Insulin-like growth factor I does not inhibit insulin secretion in adult human pancreatic islets in tissue culture
Decio Laks Eizirik, Anna Skottner, Claes Hellerström
Abstract
Decio Laks Eizirik, Anna Skottner, Claes Hellerström
Abstract
Eizirik DL, Skottner A, Hellerström C. Insulin-like growth factor I does not inhibit insulin secretion in adult human pancreatic islets in tissue culture. Eur J Endocrinol 1995;133:248–50. ISSN 0804–4643 Insulin-like growth factor I (IGF-I) has been found to increase insulin sensitivity and suppress insulin secretion, thereby having a potential interest as a therapeutic agent for non-insulin-dependent diabetes mellitus (NIDDM). The aim of the present study was to investigate the direct actions of IGF-I (400 ng/ml) on human pancreatic islets, or on rat pancreatic islets, during a 48 h period in tissue culture. Insulin-like growth factor I did not affect medium insulin accumulation, DNA or insulin content or short-term glucose-induced insulin release of human islets. However, in rat islets the peptide induced a significant decrease in the insulin increase ratio in response to 16.7 mmol/l glucose. In conclusion, the present data suggest that IGF-I does not directly affect the function of human pancreatic β-cells If this in vitro data can be extrapolated to the in vivo situation, it suggests that the observed inhibitory effects of IGF-I on serum insulin levels may be secondary to peripheral effects of the peptide. Décio L Eizirik, Department of Medical Cell Biology, Biomedicum, PO Box 571, S-751 23 Uppsala, Sweden
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Eizirik DL, Skottner A, Hellerström C. Insulin-like growth factor I does not inhibit insulin secretion in adult human pancreatic islets in tissue culture. Eur J Endocrinol 1995;133:248–50. ISSN 0804–4643 Insulin-like growth factor I (IGF-I) has been found to increase insulin sensitivity and suppress insulin secretion, thereby having a potential interest as a therapeutic agent for non-insulin-dependent diabetes mellitus (NIDDM). The aim of the present study was to investigate the direct actions of IGF-I (400 ng/ml) on human pancreatic islets, or on rat pancreatic islets, during a 48 h period in tissue culture. Insulin-like growth factor I did not affect medium insulin accumulation, DNA or insulin content or short-term glucose-induced insulin release of human islets. However, in rat islets the peptide induced a significant decrease in the insulin increase ratio in response to 16.7 mmol/l glucose. In conclusion, the present data suggest that IGF-I does not directly affect the function of human pancreatic β-cells If this in vitro data can be extrapolated to the in vivo situation, it suggests that the observed inhibitory effects of IGF-I on serum insulin levels may be secondary to peripheral effects of the peptide. Décio L Eizirik, Department of Medical Cell Biology, Biomedicum, PO Box 571, S-751 23 Uppsala, Sweden
Key concepts: Internal medicine, Endocrinology, Insulin, Pancreatic islets, Islet, Insulin oscillation, Growth factor, Diabetes mellitus