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GIGU Exam 1 > Regulation Of Food Intake > Flashcards

Regulation Of Food Intake Flashcards

1
Q

Neuronal Centers for feeding control

A 
Lateral Nucleus 
Ventromedial Nucleus
Paraventricular Nucleus 
Dorsomedial Nucleus 
Arcuate Nucleus
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2
Q

Neural signals from GI to brain is by

A

VAGUS

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3
Q

Hs. For appetite

A
  1. GI : PYY, CCK
  2. Fat : Leptin
  3. Stomach : Ghrelin
  4. Pancreas : Insulin
  5. Cerebral Cortex: Sight, smell, taste
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4
Q

Anorexigenic Pathway (Part 1 pathway)

A

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

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5
Q

Orexigenic Pathway (Part 2 pathway)

A

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.

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6
Q

MCR-3

A

Found on AGRP and NPY nucleus in AN and inhibits it when

a-MSH binds

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7
Q

Some obesity mutations have

A

Mutations in the POMC and MCR-4 genes

MCR-4 tells you you are full

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8
Q

causes of obesity not mutations

A
  1. X Leptin or LeptinR
  2. Prayer-Willi Syndrome (deleted Chr15)
  3. X POMC
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9
Q

Paradox in prayer Willi Syndrome

A

High Ghrelin

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10
Q

Vagal activity and feeding behavior

A

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

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11
Q

Feeding behavior signals are

A

Able to operate without any Higher Brain Centers input

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12
Q

Orexigenic Promotes and some areas in charge

A

EATING (Ghrelin——>NYP + AGRP- in Arcuate Nucleus)——> :

  1. Lateral Hypothalamic Area (LHA) is the huger center ———> brain releasing MCH or orexins A and B
  2. Dorsomedial Hypothalamus (DMN)
  3. Paraventricular Nucleus gets all signals——> cerebral cortex and brainstem
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13
Q

Anorexigenic promotes and some areas in charge

A

SATIETY(Leptin,CCK, Insulin, stretch)——>POMC + CART- in Arcuate Nucleus)——> :

  1. Ventromedial Hypothamic Nucleus : *major satiety center
  2. Dorsomedial Hypothalamus (DMN)
  3. Paraventricular Nucleus gets all signals——> cerebral cortex and brainstem
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14
Q

Ghrelin

A

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

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15
Q

Insulin

A 
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
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16
Q

CCK

A

Released by I cells in duodenum
Binds to Vagal neuron ——> Nucleus Slitarius ——> Hypothalamus = decrease Ghrelin
= decrease Gastric emptying —> increase gastric distention

17
Q

PYY

A

Released from L cells from ileum and colon
Binds to Y2R in the hypothalamus——I NYP/AGRP neurons +
——> POMC
= full decrease food intake

18
Q

Leptin

A

Released from adipose
Binds to ——> POMC and ——I NYP/AGRP
= increase metabolism
= decrease food intake + Ghrelin release

19
Q

Obesity is usually due to what )involving Leptin

A

High levels of Leptin and low responses to it (resistance)

20
Q

a-MSH

A

POMC releases a-MSH——> Bind to MC4R neurons in Paraventricular N
= increase metabolism and decrease appetite

21
Q

AGRP

A

AGRP/NYP releases it——I MC4R neurons in the Paraventricular nucleus
= inhibit metabolism
= inhibit satiety = hunger to eat

22
Q

NYP

A

AGRP/NYP releases it——> Y2R neurons in the Paraventricular nucleus
= increase appetite and decrease metabolism

23
Q

What is responsible for long-term energy balance

A

Adiposity

24
Q

Glucagon- like peptide (GLP-1)

A

Secreted with PYY from L- cells in the SI
Rise after meal
= satiety
= lower glucagon
= inhibit gastric emptying
= increase INCRETIN = release insulin from pancreas

25
Q

Oxyntomodulin

A

From L cells on of the SI also
When food is present and in proportion to caloric intake
= Anorectic effect or satiety

26
Q

Pancreatic Peptide (PP)

A

From islet of langerhans in pancreas cells
= satiety ——> binds to Y4R ——I NPY receptors(Y2R) in hypothalamus Paraventricular Nucleus
= also ——> vagus N

27
Q

Glucagon

A

Secretary by a-cells in pancreas islets
= increase blood glucose + insulin
= satiety

28
Q

Amylin

A

Released with insulin from pancreas B-cells
= ———I NYP release from NYP/AGRP
= satiety

29
Q

What does the Paraventricular Nucleus release

A
  1. TRH + CRH = don’t eat (satiety) - when MC4R is stimulated

2. MCH + orexin = eat (appetite) - when Y2R is stimulated

30
Q

Anorexia Nervosa what happens in their brains to restrict eating

A

Polymorphism of genes involved in eating behavior
Loss of Leptin pulsatile secretion (due to loss of fat)
HOWEVER
1. Ghrelin resistance (Ghrelin level is high)
2. High PPY due to decreased nutrients and eating disorder pathophysiology

GIGU Exam 1 (19 decks)

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