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Block X; Week 2-M > Valencik-Hunger > Flashcards

Valencik-Hunger Flashcards

1
Q

What is anorexigenic?

A

suppresses appetite

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2
Q

What is orexigenic?

A

increases appetite

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3
Q

What is satiation? satiety?

A

satiation: cessation of hunger
satiety: sensation of being full

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4
Q

What are enteroendocrine cells?

A

endocrine cells of the GI tract & pancreas

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5
Q

What are incretins?

A

gut hormones that stimulate insulin secretion

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6
Q

What are oxyntic cells?

A

gastric parietal cells that release gastric acid

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7
Q

What are orexins? or aka hypocretins

A

NT that regulates arousal, wakefulness, hunger

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8
Q

Which 3 areas give peripheral signals to the hypothalamus and brainstem to control energy homeostasis?

A

adipose tissue
pancreas
GI tract

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9
Q

What are some long term signals related to hunger?

A

leptin-decreases hunger

insulin–decreases appetite

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10
Q

What are some short-term signals related to appetite?

A

ghrelin-increases hunger
tells you I’m full! With gastric emptying:
CCK
PYY

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11
Q

What’s the deal with leptin?

A

hormone that decreases hunger released in proportion to fat stores.
If you eat less & have less body fat–>less leptin will be produced.

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12
Q

Say you have a lot of leptin released….what are some mechanisms that counteract that?

A

minimizing energy usage

increasing appetite

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13
Q

The short term signals of the GI tract are released based off of which 2 things?

A

size of meals

number of meals

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14
Q

What are the different nuclei in the hypothalamus that are related to food intake?

A 
Lateral nuclei (LN)
Ventromedial nuclei (VMN) 
Paraventricular nuclei (PVN)
Dorsomedial nuclei (DMN)
Arcuate nuclei (ARC)
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15
Q

The laternal nuclei of the hypothalamus is the _______ center. The ventromedial nuclei of the hypothalamus is the _____ center.

A

LN: feeding center
VMN: satiety center

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16
Q

When you stimulate LN what do you get? When you destroy it–what happens?

A

lots of hunger–hyperphagia

destroyed–>no urge to eat (inanition), weight loss, muscle weakness, decreased metabolism

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17
Q

When you stimulate VMN what happens? When you destroy it?

A

Stimulate: aphagia, no urge to eat.
Destroyed: eat & become obese.

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18
Q

A lesion to the paraventricular nucleus leads to what?

A

excessive eating

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19
Q

A lesion to the dorsomedial nucleus leads to what?

A

less eating

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20
Q

What’s the deal with the arcuate nucleus?

A

multiple hormones are released from GI & adipose tissue & converge at AN to regulate eating.

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21
Q

So…it appears that which guys are on the anti-eating train?

A

PVN

VMN

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22
Q

Which guys are on the eating train?

A

LN

DMN

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23
Q

What are the 2 types of neurons found in the arcuate nuclei?

A
  1. anorexigenic

2. orexigenic

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24
Q

What do the anorexigenic neurons produce in the arcuate nucleus?

A

POMC/CART
CART–cocaine & amphetamine regulated transcript
**get alpha-MSH & CART peptide

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25
Q

What is produced by the orexigenic neurons in the arcuate nucleus?

A

AgRP/NPY

make agouti-related protein & neuropeptide Y

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26
Q

What are the gut hormones from the GI tract that affect the brain stem & hypothalamus in controlling hunger?

A 
PP
GLP-1
CCK
PYY
OXM
Ghrelin
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27
Q

What are the adiposity signals that affect the hypothalamus & control hunger?

A

adiponectin
insulin
leptin

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28
Q

T/F the state of the nuclei in the hypothalamus affect secretion of the thyroid, pancreatic islet cells, adrenal gland.

A

True.

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29
Q

How does the arcuate nucleus in the hypothalamus receive info from the body?

A

mainly through the median eminence, lacks a BBB

receptors for a number of things, including insulin, GH, leptin & other peripheral signals.

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30
Q

Describe in basic terms how the arcuate nucleus neurons interact with the PVN to control hunger.

A

POMC/CART neuron in arcuate nucleus stimulates the neuron of the PVN causing decreased food intake & (via nucleus tractus solitarius) increased energy expenditure.
AGRP/NPY neuron in arcuate nucleus inhibits the neuron of PVN & POMC/CART causing increased food intake & decreased energy expenditure.

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31
Q

In more detail…how does POMC/CART neuron stimulate the neuron of the PVN to increase energy expenditure & decrease food intake?

A

POMC release alpha MSH which activates MCR3 & 4 on PVN.

CART peptide when released binds to unknown receptor on PVN.

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32
Q

What does inhibition of MCR4 play a role in? Excessive activation of MCR4?

A

MCR4 inhibition: obesity in children

MCR4 excessive activation: role in anorexia

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33
Q

Describe in more detail how AGRP/NPY inhibits PVN & POMC/CART to increase food intake.

A

AgRP is an antagonist of MCR4 (alphaMSH can’t affect PVN)
AgRP inhibits POMC via GABA release
NPY inhibits PVN & POMC/CART via Y1 receptors (hyperpolarization/inhibition).

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34
Q

What is excessive AgRP associated with?

A

obesity

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35
Q

What does NPY stimulate food intake of? What else does it do?

A

preferentially carbs

It reduces fatty acid oxidation, promotes carbohydrate oxidation and promotes fatty acid synthesis.

36
Q

What does AgRP control in rodents?

A

coat color

37
Q

Which family of hormones is NPY a member of? What are some of its family members?

A

pancreatic polypeptide family of hormones

other family members: pancreatic polypeptide (PP), peptide tyrosine tyrosine (PYY)

38
Q

Where is NPY found? When does it increase?

A

arcuate nucleus

increases when you lose weight.

39
Q

Where are orexins found? Where are their receptors found?

A

orexins–in the lateral & posterior hypothalamic areas.
have axonal projections throughout the brain
receptors throughout the CNS

40
Q

What is the function of orexins?

A

increase eating
role in emotional & motivational aspects of feeding behavior
increase wakefulness

41
Q

Where do anorexigenic responses mainly work? What are some examples of these?

A

hypothalamus

Glucagon-like peptide-1 (GLP-1)
Cholecystokinin (CCK)
Peptide tyrosine tyrosine (PYY)
Pancreatic polypeptide (PP)
Oxyntomodulin (OXM or OXY)
Insulin-pancreas
Leptin-fat
42
Q

What are some examples of orexigenic hormones?

A

Ghrelin
Galanin (GAL)
Cortisol

43
Q

What are the 2 main adipocyte hormones?

A

leptin

adiponectin

44
Q

What does leptin do?

A

limits food intake
promotes synthesis of alpha-MSH (also anorexigenic)
reduces the effects of NPY at first
**leptin conc’n proportional to body fat (more w/ more fat)

45
Q

How exactly does leptin control food intake?

A

leptin causes an increase in alphaMSH & CART, which bind to PVN. decrease in food intake.
leptin inhibits AGRP/NPY, limits ability of AGRP to antagonize MCR4 & limits NPY’s ability to bind Y1r. decrease in food intake.

46
Q

Once again, what does alpha MSH bind to?

A

MCR4 receptor

47
Q

How do you treat a leptin deficient patient?

A

subcu injections of recombinant leptin.

Note: most obese patients have a lot of leptin, but it doesn’t decrease their weight.

48
Q

Is adiponectin anorexigenic or orexigenic?

A

depends

49
Q

What is the function of adiponectin?

A

regulates basal metabolic rate

increases insulin sensitivity & fatty acid oxidation

50
Q

What inhibits the activity of adiponectin? Levels are reduced in which people? increased in which people?

A

activity inhibited by adrenergic stimulation & glucocorticoids
high adiponectin levels in anorexic people & low levels in obese people.

51
Q

What are some receptors for adiponectin & where are they found?

A

AdipoR1-muscle

AdipoR2-liver & brain (hippocampus & some hypothalamic nuclei)

52
Q

What is the largest endocrine organ?

A

the GI tract

30 peptides expressed–>hormones, peptide NT, growth factors

53
Q

T/F Gi tract mainly produces orexigenic hormones.

A

False. Mainly anorexigenic.

54
Q

What are incretins?

A

Hormones that stimulate a decrease in blood glucose levels by increasing insulin secretion from the pancreas.
Ex: GLP-1 (glucagon-like peptide) & GIP (gastric inhibitory peptide OR glucose-dependent insulinotropic peptide)

55
Q

What exactly does GLP-1 do?

A

Potentiates glucose-dependent insulin secretion
Inhibit glucagon secretion
Inhibit gastric acid secretion
Inhibit gastric emptying
Decrease appetite
also pancreatic beta cell proliferation & decreased apoptosis.
increases cardiac function & Cardioprotection
decreases endothelial dysfunction

56
Q

Where is GIP expressed?

A

enteroendocrine K-cells of the duodenum & proximal jejunum

57
Q

How does GIP begin? How is it inactivated?

A

pre-pro GIP
After cleavage–>GIP
inactivated by DPP-4 (dipeptidyl peptidase-4)

58
Q

Which cells express genes for glucagon derived peptides?

A

L-cells of the small intestine
have a long prepropeptide to make glucagon
sequential processing is tissue specific

59
Q

What is GRPP+Glucagon+IP-1?

A

Glicentin

60
Q

What is Glucagon+IP1?

A

Oxintomodulin

61
Q

What is GRPP+Glucagon?

A

proglucagon

62
Q

What does GIP do?

A

increases lipogenesis

increase insulin secretion

63
Q

What is oxyntomodulin?

A

Glucagon+IP-1
37 AA peptide derived from proglucagon
from enteroendocrine L cells of the distal gut
**incretin activity

64
Q

When is oxyntomodulin secreted? Which receptor does it bind? What does it do?

A

secreted w/i 5-10 minutes of meal
binds GLP-1 receptor
**incretin activity
**suppresses gherkin effects in the brain

65
Q

What happens when oxyntomodulin is injected subcu in obese patients?

A

suppresses appetite for 4 weeks.

66
Q

Where is cholecystokinin expressed? How many forms?

A

expressed in duodenum & jejunum
also produced in the brain
4 forms–>CCK-33 most common

67
Q

When does CCK increase? What is its half life?

A

increases w/i 15 minutes of eating
peaks @ 25 min
t1/2=1-2 minutes

68
Q

What does CCK bind to?

A

GPCRs (CCK-1, CCK-2)

69
Q

What happens when CCK binds to its receptors?

A

Gallbladder contracts
Pancreatic enzymes release
Gastric emptying is inhibited
**synergistic w/ leptin (reduces food intake)

70
Q

What are the major members of the pancreatic polypeptide family?

A

pancreatic polypeptide
peptide tyrosine-tyrosine
NPY

71
Q

Where is PP expressed? When does it increase?

A

expressed in distal GI
can’t cross BBB
increases 6 hours after meal
more secreted w/ higher caloric content of meal

72
Q

When does PP increase aside from after a meal? What does it do?

A

w/ ghrelin, motilin, gastric distention, secretion of PP increases.
**action: decreases ghrelin expression.

73
Q

What happens when you inject PP into healthy people?

A

decreases food intake by 25% w/i 24 hours.

74
Q

Where is PYY produced/secreted?

A

enteroendocrine L-cells of ileum & colon

75
Q

What leads to increased levels of PYY?

A

high fat–high PYY.

76
Q

Which receptors does PYY bind?

A

Y1, but mainly Y2 receptor.

increases POMC & decreases NPY

77
Q

What is the action of PYY?

A

Reduces ghrelin, gut motility, delays in gastric emptying, inhibits pancreatic bicarbonate and protein secretion and inhibits gallbladder contraction.
satiety effects via arcuate nuclei

78
Q

What is ghrelin?

A

pre protein makes either it or obestatin, endogenous agonist of growth hormone, specifically GHS-R, stimulating release of GH

79
Q

What is ghrelin secreted from?

A

stomach (gastric oxyntic cells), SI, colon

80
Q

What is the structure of ghrelin?

A

28 AA protein w/ acyl side chain, n-octanoic acid (necessary to bind GHS-R)

81
Q

What does ghrelin stimulate in the hypothalamus?

A

stimulates NPY/AgRP in arcuate nucleus

82
Q

What is galanin? Where is it expressed?

A

29 AA peptide, orexigenic

expressed in gut & brain & binds GALR1 in hypothalamus

83
Q

Insulin & leptin stimulate _____.

A

POMC/CART

84
Q

Ghrelin activates ____.

A

AgRP/NPY

85
Q

Leptin & PYY inhibit _____.

A

AgRP/NPY

86
Q

The liver & GI can stimulate the vagus nerve–>NTS & cause____.

A

satiety, meal termination

Block X; Week 2-M (7 decks)

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