To eat or not to eat-Valencik Flashcards
1
Q
What is anorexigenic?
A
suppresses appetite
2
Q
What is orexigenic?
A
increases appetite
3
Q
What is satiation?
A
cessation of hunger
4
Q
What is satiety?
A
sensation of being full
5
Q
What are enteroendecrine cells?
A
endocrine cells of the GI tract and pancreas
6
Q
What are incretins?
A
gut hormones that stimulate insulin secretion
7
Q
What are oxyntic cells?
A
gastric parietal cells that release gastric aid
8
Q
What are orexins?
A
hormone that regulates sleep and appetite
9
Q
What are the adiposity signals?
A
- insulin
- adiponectin
- leptin
10
Q
What are the gut hormones?
A
- PYY
- OXM
- Ghrelin
- PP
- GLP-1
- CCK
11
Q
What are the long term signals for energy homeostasis?
A
Leptin
Insulin
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
13
Q
What does insulin do?
A
decreases appetite
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)
15
Q
Their are neurons and neurotransmitters in the (blank) that stimulate or inhibit feeding
A
hypothalamus
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)
17
Q
The lateral nuclei (LN) is the (blank) center of the brain
A
feeding
18
Q
When LN is stimulated what happens?
A
hunger increases a lot-> hyperphagia
19
Q
What happens if you destroy your LN?
A
no urge to eat (inanition)
-weight loss, muscle weakness, and decreased metabolism
20
Q
What is the satiety center?
A
Ventromedial nuclei (VMN)
21
Q
When the VMN is stimulated, what happens?
A
no urge to eat
refusal to eat (aphagia)
22
Q
What happens if the VMN is destroyed?
A
you have a voracious appeptide and continued eating can lead to obesity
23
Q
What part of the brain is this:
lesions lead to excessive eating
A
paraventricular nuclei (PVN)
24
Q
What part of the brain is this:
lesions depress eating
A
Dorsomedial nuclei (DMN)
25
What part of the brain is this:
| Site where multiple hormones released from GI and adipose tissue converge to regulate eating and energy consumption
Arcuate nuclei (AN)
26
What are the 2 distinct types of neurons in the arcuate nuclei?
Anorexigenic
Orexigenic
27
What are the anorexigenic neurons and what do they do?
POMC/CART
pro-opiomelanocortin/ cocaine-and amphetamine-regulated transcript (CART)
These neurons produce alpha-melanocyte-stimulating hormone (a-MSH) and CART peptide
28
What are the orexigenic neurons and what do they do?
AgRP/NPY these produce agouti-related protein (AgRP) neuropeptide Y (NPY)
29
Insulin, leptin and CCK cause you to feel full or hungry?
full
30
Ghrelin causes you to feel full or hungry?
hungry
31
(blank) neurons release alpha-MSH leading to the activation of melanocortin MCR-3 and MCR-4 receptors on the PVN
POMC/CART
32
When POMC/CART neurons are releasing alpha-MSH, what else is being released simultaneously?
CART peptide is released and binds to an unknown receptor.
33
What does POMC/CART stimulate?
the PVN regulation pathways that inhibit eating and stimulate energy expenditure (anorexigenic control)
34
Additional (blank) can augment or inhibit the POMC/CART function
peripheral peptide hormones
35
Orexigenic neurons release (Blank) and (blank) in response to low energy stores.
AgRP
| NPY
36
(blank) is an antagonist of MCR-4 blocking the signaling by a-MSH in the PVN
AgRP
37
(blank) stimulates the release of GABA resulting in inhibition of POMC
AgRP
38
So orexigenic neurons release AgRP and NPY which blocks a-MSH and stimulates GABA which results in...?
PVN are not subject to a-MSH binding to MCR-4 and appetite increase.
39
(blank) can stimulate or inhibit AgRP actions
Gut endocrine factors
40
Where do you find agouti related peptide? What kind of relationship does it have wth NPY?
in arcuate nucleus -> next to NPY neurons
| -Functional (similarly modulated under identical physiological conditions)
41
Agouti related peptide make you hungry and antagonize (blank)
melanocortins
42
What is this:
- hypothalamic neuroendocrine protein
- part of the pancreatic polypeptide family hormones
Neuropeptide Y (NPY)
43
Where is NPY found?
in the ARC
44
(Blank) is one of the most potent orexigenic factors. When you lose weight (blank) increases. (blank) stimulates a craving for carbs
NPY
NPY
NPY
45
Where do you find orexins? where do you find orexin receptors?what do they do?
- 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
In response to food, what are the anorexigenic responses in the brain (Hypothalamus mostly)?
- GLP-1
- (cholecystokinin) CCK
- (peptide tyrosine tyrosine) PYY
- (pancreatic polypeptide) PP
- (oxyntomoduin) OXM or OXY
- insulin
- leptin
47
In response to hunger what is released?
Ghrelin
Galanin (GAL)
Cortisol
48
What are the adipocyte hormones?
leptin
| adiponectin
49
(blank) regulates overall body weight by limiting food intake. (blank) concentrations directly correlate with body fat.
Leptin
| Leptin
50
Leptin promotes the synthesis of (blank) suppressing hunger
a-MSH (anorexigenic)
51
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
neuropeptide-Y (NPY)
52
(blank) is thought to mainly regulate BMR (energy). Increases insuline sensitivity and FA oxidation
Adiponectin
53
How do you inhibit adiponectin?
adrenergic stimulation and glucocorticoids
54
Adiponectin levels are reduced in (blank) individuas and increased in patients with (blank)
obese
| anorexia nervosa
55
Where are the majority of adiponectin receptors?
AdipoR1-muscle
| AdipoR2-liver
56
AdipoR2 expression in the brain is restricted to the (blank) and specific hypothalamic nuclei but function there is unknown.
hippocampus
57
The (blank) is the largest endocrine organ and at least (blank) peptides are expressed such as...?
gut
30
-hormones, peptide neurotransmitters, growth factors
58
What are some examples of peptides excreted by the gut?
```
GLP-1 and GIP
Oxyntomodulin
Cholecystokinin
Ghrelin and Obestatin
Pancreatic Polypeptide
Protein tyrosine tyrosine, PYY
```
59
What is this:
| hormones that stimulate a decrease in blood glucose levels by increasing insulin secretion from pancreas
Incretins
60
What does GLP-1 do?
- potentiates glucose-dependent insulin secretion
- inhibit glucagon secretion
- inhibit gastric acid secretion
- inhibit gastric emptying
- decrease appetite
61
What is this:
| expressed by enteroendocrine K-cells of the duodenum and proxima jejunum
GIP
62
GLP-1 and GIP are rapidly inactivated by (blank)
dipeptidyl peptidase-4 (DPP-4)
63
Glucagon derived peptides are expressed by (blank) cells of the (blank)
L cells
| of the small intestine
64
What is this:
| a 37 AA peptide derived from proglucagon containing the entire 29 AA of glucagon
oxyntomodulin
65
(blank) is synthesized and released in the enteroendocrine L cells of the distal gut.
Oxynotomodulin
66
Oxynotomodulin is secreted in response to food intake within (blank) minutes
5-10 minutes
67
Oxynotomodulin has (blank) activity and is thought to use the (blank) receptor. In the brain it suppresses (blank) effects
incretin
GLP-1
ghrelin
68
(blank) is expressed mainly in the duodenum and jejunum.
Cholecystokinin CCK
69
There are several active forms of CCK, there are (blank) major forms. In human plasma it is the (blank) form.
4 major forms
| CCK-33
70
CCK increases within (blank) minutes after eating and peaks at (blank) but the half life is only (blank) minutes.
15
25
1-2
71
CCK (CCK-1 and CCK-2) binds to (blank) and causes what three things to happen?
GPCRs
- gallbladder contracts
- pancreatic enzymes release
- gastric emptying is inhibitd
72
CCK is synergistic with (blank) i.e reduces food intake
leptin
73
The pancreatic polypeptide (pp) family of hormones comprises 2 gut hormones which are? And one CNS hormone?
```
pancreatic polypeptide (PP) and peptide tyrosine tyrosine (PYY)
CNS hormone neuropeptide Y (NPY)
```
74
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.
BBB
GI
6
75
PP increases in response to (blank X 3)
ghrelin, motilin and gastric distention
76
PP decreases (blank) expression
ghrelin
77
(blank) is produced and secreted from enteroendocrine L-cells of the ileum and colon
PYY (protein tyrosine tyrosine)
78
What is a potent regulator of PYY and what will lead to the highest levels of PYY?
food composition
| fat
79
PYY is a potent agonist of (blank) but predominantly the (blank) receptor (increased POMC and decreased NPY)
Y1
| Y2
80
What does PYY do?
- reduces ghrelin
- reduces gut motility
- delays in gatric emptying
- inhibits pancreatic bicarb and protein secretion
- inhibits gallbladder contraction
- satiety effects
81
Where do the satiety effects caused by PYY come from?
actions on the ARC nuclei in the hypothalamus
82
(blank) is an endogenous agonist of growth hormone secretagogue receptor (GHS-R) stimulating the release of growth hormone.
Ghrelin
83
(blank) can be processed to either ghrelin or obestatin
Prepro-ghrelin (human)
84
What is ghrelin secreted by?
stomach (oxyntic cells), small intestine and the colon
85
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.
Octanolyation
86
Where does ghrelin have its major effect?
| WHat does it stimulate?
Hypothalamus at arcuate nucleus
- NPY and Agrp
- increase GABA release which inhibits POMC nuclei
87
```
What is galanin?
Where is it expressed?
What does it bind?
Does it impact food preference?
Are its effects large or small?
```
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
What are the major signals of satiety?
| What does this result in?
- leptin
- insulin
- CCK, PYY
-decreased appeptite and increased energy expenditure
