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Preferential suppression of insulin‐stimulated proliferation of cultured hepatocytes by somatostatin: Evidence for receptor‐mediated growth regulation
Author(s) -
Kothary Piyush C.,
Kokudo Norihiro,
Eckhauser F. E.,
Delvalle John,
Raper Steven E.
Publication year - 1995
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240590214
Subject(s) - liver regeneration , hepatocyte , somatostatin , thymidine , hepatectomy , medicine , glucagon , biology , endocrinology , dna synthesis , receptor , intracellular , microbiology and biotechnology , insulin , dna , chemistry , biochemistry , regeneration (biology) , in vitro , surgery , resection
The role of somatostatin (SS‐14) in the regulation of rat liver regeneration was examined by using thymidine incorporation into hepatocyte DNA labeled with tritiated thymidine, a nuclear‐labeling index, and the binding of 125 I‐tyr 11 ‐SS‐14 to hepatocytes isolated at various times after partial hepatectomy. The data demonstrated no suppressive effect of SS‐14 on insulin and glucagon‐stimulated thymidine incorporation into hepatocyte DNA as early as 2 h after partial hepatectomy. These data were substantiated by a nuclear labeling index studies. At 2 h, 125 I‐tyr 11 ‐SS‐14 binding to its specific sites on isolated hepatocytes was undetectable. There was a time‐dependent increase in binding of 125 I‐tyr 11 ‐SS‐14 to hepatocytes obtained at various times after partial hepatectomy. There was a significant decrease in the number of binding sites after partial hepatectomy as determined by Scatchard analysis. The data were supported by autoradiography analysis of affinity labeled 125 I‐tyr 11 ‐SS‐14‐binding protein complex followed by SDS‐PAGE. SS‐14 also inhibited intracellular cAMP in hepatocytes obtained at 18 h after hepatectomy. The data are consistent with the hypothesis that SS‐14 participates via its own receptor in the regulation of the liver regeneration. © 1995 Wiley‐Liss, Inc.