A role for the endocrine and pro-inflammatory mediator MIF in the control of insulin secretion during stress
✍ Scribed by Gérard Waeber; Thierry Calandra; Christophe Bonny; Richard Bucala
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 205 KB
- Volume
- 15
- Category
- Article
- ISSN
- 1520-7552
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✦ Synopsis
The systemic response to injury or infection is often accompanied by signi®cant 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 in¯ammatory response. The protein known as macrophage migration inhibitory factor (MIF) has been identi®ed recently to play a central role in host immunity and to regulate glucocorticoid effects on the immune and in¯ammatory 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 b-cells and to act as an autocrine factor to stimulate insulin release. Since circulating MIF levels are elevated during stress or systemic in¯ammatory processes, this protein may play a central role in the control of insulin secretion during various disease states.