Regulation of Food Intake Flashcards

1
Q

What controls feeding and satiety?

what is within this structure?

A

there is the hypothalamus

within it are an arrangement of neuronal populations..

1) lateral nucleus (LH)
2) Ventromedial nucleus (VM)
3) Paraventricular Nucleus (PV)
4) Dorsomedial Nucleus (DM)
5) Arcuate Nucleus (Arc)

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2
Q

Where does most of the the signaling integration happen in the hypothalamus?

A

mostly in the arcuate nucleus.

within the arcuate nucleus we have 2 pathways:

1) stimulates the feeding behavior
2) inhibits the feeding behavior.

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3
Q

which pathway of the arcuate nucleus inhibits the feeding behavior?

what stimulates this pathway?

what is the pathway?

how does this stimulation work?

A

Anorexigenic pathway!

Insulin, Leptin, CCK stimulate this pathway! (anaroxigenic hormones)

for this pathway we have POMC/CART… this releases a-melanocortin (a-msh) into another level of neurons (PVN) is going to have receptor for alpha MSH.. known as MCR-4.

the outcome of that binding is going to signal the decrease in food intake!

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4
Q

What pathway of the arcuate nucleus stimulates feeding behavior?

What up regulates this pathway and where is it from?

What is the pathway?

A

Orexigenic pathway!

Ghrelin is something that up regulates this (secreted from the stomach)!

Activation of the AGRP/NPY population of neurons leads to the release of substances that stimulate the Y1 receptor of the PVN neurons

this binding signals the increase in food intake

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5
Q

What’s good to know about the Orexigenic vs Anorexigenic pathways and how they work on each other?

A

both pathways antagonize each other.

Insulin, leptin, CCK inhibit food intake while simultaneously stimulating the lowering food intake pathway..

so peptides that stimulate the a-MSH pathway inhibit the NPY system

AGRP is an antagonist of MCR-4 receptor. the activation of AGRP and release of these are going to inhibit the activity of POMC.

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6
Q

The vagus nerve

A

Vagal –> NTS –> Hypothalamus circuit produces responses related to feeding behavior and metabolism.

take out the vagus, we can disrupt the mechanism that senses distention and that can affect the satiety. so it might not detect the large size of a meal. this would affect satiety

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7
Q

Ghrelin is what kind of enzyme?

where is it secreted?

where does it bind?

what is its effect on the hypothalamus

what is the actions of Ghrelin? (5 of them)

A

from the periphery, the main oxynogenic that is the main feeding stimulating mechanism.

The stomach mostly secretes ghrelin.

Ghrelin binds to the secretagogue receptors (GHSR)…

the effect in the hypothalamus stimulates the release of NPY.. the actions then would be are to..

1) increase appetite!!!
2) increase gastric motility (all of that wants to move stuff out of the stomach so we don’t feel full.. i.e. increase eating!
3) increase gastric acid secretion
4) adipogenesis.
5) decreasing insulin secretion (no one knows why)

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8
Q

Insulin is what kind of enzyme?

where does it bind? what does it do in each?

2 actions?

what happens with people with type 1 diabetes?

A

anoxygenic peptide.

binds to receptors in POMC/NPY systems.

in the case of insulin, it INHIBITS NPY pathway, but stimulates POMC!!

Actions:

1) decrease appetite (because of inhibiting NPY)
2) increase metabolism

DM1 = low insulin increases food intake.. this makes sense with the action of insulin.. so no insulin means not inhibiting NPY so increased food intake.

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9
Q

What does CCK do?

where is it released from?

what does it do and what 2 ways does it do it?

A

anoxygenic

released by I cells in the duodenum

Elicits gastric emptying (by distending the stomach) so increasing distention creates SATIETY:

vagal –> NTS –> Hypothalamus circuit –> lowers ghelin!!

1) decreases ghrelin
2) decreasing gastric emptying by increasing gastric distention.

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10
Q

what type of peptide is PYY?

where does it come from?

A

an anoroxygenic molecule

released by L cells of the ileum and colon following a meal

1) it binds to Y2R in the hypothalamus, which will inhibit NPY neurons.
2) releases inhibition (stimulating) of POMC neurons.. making it so we are decreasing food intake… Satiety.

SO INHIBITS NPY BUT UP REGULATES POMC

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11
Q

What does leptin do?

where is it secreted from?

A

Anorexigenic

secreted by adipose tissue

Leptin binds to receptors in POMC and NPY systems… it inhibits NPY and Stimulates POMC…

1) lower appetite
2) increase metabolism
3) lower ghrelin release

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12
Q

what happens in kids with a congenital leptin deficiency and you give them leptin?

what is obesity in humans is associated with?

A

reduces fat mass, hyperinsulinaemia, and hyperlipidemia.

high leptin levels and failure to respond to exogenous leptin… so LEPTIN RESISTANCE!!

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13
Q

Satiety does what to NPY/AgRP?

what about hunger?

A

inhibits NPY

stimulates NPY

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14
Q

What does Glucagon-like peptide-1 do? (GLP-1)

what kind of peptide is GLP-1? (2 things)

where is it synthesized?

what does it do?

A

in addition to being anorexigenic, it also is an Incretin !

co-secreted with PYY from L cells in the intestine

incretin causes insulin release from the pancreas.

it reduces food intake, suppresses glucagon secretion, and delays gastric emptying.

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15
Q

What is Oxyntomodulin?

A

anorexigenic.

coming from L cells of the intestine in response to ingested food.

reduces food intake.

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16
Q

Pancreatic Peptide (PP)

A

anoroxygenic (decreasing food intake)

come from endocrine pancreas

decreases intake by directly interacts with Y4R receptors in the brainstem and hypothalamus.

17
Q

Glucagon?

  1. where is it secreted?
  2. what is it’s goal?
  3. what kind of compound is it then?
A

secreted by alpha cells of the pancreatic islets

reduces food intake

anoroxygenic

18
Q

Amylin?

A

stored and released from the pancreas (with insulin) in response to food intake

anoroxygenic effects (inhibition of NPY release)

19
Q

Anorexia nervosa (AN)?

4 symptoms

what does it lead to?

A

self-starvation and excessive weight loss

severely malnourished and emaciated

dysfunctions in hormones and cardiological dysfunctions, abnormalities with digestive, skeletal, reproductive systems.

20
Q

what are some biological factors that are related to the gut-brain axis associated with people with AN?

Ghrelin?

PYY?

Leptin?

A

Increase in Ghrelin but patients aren’t overfeeding themselves… so patients have a resistance to ghrelin!

elevated peptide YY (PYY) contributes to the decrease in food intake and this leads to the psychological trait of the disease.

Leptin is decreased, which is by decreasing the fat associated with the emaciation.

21
Q

what has more, anoroxygenic hormones or orexigenic hormones?

A

anorexygenic!

22
Q

what’s to note about AGRP/NPY and the POMC/CART systems and obesity?

A

obesity are sometimes related to mutations in the POMC and MCR-4 genes… making it hard to decrease your food intake

23
Q

What is crucial for interpretation and relaying of peripheral signals?

how does this do it?

what happens in the hindbrain because of this?

A

Vagus

it signals to the NTS through the NODOSE GANGLION –> received by the hypothalamus and produces the appropriate feeding behavior.

the hindbrain is able to regulate food intake in response to peripheral signals EVEN IN THE ABSENSE OF HIGHER CENTER’S INPUT!

24
Q

Of the NPY/AgRP, which one is acting on MC4R, which one is acting on Y1R?

A

AgRP is acting on MC4R receptors TO INHIBIT IT

NPY is activating Y1R receptors to ACTIVATE

25
Q

Once MC4R is activated , what is it going to do to metabolism and food intake?

A

stimulate metabolism

inhibit food intake

26
Q

Once Y1R is activated , what is it going to do to metabolism and food intake?

A

inhibit metabolism

stimulate food intake

27
Q

gastric bypass come with what?

A

malabsorption and changes the food preference and hormones + food intake.