Hypothalamic Control of Eating Flashcards
Why do we stop eating
satiety
Gastric stretch causes
decrease in food intake
Gastric nutrient: sucrose –>
decreased food intake
Intestinal nutrient: sucrose –>
decrease food intake
liver factors via the portal vein senses Glucose and Free fatty acids –>
decreased food intake
In gastric distention, mechanoreceptors - vagal afferents relay to what center which causes a decrease in food intake
Nucleus Tractus Solitarius (NTS)
[solitary nucleus in the medulla]
Cholecytokinin (CCK) is a hormone that is released from the …
Duodenum
Cholecytokinin (CCK) causes
increased gallbladder contraction –> release of bile –> fat digestion
increased pyloric constriction –> increased stomach activity
Increased gastric contractions –> stomach activity digestion
______________ works on CCK receptors to increase excitation of vagal affernts (gastric mechanorecptors) which excites the NTS and decreased food intake
Cholecystokinin (CCK)
This hormone in the stomach is increased by fasting and is orexigenic (increases appetite)
Ghrelin
Prader-Willi Syndrome (deletion on chromosome 15)
Symptoms:
fetal hypotonia mental retardation obesity hyperphagia (excessive eating) hypogonadotropic hypogonadism (dcreased FSH and LH --> decreased gonadal function)
hypothalamic control of eating short-term signals
gastric distention
cholecytokinin (CCK)
Ghrelin
Hypothalamic control of eating long-term signals
Leptin
Leptin - the ob protein - is released from ________ and causes a decrease in food intake
adipocytes
Site of action for leptin
brainstem –> solitary nucleus
hypothalamus
Hypothalamic Nuclei implicated in control of food intake
Lateral hypothalamic area (LHA) Paraventricular nucleus (PVN) Arcuate nucleus (ARC)
Lateral hypothalamic area (LHA) lesion could cause
aphagia (cessation of eating)
aphagia due to damage to medial forebrain bundle
reduced motivation to eat (meso-limbic system –>DA)
reduced motor function
In the solitary nucleus, this increases responsiveness to gastric stretch
leptin
Lateral hypothalamic area (LHA)
Aphagia due to: loss of neurons that synthesze ________peptide
“orexigenic” OREXIN
Activation of LHA –> causes release of ______ neurotransmitter into the brainstem
anabolic (increased eating, increased eating/growth)
Paraventricular nucleus (PVN) neurons send axons to the brainstem to regulate food intake and causes _________
decrease in eating
Activation of the Paraventricular nucleus (PVN) causes
release of “catabolic” neurotransmittor(s) in the brainstem which causes decrease in eating and growth
Neurotransmitter released in the brainstem by the paraventricular nucleus
Corticotropin releasing hormone (CRH)
two populations of neurons in the Arcuate nucleus (ARC)
Neuropeptide Y (NPY) Melanocortin (POMC-derived peptide)
Neuropeptide Y (NPY) neurons project to
PVN and LHA which increases eating
Leptin acts in the ARC to inhibit
NPY neuronal activity (causes a decrease in food intake)
Melanocortin (POMC-derived peptide) neurons project both to
PVN and to LHA
Leptin acts in the ARC to activate
Melanocortin neuronal activity (causes decreased eating)
Ghrelin acts in the ARC to increase
NPY neuronal activity (causes increased food intake)
