Regulation Of Food Intake Flashcards
Neuronal Centers for feeding control
Lateral Nucleus Ventromedial Nucleus Paraventricular Nucleus Dorsomedial Nucleus Arcuate Nucleus
Neural signals from GI to brain is by
VAGUS
Hs. For appetite
- GI : PYY, CCK
- Fat : Leptin
- Stomach : Ghrelin
- Pancreas : Insulin
- Cerebral Cortex: Sight, smell, taste
Anorexigenic Pathway (Part 1 pathway)
Insulin, Leptin, CCK ——> Arcuate Nucleus (POMC, CART) ——> a-melanocytes stimulating H. (a-melanocortin) released from AN and binds to the MCR-4 receptor in the NEURON of HYPOTHALAMUS (paraventricular Nuc.)
= NO TO FOOD INTAKE
= Nucleus Tractus ——> energy expenditure by activating sympathetic pathway
Orexigenic Pathway (Part 2 pathway)
Ghrelin ——> ARCUTE NUCLEUS (AGRP/NYP) ——> Nueropeptide Y is released and binds to receptors Y1r in
1. Neurons in HYPOTHALAMUS (paraventricular Nuc.)= YES TO FOOD INTAKE
AGRP is released and binds to Y1r ——I MCR-4 receptor to bind to a-MSH in paraventricular Nuc.
MCR-3
Found on AGRP and NPY nucleus in AN and inhibits it when
a-MSH binds
Some obesity mutations have
Mutations in the POMC and MCR-4 genes
MCR-4 tells you you are full
causes of obesity not mutations
- X Leptin or LeptinR
- Prayer-Willi Syndrome (deleted Chr15)
- X POMC
Paradox in prayer Willi Syndrome
High Ghrelin
Vagal activity and feeding behavior
Amount of food in stomach and distention in stomach signals using the vagus N to feel hungry or full ——-> Nucleus Solitarius (dorsal Vagus Complex)——> Hypothalamus
Feeding behavior signals are
Able to operate without any Higher Brain Centers input
Orexigenic Promotes and some areas in charge
EATING (Ghrelin——>NYP + AGRP- in Arcuate Nucleus)——> :
- Lateral Hypothalamic Area (LHA) is the huger center ———> brain releasing MCH or orexins A and B
- Dorsomedial Hypothalamus (DMN)
- Paraventricular Nucleus gets all signals——> cerebral cortex and brainstem
Anorexigenic promotes and some areas in charge
SATIETY(Leptin,CCK, Insulin, stretch)——>POMC + CART- in Arcuate Nucleus)——> :
- Ventromedial Hypothamic Nucleus : *major satiety center
- Dorsomedial Hypothalamus (DMN)
- Paraventricular Nucleus gets all signals——> cerebral cortex and brainstem
Ghrelin
Endocrine cells in stomach, SI, LI, Hypothalamus
Bind to——> GHSR in the NYP/POMC (arcuate nucleus)——> Release NYP
= increase appetite, gastric acid + motility, adipogenesis,
= decrease insulin
Insulin
From B-cells in pancreas : Binds to ——I NYP Binds to ——> POMC = increase metabolism = decrease food intake T1D : increase food intake due to low insulin
CCK
Released by I cells in duodenum
Binds to Vagal neuron ——> Nucleus Slitarius ——> Hypothalamus = decrease Ghrelin
= decrease Gastric emptying —> increase gastric distention
PYY
Released from L cells from ileum and colon
Binds to Y2R in the hypothalamus——I NYP/AGRP neurons +
——> POMC
= full decrease food intake
Leptin
Released from adipose
Binds to ——> POMC and ——I NYP/AGRP
= increase metabolism
= decrease food intake + Ghrelin release
Obesity is usually due to what )involving Leptin
High levels of Leptin and low responses to it (resistance)
a-MSH
POMC releases a-MSH——> Bind to MC4R neurons in Paraventricular N
= increase metabolism and decrease appetite
AGRP
AGRP/NYP releases it——I MC4R neurons in the Paraventricular nucleus
= inhibit metabolism
= inhibit satiety = hunger to eat
NYP
AGRP/NYP releases it——> Y2R neurons in the Paraventricular nucleus
= increase appetite and decrease metabolism
What is responsible for long-term energy balance
Adiposity
Glucagon- like peptide (GLP-1)
Secreted with PYY from L- cells in the SI
Rise after meal
= satiety
= lower glucagon
= inhibit gastric emptying
= increase INCRETIN = release insulin from pancreas
