AJP - Endocrinology and Metabolism, Vol 242, Issue 2 115-E120, Copyright © 1982 by American Physiological Society
Mechanism of hyperinsulinemia after reticuloendothelial system phagocytosis
J. P. Filkins and M. R. Yelich
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.
