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anat 322 > food intake > Flashcards

food intake Flashcards

1
Q

how is obesity defined

A

state of body energy stores that exceeds physiological needs

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2
Q

how is the degree of obesity measured and what does it correlate with

A

BMI; correlates with total body fat

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3
Q

what creates an obesogenic environment (4)

A
  1. increased food availability
  2. increased portion size
  3. increased sedentary leisure time activities
  4. decreased occupational physical activity
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4
Q

health risks associated with obesity (6)

A
  1. type 2 diabetes
  2. CVD
  3. sleep-breathing abnormalities
  4. gallstones
  5. menstrual irregularities or difficulty getting pregnant
  6. cancer
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5
Q

describe energy homeostasis

A

energy intake balances energy expenditure

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6
Q

what systems regulate food intake (2)

A
  1. homeostatic system
  2. hedonic system
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7
Q

role of homeostatic system

A

motivation to eat when energy goes down (biological needs)

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8
Q

role of hedonic system

A

eat because of pleasure (can override homeostasis)

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9
Q

which system is main cause of obesity

A

hedonic system

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10
Q

which brain area control hedonic system

A

VTA

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11
Q

which brain areas control homeostatic system (2)

A
  1. brainstem
  2. hypothalamus
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12
Q

hypothalamic regions regulating food intake (4)

A
  1. 3rd ventricle (3V)
  2. dorsomedial nucleus (DMN)
  3. ventromedial nucleus (VMN)
  4. ARC
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13
Q

how did they find that hypothalamus controls food intake

A

lesioning PVN, VMN and DMN caused obesity; lesioning LHA caused weight loss

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14
Q

what are parabiosis experiments

A

surgical union of 2 individuals so they share common blood circulation

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15
Q

result of ob/ob + normal parabiosis mice

A

weight gain of ob/ob mouse suppressed (indistinguishable from WT)

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16
Q

result of db/db + normal parabiosis mice

A

normal mouse slowly loses weight and dies of apparent starvation

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17
Q

result of db/db + ob/ob parabiosis mice

A

ob/ob mouse rapidly loses weight and ides of apparent starvation

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18
Q

conclusions from parabiosis experiments (2)

A
  1. circulating factor involved in energy balance regulation
  2. defects in ob/ob and db/db mice may be in signal and receptor for signal
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19
Q

ob/ob mice are deficient in

A

leptin

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20
Q

db/db mice are deficient in

A

leptin receptor

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21
Q

leptin is produced by

A

adipocytes (proportionally)

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22
Q

increase in leptin leads to (2)

A
  1. decreased food intake
  2. increased energy expenditure
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23
Q

decrease in leptin leads to (2)

A
  1. increased food intake
  2. decreased energy expenditure
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24
Q

effect of leptin administration on ob/ob mice

A

restores normal body mass

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25
Q

why doesn’t leptin administration affect obese people (not leptin deficient)

A

obesity associated with increased circulating leptin; person becomes leptin-resistant; lack of response to exogenous leptin administration

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26
Q

action of leptin at genomic level (5 steps)

A
  1. leptin binds to leptin receptor (LepR) causing dimerization of receptor
  2. JAK phosphorylates LepR
  3. STAT binds to phosphate
  4. STAT dimerizes with other STAT
  5. dimer binds to gene in nucleus and induces transcription
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27
Q

orexigenic and anorexigenic hormones

A

orexigenic: ghrelin
anorexigenic: leptin

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28
Q

orexigenic and anorexigenic neurons

A

orexigenic: NPY/AgRP
anorexigenic: POMC

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29
Q

location of NPY/AgRP and POMC neurons

A

ARC

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30
Q

NPY/AgRP and POMC neurons synapse on

A

MC3/4R neurons

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31
Q

action of ghrelin in ARC

A

activates NPY/AgRP neurons (increase food intake)

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32
Q

action of leptin in ARC

A

activates POMC neurons and inhibits NPY/AgRP neurons (decrease food intake)

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33
Q

how did they determine colocalization of NPY/AgRP neurons

A

IHC; NPY & AgRP overlapped; NPY & POMC or AgRP & POMC didn’t overlap

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34
Q

how did they create a LepR KO

A
  1. expressed Cre under a neuron specific promoter
  2. crossed with mouse with LepR flanked with loxP sites
  3. Cre cleaves LepR in Cre-dependent manner (in neurons)
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35
Q

LepR KO on POMC or AgRP neurons leads to

A

mild obesity (similar to db/db mice, but not as obese)

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36
Q

LepR KO on VMH neurons leads to

A

very mild obesity

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37
Q

double KO of LepR on POMC and VMH neurons leads to

A

higher body weight than single mutant (potentiation), but still not db/db phenotype

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38
Q

what leads to replication of db/db mouse (2)

A
  1. whole body LepR KO
  2. brain-specific LepR KO
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39
Q

effect of leptin action on GABAergic neurons (2)

A
  1. prevents obesity
  2. reduces inhibitory tone to POMC neurons (decreased appetite)
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40
Q

leptin’s anti-obesity effects are mediated by what type of neuron

A

GABAergic neurons

41
Q

result of Vgat-LepR-KO mice and Vglut2-LepR-KO mice

A

GABA: mimics whole body LepR KO (db/db phenotype)
glut: similar to control

42
Q

which ARC neuron is GABAergic

A

AgRP

43
Q

why are AgRP neurons the only neurons (known) to contribute directly to obesity (not POMC for ex.)

A

AgRP neurons are GABAergic; leptin’s effects are mediated by GABAergic neurons as seen in Vgat-LepR-KO mice that have db/db phenotype (compared to vglut2-LepR-KO mice that look like control)

44
Q

what leads to the hypothesis that the majority of leptin’s anti-obesity effects are uncharacterized

A

vgat-LepR-KO mice leads to db/db phenotye -> AgRP neurons are known to be involved in leptin’s anti-obesity effects (because they are GABAergic) -> but LepR KO in AgRP neurons only leads to mild obesity (not db/db phenotype) -> other GABAergic neurons must be involved

45
Q

AgRP expression in fasted & fed mice and potential conclusion from this

A

increased expression in fasted mice (activity of AgRP neurons correlated with fasting behavior; activity of AgRP neurons induces feeding?)

46
Q

tools used to conduct experiments (5)

A
  1. neurosurgery
  2. IHC
  3. Cre
  4. GCaMP
  5. optogenetics
47
Q

explain GCaMP

A
  1. GFP bound to calmodulin and M13 in inactive conformation
  2. calcium binds to calmodulin and induces conformational change
  3. fluorescence
48
Q

activity of AgRP neurons when (a) fasted; (b) being fed

A

(a) fasted: high activity
(b) get food: activity drops fast

49
Q

activity of AgRP neurons when being fed false food

A
  1. fasted: high activity
  2. get false food: activity drops
  3. when realize not food: activity increases
    -> activity is related to food specifically
50
Q

when do AgRP neurons decrease activity

A

in the discovery or consumption of food

51
Q

effect of non-nutritive value things on AgRP neurons

A

fail to sustain decreased AgRP neuronal activity

52
Q

effect of shining blue light on AgRP neurons with ChR2

A

induces food intake

53
Q

how did they prove that hunger has a negative valence

A
  1. conditioned mice to eat orange flavor by shining light when eat orange flavor (AgRP-ChR2 neurons)
  2. no shining light: mice preferred to eat pink flavor (associate orange with hunger, so want to avoid)
54
Q

how did they prove that hunger has negative valence, but isn’t food specific

A
  1. photostimulation of AgRP-ChR2 neurons in place #1
  2. no photostimulation: mice avoid place #1 (prefer place #2) because associate with hunger
55
Q

valence of AgRP activity

A

negative (try to avoid it)

56
Q

how do we avoid AgRP activity

A

eating

57
Q

for what physiological purpose did leptin evolve

A

serve as a metabolic signal of energy sufficiency (rather than excess)

58
Q

ob/ob mice and fertility

A

ob/ob mice are infertile and obese

59
Q

why do opposite body weight types have same repoduction deficit

A

lean: not enough adipocytes, not enough leptin = no leptin signalling
obese: too much leptin, leptin resistance = no leptin signalling

60
Q

relationship bw starvation and gonadal hormone

A

starvation = decreased gonadal hormone and delays ovulation in females

61
Q

delayed ovulation and leptin administration in fasted mice

A

fasted + saline = delayed ovulation
fasted + leptin = no delay (like control)

62
Q

what causes fertility dysregulation in lean people

A

specific impairment of leptin signalling, not the body weight change

63
Q

result of leptin administration to female athletes that lost their period

A

improvement of reproductive function after (only) few months (not due to altered exercise patterns or weight gain)

64
Q

when are ghrelin levels maximal

A

just before eating

65
Q

where is ghrelin produced from

A

stomach cells

66
Q

ghrelin is mediated by which receptor

A

GH receptor

67
Q

what activities does ghrelin have (2)

A
  1. appetite-stimulating activities
  2. GH-releasing activities
68
Q

what role does ghrelin presumably have

A

meal initiation

69
Q

how does ghrelin impact body weight

A

increases body weight

70
Q

interindividual variability of ghrelin

A
  1. wide range of circulating ghrelin values
  2. maximal value always before eating
71
Q

relationship bw ghrelin and diet-induced weight loss

A

after diet-induced weight loss, plasma ghrelin levels increase -> maybe mechanism of rebound weight gain

72
Q

relationship bw bariatric surgery and ghrelin

A

bariatric surgery suppresses ghrelin levels (remove stomach cells -> less ghrelin release): contributes to weight-reducing effect and maintenance of reduced weight

73
Q

relationship bw cancer patients and ghrelin

A

ghrelin increases energy intake in cancer patients with impaired appetite

74
Q

location of LepR expression

A

VTA, which releases DA to striatum/NAc, amygdala and PFC (reward and motivation processing centers) and LHA (projects to VTA)

75
Q

effect of presenting highly palatable food

A

release of DA into nucleus accumbens

76
Q

high vs low fat diet and DA release

A

high fat diet induces more DA release than low fat diet

77
Q

brain activation towards high vs low calorie food & obese vs non-obese patients + conclusion

A
  1. higher response to high calorie foods
  2. obese people show stronger response
  3. conclusion: some people (obese people) are more attracted to caloric food than others
78
Q

relationship bw leptin and DA release in response to palatable food

A

leptin decreases DA release even before food presentation

79
Q

direct leptin administration to VTA + conclusion

A

reduces food intake -> VTA regulation important component of leptin’s ability to regulate food intake

80
Q

leptin and brain response to food images

A
  1. leptin-deficient state: even when fed, high brain response to food
  2. post-leptin treatment: when fed, no brain activation when shown food
  3. conclusion: enhanced neuronal activation normalized by leptin replacement therapy
81
Q

relationship bw ghrelin injection and brain response to food pictures

A

dramatic increase in brain response in VTA to food images following ghrelin injection -> ghrelin favors consumption by enhancing hedonic response to food-related cues

82
Q

receptor involved in sweet tasting

A

TRPM5 ion channel expressed in taste receptors cells

83
Q

WT vs trmp5-KO mice

A

WT -> strong attraction for sucrose solutions
trmp5-KO -> no preference for sucrose solution over water (no distinction bw both)

84
Q

long-term result of trmp5-KO mice

A

even lacking sweet receptors, mice eventually developed a preference for sucrose solutions (learned to distinguish)

85
Q

does TRMP5 distinguish sweet from non-sweet or calories and why (how do they know)

A

calories (and sweet) -> trmp5-KO presented with water and sucralose (noncaloric sweetener) and weren’t able to distinguish bw them

86
Q

barrel cortex plasticity (when eat something highly caloric?) after whisker trimming

A

dendritic spine turnover in pyramidal neurons -> some spines are lost, some new spines, some spines always present, some transient spines

87
Q

activity-dependent morphological plasticity of astrocytic processes in SON

A
  1. unstimulated SON: astroglia separates magno neurons
  2. stimulated (lactation) SON: astroglia retract & increased neuronal communication (NTs)
88
Q

synapse type and number in ob/ob mice: NPY neurons

A

more excitatory synapses in ob/ob mice than WT; less inhibitory synapses in ob/on mice than WT -> leads to increased appetite

89
Q

synapse type and number in ob/ob mice: POMC neurons

A

less excitatory synapses in ob/ob mice than WT; more inhibitory synapses in ob/ob mice than WT -> leads to increased appetite (decrease of loss of appetite)

90
Q

changes in synaptic density and properties in hypothalamus after leptin replacement: NPY neurons

A
  1. decreased excitatory synapses
  2. increased inhibitory synapses
  3. result: silencing of NPY neurons (decreased appetite)
91
Q

changes in synaptic density and properties in hypothalamus after leptin replacement: POMC neurons

A
  1. increased excitatory synapses
  2. no change in inhibitory synapses
  3. result: excitation of POMC neurons (increased appetite)
92
Q

differences bw ob/ob mice and WT synapses

A

different excitatory & inhibitory inputs onto NPY and POMC neurons

93
Q

what is DiI

A

fluorescent lipophilic dye that labels axonal projections

94
Q

leptin deficiency effect on projections from ARC to PVN

A

leptin deficiency disrupts normal pattern of projections from ARC to PVN: decrease in processes, less communication

95
Q

relationship bw leptin and neurite outgrowth

A

leptin promotes neurite outgrowth directly from ARC

96
Q

neurite outgrowth in ob/ob mice vs ob/ob + leptin mice

A

increases neurite outgrowth when leptin administration

97
Q

leptin actions in hypothalamus (3)

A
  1. acts directly on neurons of ARC by binding to LepR -> changes in their production & release of neuropeptides NPY and a-melanocyte (POMC product)
  2. produces rapid changes in strength and number of excitatory and inhibitory synapses that input onto NPY and POMC ARC neurons
  3. induces neurite outgrowth of ARC neurons -> stimulating projections from ARC to PVN during critical postnatal period
98
Q

projections of ARC -> PVN in obesity-resistant and obesity-prone rats

A

obesity-resistant rats have more processes than obesity-prone rats (more communication) -> obesity-prone rats become obese when given moderate diet compared to obesity-resistant rats (obesity-prone have defective ARC projections seen as early as 1st week and can persist into childhood)

99
Q

response of ARC neurons to leptin in obesity-prone rats

A

fail to respond to leptin (no neurite outgrowth)

anat 322 (7 decks)

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