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Betacellulin improves glucose metabolism by promoting conversion of intraislet precursor cells to -cells in streptozotocin-treated mice

¹Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512; and ²Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University, Okayama 700-8530, Japan

Submitted 20 March 2003 ; accepted in final form 12 May 2003

Betacellulin (BTC) induces differentiation of pancreatic -cells and promotes regeneration of -cells in experimental diabetes. The present study was conducted to determine if BTC improved glucose metabolism in severe diabetes induced by a high dose of streptozotocin (STZ) in mice. Male ICR mice were injected with 200 µg/g ip STZ, and various doses of BTC were administered daily for 14 days. The plasma glucose concentration increased to a level of >500 mg/dl in STZ-injected mice. BTC (0.2 µg/g) significantly reduced the plasma glucose concentration, but a higher concentration was ineffective. The effect of BTC was marked by day 4 but became smaller on day 6 or later. The plasma insulin concentration and the insulin content were significantly higher in mice treated with 0.1 and 0.2 µg/g BTC. BTC treatment significantly increased the number of -cells in each islet as well as the number of insulin-positive islets. Within islets, the numbers of 5-bromo-2-deoxyuridine/somatostatin-positive cells and pancreatic duodenal homeobox-1/somatostatin-positive cells were significantly increased by BTC. These results indicate that BTC improved hyperglycemia induced by a high dose of STZ by promoting neoformation of -cells, mainly from somatostatin-positive islet cells.

pancreas

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