Premium
A role for the endocrine and pro‐inflammatory mediator MIF in the control of insulin secretion during stress
Author(s) -
Waeber Gérard,
Calandra Thierry,
Bonny Christophe,
Bucala Richard
Publication year - 1999
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/(sici)1520-7560(199901/02)15:1<47::aid-dmrr9>3.0.co;2-j
Subject(s) - macrophage migration inhibitory factor , medicine , endocrinology , insulin , glucose homeostasis , autocrine signalling , immune system , glycogenesis , insulin resistance , inflammation , homeostasis , biology , glucocorticoid , immunology , cytokine , receptor , glycogen synthase
Abstract The systemic response to injury or infection is often accompanied by significant alterations in host metabolism and glucose homeostasis. Within the liver, these changes include a decrease in glycogenesis and an increase in gluconeogenesis, and in peripheral tissues, the development of insulin resistance and the increased utilization of glucose by non‐insulin‐dependent pathways. Depending on the severity and the duration of the response, both hyper‐ and hypoglycemia can ensue and each can become a clinically important manifestation of the systemic inflammatory response. The protein known as macrophage migration inhibitory factor (MIF) has been identified recently to play a central role in host immunity and to regulate glucocorticoid effects on the immune and inflammatory systems. MIF is released in vivo from activated immune cells as well as by the anterior pituitary gland upon stimulation of the hypothalamic‐pituitary‐adrenal axis. MIF also has been found to be secreted together with insulin from the pancreatic β ‐cells and to act as an autocrine factor to stimulate insulin release. Since circulating MIF levels are elevated during stress or systemic inflammatory processes, this protein may play a central role in the control of insulin secretion during various disease states. Copyright © 1999 John Wiley & Sons, Ltd.