Central Control of Feeding Balance
Depletion-repletion Hypothesis states feeding is controlled by caloric set point. Individuals match energy expenditures with intake without reference to fat storage.
Primed Response Hypothesis states that feeding essentially boils down to idea that animals will eat whenever an opportunity arises unless it is specifically inhibited. Satiety controlled.
Mechanisms of Satiety Control and Satiety Network
Neural signals are Vagus dependant. Afferent signals conveyed by vagus limit meal size. Vagus also sends signals to mediate cephalic phase of glucose release.
Humoral signals are insulin and leptin. Insulin regulates satiety related to caloric control while leptin with relation to specific set point of body weight.
Dual Center hypothesis centers on bilateral control of feeding/satiety by Ventrolateral hypothalamus and Vetromedial hypothalamus. (VLH/VMH)
Ventromedial Hypothalamus lesion:
-SATIETY center
-controlled by ARCUATE nucleus
-decreased sympathetic tone
-increased parasympathetic tone
-no COMPLETE loss of satiety- meal interval shorter so NEW SET POINT
-prevented by vagotomy
-causes obesity
Ventrolateral hypothalamic lesion:
-FEEDING center
-slowed gastic emptying
-increased sympathetic tone
-decreased parasympathetic tone
-produces severe anorexia
-Parkinson’s disease
Neuropeptide Y (arcuate nucleus) controls INCREASE in appetite. Secreted within 6 hours of food deprivation.
POMC inhibits feeding and is a satiety mediator.
Weight Loss Pathway Hypothalamic Response:
Decrease of body fatà Decrease leptin/insulinà decrease POMC/CART in Arcà increase NPY/AGPR binding of NPY to VLHyothalamus/PVN R5 receptors inhibition of R3/R4 receptors in VMHypothalamus — FEEDING
Weight Gain Pathway Hypothalamic Response
Increase in body fat increase leptin/insulin increase POMC/CART in Arc decrease NPY/AGRP binding of POMC to R3/R4 receptors in VMH/Arc/PVN inhibition of R5 receptors of NPY SATIETY
Tags: anorexia, arcuate nucleus, insulin, lelptin, neuropeptide Y, obesity, parasympathetic tone, Parkiknson's disease, satiety control, vagus, Ventrolateral hypothalamus
