apoptosis; proliferation
资金
- Swedish Research Council [6834, 4216, K2009-55X-21111-01-4]
- Region Skane
- Albert Pahlssons Foundation
- Novo Nordisk Foundation
- Faculty of Medicine, Lund University
As we previously demonstrated, there is an adaptive increase in insulin secretion in insulin resistance in the model of high-fat fed female mice. Since it is assumed that islets also adapt to insulin resistance with beta-cell expansion, we have now examined beta-cell volume in this experimental model. Female C57BL/6JBomTac mice were therefore fed a high-fat diet (60% fat from lard) for three, six or twelve months and beta-cell volume was estimated as beta-cell area per islet, individual beta-cell size and beta-cell number per islet. Control animals were fed a normal chow (11% fat). We found that beta-cell area per islet and total number of beta-cells per islet were increased already after three months of high-fat feeding and that this increase was sustained throughout the twelve month study period. In contrast, individual beta-cell size showed a dynamic pattern with a reduction after three months followed by increase after six and twelve months. The number of apoptosis (caspase-3) positive beta-cells was reduced after three months, whereas there was no difference in proliferation (Ki-67) positive cells, although these were generally rarely observed. Thus, we conclude that insulin resistance accompanying high-fat feeding in mice is followed by progressive beta-cell expansion as evident by early increased islet beta-cell volume and total number of beta-cells, whereas individual beta-cell size showed a dynamic response. The model is also associated with an early reduced apoptosis, which may contribute to the increased beta-cell volume.
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