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PMCOL 344 > Obesity Intro > Flashcards

Obesity Intro Flashcards

1
Q

what are 4 adverse behavioural factors that is causing the atherosclerosis epidemic

A

fatty diets
physical inactivity
diabetes
OBESITY

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2
Q

which BMI signified morbidly obese

A

about 40

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3
Q

what does high BMI mean for their health

A

major risk factor for chronic diseases, like CV caver and diabetes

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4
Q

why can obesity and diabetes cause cancer

A

cause insulin resistance means pancreas make more insulin. but insulin is a growth factor so it promotes cancer growth

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5
Q

what generally causes obesity

A

when homeostatic mechanisms controlling energy balance become disordered or overwhelmed

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6
Q

what is a main intrinsic homeostatic mechanism that contributes to obesity

A

the hypothalamus, increases its set point so its hard to lose weight

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7
Q

is there a genetic component of obesity

A

yes, strong. also epigenetic (starved mother, then kids gain weight easier)

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8
Q

what are 3 mutations that cause mice to be obese

A

ob (lack leptin)
db (lack leptin receptor)
tub (transcription factor)

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9
Q

what do homozygote mice with those mutations do

A

eat excessively, low expenditure (BMR), very fat, metabolic abnormalities

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10
Q

what does leptin do generally

A

reduces food intake and body weight

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11
Q

what produces leptin

A

adipocytes

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12
Q

what regulates leptin

A

glucocorticoids, estrogens, insulin

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13
Q

what does high fat stores do to leptin

A

increases

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14
Q

so can you just give obese people more leptin

A

no, actually most obese people have high levels but develop leptin resistance

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15
Q

how does leptin enter the CNS

A

via saturable transporter

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16
Q

where does leptin act in the CNS

A

in the hypothalamus, leptin receptors in 2 groups of neurons in the arcuate nucleus (ARC)

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17
Q

what are the 2 groups that leptin activates like (general)

A

they have opposing actions

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18
Q

what does energy homeostasis depend on

A

balance between actions of leptin (and other mediators) on these 2 groups of neurons

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19
Q

what are the 2 pathways that leptin deals with

A
  • anorexigenic (POMC and CART)

- orexigenic (NPY and AGRP)

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20
Q

what does leptin do to anorexigenic (POMC and CART) pathway

A

stimulates

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21
Q

what does leptin do to orexigenic (NPY and AGRP) pathway

A

inhibits

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22
Q

what pathway is POMC

A

anorexigenic

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23
Q

what pathway is AGRP

A

orexigenic

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24
Q

what pathway is CART

A

anorexigenic

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25
what pathway is NPY
orexigenic
26
what does leptin do to anorexigenic pathways
stimulates
27
what does leptin do to orexigenic pathways
inhibits
28
what does leptin do to POMC pathway
stimulates
29
what does leptin do to AGRP pathway
inhibits
30
what does leptin do to NPY pathway
inhibits
31
what does leptin do to CART pathway
stimulates
32
what does starvation and weight loss do to leptin levels
decreases
33
what does overfeeding and weight gain do to leptin levels
increase
34
what does stimulation of POMC and CART and MSH pathway cause
decrease food intake, decrease storage and synthesis of fat (catabolism), increase energy expenditure
35
what does stimulation of NPY and AGRP pathway cause
increased food intake, increased synthesis and storage of fat (anabolism), decreased energy expenditure
36
which receptor does AGRP effect and how
it is an inverse agonist at MC receptors
37
what happens if there is defects in POMC/MSH/melanocortin axis
link to obesity
38
how does leptin regulation compare to other factors
regulation of energy balance such as leptin occurs against background of psychological, environmental, financial and social factors that engage higher brain areas in control of food intake
39
what do you see in brain imaging scans in leptin deficient individuals
they show activation of neural circuits involved in reward processing after the visual presentation of food - decreased when treated with leptin
40
how does the gut link to the brain and make you hungry (example)
bacteria want fibre, so they keep telling you you are hungry until they get what they want
41
what are 5 examples of gut peptides
ghrelin, CCK, PYY, OXM, GLP-1
42
what is the role of gut peptides
food intake is also modulated by feedback loops in which signals transmitted from GI tract to CNS
43
where is ghrelin secreted
by gastric mucosa
44
what kind of molecule is ghrelin
peptide
45
when are plasma levels of ghrelin high
during fasting, and peak when expecting a meal
46
what causes a fall in ghrelin levels
feeding
47
what does ghrelin do to leptin levels
decrease its release
48
what does leptin do to ghrelin levels
decrease its release
49
what does CCK stand for
cholecystokinin
50
where is cholecystokinin secreted from
mucosal cells
51
when is cholecystokinin released
in process of digesting foods, especially fat
52
where does cholecystokinin act
on CCK A receptors on afferent nerves | and CCK B receptors in the brain
53
what happens once cholecystokinin acts on CCK A receptors on afferent nerves
they send signal to CNS to inhibit food intake
54
what is the afferent nerve
one that sends signal to CNS
55
does efferent or afferent send signal to CNS
aferent
56
what happens once cholecystokinin acts on CCK B receptors in the brain
it causes the satiety factor
57
how does CCK cause the satiety factor
by activating CCK B receptors in the brain
58
what does CCK mediate
short term inhibition of food intake, like the size of meals
59
what does PYY stand for
peptide tyrosine tyrosine
60
what does OXM stand for
oxyntomodulin
61
what does GLP-1 stand for
glucagon like peptide
62
what is the role of PYY OXM and GLP-1
short term satiety signals
63
where are PYY OXM and GLP-1 produced
by cells of the GI mucosa
64
where does PYY OXM and GLP-1 act
afferent nerves and ARC (in hypothalamus)
65
where is the ARC
in the hypothalamus
66
when are PYY OXM and GLP-1 released
within 5-10 mins after starting to eat
67
when does PYY OXM and GLP-1 levels plateau
within 30-90 mins of eating
68
how long does PYY OXM and GLP-1 remain elevated
for up to 6 hours
69
what does PYY OXM and GLP-1 cause to hunger
reduces time before feeling hungry again
70
what does a rapid rise in PYY OXM and GLP-1 cause
change in energy status to brain and acts locally to enhance digestive process
71
which gut peptide peaks the quickest
ghrelin
72
which gut peptide peaks the slowest
PYY OXM and GLP-1
73
which gut peptide peaks the middle-ist
CCK, insulin and amylin too
74
which hormones give the feeling of satiety
PYY OXM and GLP-1
75
which pathways do PYY OXM and GLP-1 inhibit (like the anorexigenic or orexigenic)
inhibit the NPY and AGRP pathways , the orexigenic ones (cause they switch off food intake, give satiety signal)
76
which pathways do PYY OXM and GLP-1 enhance (like the anorexigenic or orexigenic)
enhance POMC CART, anorexigenic (decrease food intake)
77
which pathways does ghrelin enhance (like the anorexigenic or orexigenic)
enhance the NPY and AGRP pathways (increases food intake, orexigenic)
78
which pathways does ghrelin inhibit (like the anorexigenic or orexigenic)
POMC CART, anorexigenic (they want to increase food intake, so they inhibit the inhibitory ones)
79
what does ghrelin do to orexigenic pathway
enhance
80
what does ghrelin do to anorexigenic pathway
inhibit
81
what does PYY OXM and GLP-1 do to aoorexigenic pathway
enhance
82
what does PYY OXM and GLP-1 do to orexigenic pathway
inhibit
83
what does noradrenaline do to the 2 pathways
positive on orexigenic (enhances NPY) pathway cause it increases energy expenditure
84
what does 5-HT do to the 2 pathways
enhances the anorexigenic pathways to decrease food intake (enhances POMC CART)
85
what does GABA do to the 2 pathways
inhibits the NPY to decrease food intake
86
what is the source of leptin
adipose
87
what is the source of ghrelin
stomach
88
what is the source of CCK
GI tract
89
what is the source of PYY
GI tract
90
what is the source of OXM
GI tract
91
what is the source of GLP-1
GI tract
92
what is the source of noradrenaline
neurons
93
what is the source of GABA
neurons
94
what is the source of 5-HT
neurons
95
what is the target of leptin
ARC (arcuate nucleus in hypothalamus)
96
what is the target of Ghrelin
ARC (arcuate nucleus in hypothalamus)
97
what is the target of CCK
ARC (arcuate nucleus in hypothalamus) and afferent nerves
98
what is the target of PYY
ARC (arcuate nucleus in hypothalamus) and afferent nerves
99
what is the target of OXM
ARC (arcuate nucleus in hypothalamus) and afferent nerves
100
what is the target of GLP-1
ARC (arcuate nucleus in hypothalamus) and afferent nerves
101
what is the target of noradrenaline
ARC (arcuate nucleus in hypothalamus)
102
what is the target of GABA
ARC (arcuate nucleus in hypothalamus)
103
what is the target of 5-HT
ARC (arcuate nucleus in hypothalamus)
104
what is the effect of decreased leptin
fall in leptin levels increases food intake
105
what is the effect of increase leptin
decrease food intake
106
what is the effect of ghrelin
increase food intake
107
what is the effect of CCK
decrease food intake (limit meal size)
108
what is the effect of PYY
decrease food intake by delaying next meal
109
what is the effect of OXM
decrease food intake by delaying next meal
110
what is the effect of GLP-1
decrease food intake by delaying next meal
111
what is the effect of noradrenaline (with food intake)
enhances NPY to increase food intake but also enhance energy expenditure at other sites
112
what is the effect of GABA
inhibits NPY, decrease food intake
113
what is the effect of 5-HT
enhances POMC/MC, decreases food intake
114
what does leptin do to MSH pathway
stimulate
115
is MSH anorexigenic or orexigenic
anorexigenic
116
what does low leptin do to NPY AGRP
relieves inhibition
117
what does low leptin levels do to POMC CART MSH
reduces stimulation

PMCOL 344 (27 decks)

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