ABSTRACT
Observations of glucosuria during infections were already made at the end of the 19th century, which was followed by the demonstration of hyperglycemia and insulin resistance in infectious disease. The immune system is activated nonspecifically during injury which leads to a pattern of cytokine production similar to acute infections and may culminate in endocrine and metabolic responses characteristic of the acute phase response. Infection with lymphocytic choriomeningitis virus leads to growth hormone (GH) deficiency in some mouse strains which is due to the impairment of GH secreting pituitary cells by the virus. A newly isolated pituitary hormone, called suppressin, inhibited mitogen-induced and IL-2-dependent lymphocyte proliferation. Another pituitary factor isolated from bovine glands induced thymic epithelial cell proliferation in vitro. Inflammatory mediators, such as platelet activating factor, bradykinin, histamine, and prostaglandins, are also involved in the regulation of pituitary hormone secretion.
