Volume 1, Issue 5 p. 424-430
Original Article
Free Access

Hepatocyte and Kupffer cell functions during liver regeneration in streptozotocin-diabetic rats

Robert P. Cornell Ph.D.

Corresponding Author

Robert P. Cornell Ph.D.

Division of Science, Northeast Missouri State University, Kirksville, Missouri 63501

Associate Professor of Physiology, Division of Science, Northeast Missouri State University. Kirksville. Missouri 63501===Search for more papers by this author
Brenda K. Hinck

Brenda K. Hinck

Division of Science, Northeast Missouri State University, Kirksville, Missouri 63501

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Randall E. Halley

Randall E. Halley

Division of Science, Northeast Missouri State University, Kirksville, Missouri 63501

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First published: September/October 1981
Citations: 3

Abstract

The insulinoprivic influence of acute severe streptozotocin diabetes on liver regeneration in rats was evaluated by determining liver weights as well as hepatocyte and Kupffer cell functional capacities. Functional capacities were assessed by bromosulfophthalein uptake for hepatocytes and carbon phagocytosis for Kupffer cells. Evaluation immediately after partial hepatectomy revealed a 66% reduction of liver mass, a 63% decrease in hepatocyte bromosulfophthalein removal, and a 65% decline in Kupffer cell carbon phagocytosis. Per cent recovery at 48-hr posthepatectomy was considerably greater for carbon phagocytosis than for bromosulfophthalein removal by regenerating livers. This apparent difference in functional recovery was likely due in part to enhanced non-Kupffer cell carbon phagocytosis. No significant differences of the three regeneration indices were noted for untreated streptozotocin-diabetic rats compared to nondiabetic animals. However, insulin administration to fasted streptozotocin diabetics significantly stimulated liver regeneration above that of untreated fasted rats and almost equivalent to that of pair-fed animals. Fasted rats had in general slower liver regeneration than pair-fed animals as expected. Furthermore, insulin administration to fasted nondiabetic rats after partial hepatectomy caused severe hypoglycemia and resulted in a further depression of liver regeneration.