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DNA Synthesis in Pancreatic Islet and Acinar Cells in Rats with Streptozotocin-Induced Diabetes

Nancy A. Hamming, William M. Reynolds

Open publisher page 7 citations

Abstract

The rates of DNA synthesis in islet and acinar cells were compared at different intervals following streptozotocin-induced diabetes. Streptozotocin, injected I.V. at a dosage of 65 mg/kg, consistently produced a diabetic-like state in young rats, ages 33 to 42 days. At two, four, and seven days after streptozotocin administration, no significant difference in DNA synthesis per mm2 of islet and acinar tissue was evident. However, four days after streptozotocin injection, a significant increase over control values was observed in the number of cells per islet incorporating tritiated thymidine. Following streptozotocin administration, beta cells generally appeared degranulated but not necrotic. Transformation of acinar cells or ductal elements to beta cells was not observed, suggesting that proliferating beta cells are the progeny of pre-existing beta cells. This study suggests that a brief, temporary period of compensatory proliferation of beta cells follows the initial insult of the diabetogenic agent streptozotocin in young rats.

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The rates of DNA synthesis in islet and acinar cells were compared at different intervals following streptozotocin-induced diabetes. Streptozotocin, injected I.V. at a dosage of 65 mg/kg, consistently produced a diabetic-like state in young rats, ages 33 to 42 days. At two, four, and seven days after streptozotocin administration, no significant difference in DNA synthesis per mm2 of islet and acinar tissue was evident. However, four days after streptozotocin injection, a significant increase over control values was observed in the number of cells per islet incorporating tritiated thymidine. Following streptozotocin administration, beta cells generally appeared degranulated but not necrotic. Transformation of acinar cells or ductal elements to beta cells was not observed, suggesting that proliferating beta cells are the progeny of pre-existing beta cells. This study suggests that a brief, temporary period of compensatory proliferation of beta cells follows the initial insult of the diabetogenic agent streptozotocin in young rats.

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Available abstract

The rates of DNA synthesis in islet and acinar cells were compared at different intervals following streptozotocin-induced diabetes. Streptozotocin, injected I.V. at a dosage of 65 mg/kg, consistently produced a diabetic-like state in young rats, ages 33 to 42 days. At two, four, and seven days after streptozotocin administration, no significant difference in DNA synthesis per mm2 of islet and acinar tissue was evident. However, four days after streptozotocin injection, a significant increase over control values was observed in the number of cells per islet incorporating tritiated thymidine. Following streptozotocin administration, beta cells generally appeared degranulated but not necrotic. Transformation of acinar cells or ductal elements to beta cells was not observed, suggesting that proliferating beta cells are the progeny of pre-existing beta cells. This study suggests that a brief, temporary period of compensatory proliferation of beta cells follows the initial insult of the diabetogenic agent streptozotocin in young rats.

Key concepts: Streptozotocin, Endocrinology, Internal medicine, Islet, Diabetes mellitus, Beta cell, Pancreas, DNA synthesis

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DNA Synthesis in Pancreatic Islet and Acinar Cells in Rats with Streptozotocin-Induced Diabetes — Research Paper | ScholarLens