Mechanism of hyperinsulinemia after reticuloendothelial system phagocytosis
| Autor: | J. P. Filkins, M. R. Yelich |
|---|---|
| Rok vydání: | 1982 |
| Předmět: |
Blood Glucose
Male medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism Phagocytosis medicine.medical_treatment Biology Islets of Langerhans In vivo Physiology (medical) Internal medicine Insulin Secretion medicine Hyperinsulinemia Animals Insulin Secretion Mononuclear Phagocyte System Mononuclear phagocyte system medicine.disease Rats Monokine Endocrinology Liver Hepatic portal vein |
| Zdroj: | The American journal of physiology. 242(2) |
| ISSN: | 0002-9513 |
| Popis: | Endocytic loading of the reticuloendothelial system (RES) results in acute hyperinsulinemia and functional hyperinsulinism. Colloidal carbon blockade of the RES in rats resulted in elevations of both portal vein and systemic serum immunoreactive insulin and increases in the hepatic portal vein insulin glucose ratios. Two mechanisms for the hyperinsulinemia were evaluated: 1) decreased removal of insulin by the postendocytic liver and 2) increased secretion of insulin by the isolated perfused pancreas. Colloidal carbon blockade did not alter removal of 125I-insulin as evaluated in the isolated perfused rat liver. Pancreases from postendocytic donor rats when perfused according to the technique of Grodsky manifested enhanced insulin secretion. Macrophage culture-conditioned media enhanced glucose-mediated insulin secretion both as assayed in vivo and in the isolated perfused rat pancreas. The data suggest that postendocytic activated macrophages secrete a monokine that alters insulin release and thus produces the hyperinsulinemia of RES blockade. The acronym MIRA for macrophage insulin-releasing activity is proposed for the monokine. |
| Databáze: | OpenAIRE |
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