Endocrine Abstracts

Stressors engage a neural stress response network that is mediated in large part through the immediate actions of the stimuli on corticotropin-releasing factor (CRF) neurons in the amygdala (CeA) and in the long-term by the actions of glucocorticoids (GC) on increased synthesis of CRF in CeA and secretion of CRF on the monoaminergic cell groups as well as forebrain. The consequences of this bias behavioral, autonomic and endocrine outputs in the stressed organism. However, the GC also act both very rapidly and more slowly in hypothalamus and at the pituitary to damp further activity in the HPA axis. When elevations in GC are sustained, systemic insulin concentrations rise in parallel with GC. Together, elevated GC and insulin promote food intake, with a strong bias toward highly palatable calories in moderately stressed rats. This effect is also both acute and chronic. Systemically, the hormones promote increases in fat deposition. This combination over the long term increases fat depot weights. There is good evidence that a feedback signal denoting metabolic well-being acts on brain to reduce activity in the central stress response network, thus ameliorating the neural effects of stressors. Activity in common hepatic vagal afferents reduces intake of palatable calories, however, insulin overrides this action, and it is likely that the central action of insulin is responsible for fat and sucrose preferences shown in moderately stressed rats. Moreover, there is a strong, inverse relationship between mesenteric fat depot weights and hypothalamic CRF expression that supports the conclusion that metabolic well-being modulates the perception of stressors by the brain. Because the HPA axis appears to be in large part responsible for metabolic homeostasis and responds primarily to loss of metabolic stores, the dual feedback and feedforward actions of GC and insulin provide a highly appropriate means to re-establish metabolic equilibrium.