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Block 10 Week 2 > To eat or not to eat-Valencik > Flashcards

To eat or not to eat-Valencik 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?

A

cessation of hunger

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4
Q

What is satiety?

A

sensation of being full

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5
Q

What are enteroendecrine cells?

A

endocrine cells of the GI tract and pancreas

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6
Q

What are incretins?

A

gut hormones that stimulate insulin secretion

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7
Q

What are oxyntic cells?

A

gastric parietal cells that release gastric aid

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8
Q

What are orexins?

A

hormone that regulates sleep and appetite

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9
Q

What are the adiposity signals?

A
  • insulin
  • adiponectin
  • leptin
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10
Q

What are the gut hormones?

A
  • PYY
  • OXM
  • Ghrelin
  • PP
  • GLP-1
  • CCK
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11
Q

What are the long term signals for energy homeostasis?

A

Leptin

Insulin

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12
Q

What does leptin do?

A
  • secreted in proprotion to fat stores
  • eat less, less body fat, less leptin is produced
  • however body adapts by minimizing energy usage and increasing appetite
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13
Q

What does insulin do?

A

decreases appetite

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14
Q

What are the short term signals in energy homeostasis?

A 
GI tract hormones (size of meals, number of meals)
Ghreline (hunger)
CCK (full)
PYY (full)
Gastric emptying (full)
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15
Q

Their are neurons and neurotransmitters in the (blank) that stimulate or inhibit feeding

A

hypothalamus

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16
Q

What are the neural centers that regulate food intake?

A

Hypothalamus

  • lateral nuclei (LN)
  • ventromedial nuclei (VMN)
  • Paraventricular nuclei (PVN)
  • Dorsomedial nuclei (DMN)
  • Arcuate nuclei (ARC)
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17
Q

The lateral nuclei (LN) is the (blank) center of the brain

A

feeding

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18
Q

When LN is stimulated what happens?

A

hunger increases a lot-> hyperphagia

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19
Q

What happens if you destroy your LN?

A

no urge to eat (inanition)

-weight loss, muscle weakness, and decreased metabolism

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20
Q

What is the satiety center?

A

Ventromedial nuclei (VMN)

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21
Q

When the VMN is stimulated, what happens?

A

no urge to eat

refusal to eat (aphagia)

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22
Q

What happens if the VMN is destroyed?

A

you have a voracious appeptide and continued eating can lead to obesity

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23
Q

What part of the brain is this:

lesions lead to excessive eating

A

paraventricular nuclei (PVN)

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24
Q

What part of the brain is this:

lesions depress eating

A

Dorsomedial nuclei (DMN)

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25
Q

What part of the brain is this:

Site where multiple hormones released from GI and adipose tissue converge to regulate eating and energy consumption

A

Arcuate nuclei (AN)

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26
Q

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

A

Anorexigenic

Orexigenic

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27
Q

What are the anorexigenic neurons and what do they do?

A

POMC/CART
pro-opiomelanocortin/ cocaine-and amphetamine-regulated transcript (CART)

These neurons produce alpha-melanocyte-stimulating hormone (a-MSH) and CART peptide

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28
Q

What are the orexigenic neurons and what do they do?

A

AgRP/NPY these produce agouti-related protein (AgRP) neuropeptide Y (NPY)

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29
Q

Insulin, leptin and CCK cause you to feel full or hungry?

A

full

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30
Q

Ghrelin causes you to feel full or hungry?

A

hungry

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31
Q

(blank) neurons release alpha-MSH leading to the activation of melanocortin MCR-3 and MCR-4 receptors on the PVN

A

POMC/CART

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32
Q

When POMC/CART neurons are releasing alpha-MSH, what else is being released simultaneously?

A

CART peptide is released and binds to an unknown receptor.

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33
Q

What does POMC/CART stimulate?

A

the PVN regulation pathways that inhibit eating and stimulate energy expenditure (anorexigenic control)

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34
Q

Additional (blank) can augment or inhibit the POMC/CART function

A

peripheral peptide hormones

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35
Q

Orexigenic neurons release (Blank) and (blank) in response to low energy stores.

A

AgRP

NPY

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36
Q

(blank) is an antagonist of MCR-4 blocking the signaling by a-MSH in the PVN

37
Q

(blank) stimulates the release of GABA resulting in inhibition of POMC

38
Q

So orexigenic neurons release AgRP and NPY which blocks a-MSH and stimulates GABA which results in…?

A

PVN are not subject to a-MSH binding to MCR-4 and appetite increase.

39
Q

(blank) can stimulate or inhibit AgRP actions

A

Gut endocrine factors

40
Q

Where do you find agouti related peptide? What kind of relationship does it have wth NPY?

A

in arcuate nucleus -> next to NPY neurons

-Functional (similarly modulated under identical physiological conditions)

41
Q

Agouti related peptide make you hungry and antagonize (blank)

A

melanocortins

42
Q

What is this:

  • hypothalamic neuroendocrine protein
  • part of the pancreatic polypeptide family hormones
A

Neuropeptide Y (NPY)

43
Q

Where is NPY found?

A

in the ARC

44
Q

(Blank) is one of the most potent orexigenic factors. When you lose weight (blank) increases. (blank) stimulates a craving for carbs

45
Q

Where do you find orexins? where do you find orexin receptors?what do they do?

A
  • lateral and posterior hypothalamic areas with axonal projections throughout the brain
  • throughout CNS
  • role in emotional and motivational aspects of feeding behavior, increase wakefulness and suppress REM sleep
46
Q

In response to food, what are the anorexigenic responses in the brain (Hypothalamus mostly)?

A
  • GLP-1
  • (cholecystokinin) CCK
  • (peptide tyrosine tyrosine) PYY
  • (pancreatic polypeptide) PP
  • (oxyntomoduin) OXM or OXY
  • insulin
  • leptin
47
Q

In response to hunger what is released?

A

Ghrelin
Galanin (GAL)
Cortisol

48
Q

What are the adipocyte hormones?

A

leptin

adiponectin

49
Q

(blank) regulates overall body weight by limiting food intake. (blank) concentrations directly correlate with body fat.

A

Leptin

Leptin

50
Q

Leptin promotes the synthesis of (blank) suppressing hunger

A

a-MSH (anorexigenic)

51
Q

Leptin reduces the inhibitor effects of local orexigenic (blank) on POMC nuclei and suppresses hunger initially but in the long run NPY levels return to normal

A

neuropeptide-Y (NPY)

52
Q

(blank) is thought to mainly regulate BMR (energy). Increases insuline sensitivity and FA oxidation

A

Adiponectin

53
Q

How do you inhibit adiponectin?

A

adrenergic stimulation and glucocorticoids

54
Q

Adiponectin levels are reduced in (blank) individuas and increased in patients with (blank)

A

obese

anorexia nervosa

55
Q

Where are the majority of adiponectin receptors?

A

AdipoR1-muscle

AdipoR2-liver

56
Q

AdipoR2 expression in the brain is restricted to the (blank) and specific hypothalamic nuclei but function there is unknown.

A

hippocampus

57
Q

The (blank) is the largest endocrine organ and at least (blank) peptides are expressed such as…?

A

gut
30
-hormones, peptide neurotransmitters, growth factors

58
Q

What are some examples of peptides excreted by the gut?

A 
GLP-1 and GIP
Oxyntomodulin
Cholecystokinin
Ghrelin and Obestatin
Pancreatic Polypeptide
Protein tyrosine tyrosine, PYY
59
Q

What is this:

hormones that stimulate a decrease in blood glucose levels by increasing insulin secretion from pancreas

60
Q

What does GLP-1 do?

A
  • potentiates glucose-dependent insulin secretion
  • inhibit glucagon secretion
  • inhibit gastric acid secretion
  • inhibit gastric emptying
  • decrease appetite
61
Q

What is this:

expressed by enteroendocrine K-cells of the duodenum and proxima jejunum

62
Q

GLP-1 and GIP are rapidly inactivated by (blank)

A

dipeptidyl peptidase-4 (DPP-4)

63
Q

Glucagon derived peptides are expressed by (blank) cells of the (blank)

A

L cells

of the small intestine

64
Q

What is this:

a 37 AA peptide derived from proglucagon containing the entire 29 AA of glucagon

A

oxyntomodulin

65
Q

(blank) is synthesized and released in the enteroendocrine L cells of the distal gut.

A

Oxynotomodulin

66
Q

Oxynotomodulin is secreted in response to food intake within (blank) minutes

A

5-10 minutes

67
Q

Oxynotomodulin has (blank) activity and is thought to use the (blank) receptor. In the brain it suppresses (blank) effects

A

incretin
GLP-1
ghrelin

68
Q

(blank) is expressed mainly in the duodenum and jejunum.

A

Cholecystokinin CCK

69
Q

There are several active forms of CCK, there are (blank) major forms. In human plasma it is the (blank) form.

A

4 major forms

CCK-33

70
Q

CCK increases within (blank) minutes after eating and peaks at (blank) but the half life is only (blank) minutes.

71
Q

CCK (CCK-1 and CCK-2) binds to (blank) and causes what three things to happen?

A

GPCRs

  • gallbladder contracts
  • pancreatic enzymes release
  • gastric emptying is inhibitd
72
Q

CCK is synergistic with (blank) i.e reduces food intake

73
Q

The pancreatic polypeptide (pp) family of hormones comprises 2 gut hormones which are? And one CNS hormone?

A 
pancreatic polypeptide (PP) and peptide tyrosine tyrosine (PYY)
CNS hormone neuropeptide Y (NPY)
74
Q

Pancreatic polypeptide (PP) does not cross the (blank), it is expressed in the distal (blank) and it increases after about (blank) hours in proportion to caloric intake.

75
Q

PP increases in response to (blank X 3)

A

ghrelin, motilin and gastric distention

76
Q

PP decreases (blank) expression

77
Q

(blank) is produced and secreted from enteroendocrine L-cells of the ileum and colon

A

PYY (protein tyrosine tyrosine)

78
Q

What is a potent regulator of PYY and what will lead to the highest levels of PYY?

A

food composition

fat

79
Q

PYY is a potent agonist of (blank) but predominantly the (blank) receptor (increased POMC and decreased NPY)

80
Q

What does PYY do?

A
  • reduces ghrelin
  • reduces gut motility
  • delays in gatric emptying
  • inhibits pancreatic bicarb and protein secretion
  • inhibits gallbladder contraction
  • satiety effects
81
Q

Where do the satiety effects caused by PYY come from?

A

actions on the ARC nuclei in the hypothalamus

82
Q

(blank) is an endogenous agonist of growth hormone secretagogue receptor (GHS-R) stimulating the release of growth hormone.

83
Q

(blank) can be processed to either ghrelin or obestatin

A

Prepro-ghrelin (human)

84
Q

What is ghrelin secreted by?

A

stomach (oxyntic cells), small intestine and the colon

85
Q

Ghrelin is a 28 AA protein with an acyl side chain, n-octanoic acid. (blank) is essential for binding GHS-R and for ghrelin’s effects on food intake.

A

Octanolyation

86
Q

Where does ghrelin have its major effect?

WHat does it stimulate?

A

Hypothalamus at arcuate nucleus

  • NPY and Agrp
  • increase GABA release which inhibits POMC nuclei
87
Q 
What is galanin?
Where is it expressed?
What does it bind?
Does it impact food preference?
Are its effects large or small?
A

orexigenic 29 AA peptide that stimulates feeding
gut and brain and binds GALR1 in the hypothalamus
Doesn’t impact food preference
effect is small and short lived compared to NPY

88
Q

What are the major signals of satiety?

What does this result in?

A
  • leptin
  • insulin
  • CCK, PYY

-decreased appeptite and increased energy expenditure

Block 10 Week 2 (7 decks)

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