Glucose homeostasis and hypothalamic-pituitary-adrenocortical axis during development in rats

Abstract

Glucoprivation represents a model stress in which activation of different stress responses at different ages can be monitored both in vivo and in vitro. Physiological data indicate rat brain contains a liver/pancreas-type glucose sensor, yet no biochemical or immunocytochemical evidence exists for such a sensor. Young rats appear to lack normal hypothalamic glucose-sensing ability and do not show typical secretory patterns of corticotropin-releasing factor, adrenocorticotropic hormone, or corticosterone after experimentally induced glucoprivation. However, they hypersecrete catecholamines and glucagon (compared with adults) and thrive on fuel sources other than glucose that are abundant after birth. High steroid levels during the first 24 h after birth may be critical for inducing gluconeogenic enzymes and promoting differentiation of tissues like pancreas. Neonatal rats also have unique control systems to combat the damaging effects of other stresses like hypoxia; these systems may disappear in adults. Thus the definition of stress may change during development, and the compensatory mechanisms employed to combat stress change from neonatal to adult life and are intricately related to the metabolic needs of the animal.