Regeneration of Beta-cells in Response to Islet Inflammation

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Abstract
Subtotal pancreatectomy (90%) in Lewis rats induces chronic islet inflammation and tissue damage in the remaining pancreas 4 months after surgery. Concomitantly, significant enlargement of the islets of Langerhans was observed (90% pancreatectomy: islet/pancreas area: 25.6 ± 9.6 × 10−3, beta-cell/pancreas area: 12.4 ± 4.4 × 10−3; n = 4; controls without pancreatectomy: islet/pancreas area: 5.5 ± 1.7 × 10−3, beta-cell/ pancreas area: 4.6 ± 1.5 × 10−3; n = 4; p < 0.05, respectively). Islet growth is mainly due to an increase in beta-cell mass. Beta-cell regeneration was not caused by the surgical manipulations or by metabolic stress. The former was ruled out by performing 10% pancreatectomy which did not cause islet enlargement after 4 months (islet/pancreas area: 13.6 ± 11.3 × 10−3, beta-cell/pancreas area: 7.1 ± 2.0 × 10−3; n = 3). An influence of metabolic stress was excluded by continuous substitution of syngenic islet antigens, which inhibits insulitis. In the absence of islet inflammation, despite persistent metabolic stress, beta-cell regeneration did not occur (islet/pancreas area: 7.0 ± 5.5 × 10−3, beta-cell/pancreas area: 5.5 ± 4.1 × 10−3; n = 4). Continuous treatment of animals after 90% pancreatectomy by insulin implants (1.5 U/day) avoided insulitis and beta-cell growth (islet/pancreas area: 9.2 ± 1.1 × 10−3, beta-cell/pancreas area' 6.8 ± 1.0 × 10−3, n = 3): All enlarged islets observed 4 months after 90% pancreatectomy without further treatment were infiltrated. Thus, beta-cell growth appears to! be a response to insulitis. The stimulus for beta-cell growth could result from tissue damage caused by infiltrating cells or from cytokines secreted by the infiltrating cells, or both.

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