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PSYCH310 > WEEK 8- HUNGER AND SATIETY II: CENTRAL FACTORS- NEUROPEPTIDES > Flashcards

WEEK 8- HUNGER AND SATIETY II: CENTRAL FACTORS- NEUROPEPTIDES Flashcards

1
Q

in what feedback loop is leptin circulated around the body?

A

negative feedback loop

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2
Q

what is leptin released in proportion to?

A

fat mass

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3
Q

what happens to leptin in the hypothalamus

A

leptin binds to receptors on hypothalamic neurons- more leptin= reduction in food intake- received by signals to the hypothalamic neurons

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4
Q

what are the principle sites of CNS regulation?

A

hippocampus, hypothalamus, medulla oblongata (hindbrain)

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5
Q

what are the two nuclei in the medulla oblongata

A

NTS and area postrema

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6
Q

what do the NTS and area postreme receieve signals from?

A

Vagal nerve through the CCK system

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7
Q

what is the main appetite control system?

A

hypothalamus

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8
Q

what part of the hypothalamus integrates signals from various hypothalamic nuclei and signals the body how to respond?

A

the PVN (parvoventricular nucleus)

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9
Q

what do the neurons in the DMH (dorsomedial hypothalamic nucleus) have receptors for?

A

leptin and insulin (long term control of food intake- tonic factors)

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10
Q

what are the four nuclei in the hypothalamus involved in appetite regulation?

A

DMH, VMH ARC and LHA

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11
Q

What receptors does VMH have?

A

leptin receptors, mainly sensitive to glucose

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12
Q

LHA contains populations of what neurons?

A

orexigenic neurons- stimulate food intake

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13
Q

what types of neurons does the ARC contain?

A

contains functionally discrete popualtions of neurons- some stimulate some inhibit feeding- all signals communicate with each through the neurons

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14
Q

what are the two hypothalamic believed to control hunger and satiety?

A

LHA and VMH

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15
Q

destructions of what part of the hypothalamus stopped animals eating and drinking?

A

LHA

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16
Q

what did electrical stimulation of the LHA do?- anand and brobeck 1951

A

caused eating and drinking

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17
Q

what did destructions of the VMH cause?

A

hyperphagia and weight gain

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18
Q

what did electrical stimulation of the VMH do?

A

suppressed eating

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19
Q

what was found about the claim that LHA and VMH controlled hunger and satiety?

A

not so much the geographical regions that are important- it is more about the neurons going through them

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20
Q

which was claimed to be the feeding centre and which was claimed to be the satiety centre?

A

LHA= feeding centre VMH= satiety centre

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21
Q

what are two examples of neuropeptides and neurotransmitters that cause hyperphagia?

A

NPY and AGRP

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22
Q

what is an example of a neuropeptide/ neurotransmitter that causes hypophagia?

A

a- MSH

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23
Q

What is NPY

A

36 amino acid neuropeptide, folded in hairpin shape, contains tyrosine residues at each end of the molecule, one of the most abundant neuropeptides in the brain

24
Q

NPY synapses onto what?

A

many parts within the hypothalamus

25
Q

what does NPY do?

A

increases food intake, decreases thermogenic activity, increases triglyceride in white fat and increases insulin levels

26
Q

what happens if you inject NPY into the PVN of rodents?

A

leads to a doubling of fat mass- two pronged attack- also reduces energy expenditure- as a consequence of this we get more fat deposited in adipose stores, NPY effects on feeding aare through a family of receptors- N1 AND Y6

27
Q

What study suggest NPY is a hunger signal?

A

morley et al 1987- intracerebral ventricular injection of NPY into mice. found NPY decreased latency to eat, NPY increased the time spent eating, NPY decreased grooming. conclusion: NPY modulates the state of hunger, NPY is capable of overriding mechanisms of satiety– two pronged attack- not only increasing hunger but decreasing satiety (more food eaten).

28
Q

in what study did they look at the motivation of the rodents motivation to eat the food (to make sure it wasn’t because it just tasted nice)

A

flood & morley 1991- intracerebroventricular (IVC) injection of NPY into mice to determine its effect on eating in three paradigms. 1. lever press (requires work) 2. appetite passive avoidance (electric shock to the tongue) 3. Quinine- adulterated milk (bitter taste). findings: mice consumed more milk when required to work for it. mice tolerated shock to the tongue to drink milk. mice ate food made bitter with quinine. conclusion: NPY causes a specific increase in the motivation to eat, rather than non- specific behaviour

29
Q

what studies suggested that levels of NPY are also affected hunger and satiety?

A

sahu, kalra & kalra 1988 - food deprivation for 4 days elicits a gradual increase in NPY levels. following 1 day of food intake NPY levels fall dramatically to the range found in satiated rats. Myers et al 1995- hypothalamic injection of a drug that blocks NPY receptors suppresses eating caused by food deprivation. if you block NPY receptors you remove that prompt to feed

30
Q

what triggers NPY to be released?

A

glucocorticoids (steroid hormones released by the adrenal gland)

31
Q

which hormones reduce activity of NPY

A

leptin and insulin (part of the negative feedback loop)

32
Q

what does NPY turn off?

A

thermogenesis- this reduces food intake

33
Q

what was found about leptin in zucker rats?

A

can’t respond to leptin- even though they have plenty in there system their brains cannnot detect it so appetite is no suppressed and rats become more hungry increasing food intake- partially repsonsible for the excess body fat rats demonstrate

34
Q

how does NPY affect ghrelin?

A

injection of neutralising NPY antibodies abolishes the orexigenic effects of ghrelin- antibody binds to NPY so cannot bind to NPY receptor so no ghrelin= less feeding. knockout of NPY also prevents ghrelin from stimulating feeding. Y1 specific antagonists block ghrelin orexigenic signal. NPY functions to relay peripheral ghrelin signalling. all points to the fact NPY does carry ghrelin signals to the central nervous system

35
Q

what study shows the controversy about actual NPY function?

A

erickson et al 1996- examined food intake in mice deficient in NPY. Findings: NPY deficient mice have normal food intake and body weight. NPY deficient mice become hyperphagic following food deprivation. conclusion: NPY is not essential for certain feeding responses or leptin actions- it was found that other signal from other hormones might be taking over. it was originally though NPY promote ferocious feeding when animals are starving- tested this but animals went back to normal eating behaviour- then though NPY had no role in the control of food intake- actually just that there is multiple factors involved

36
Q

In what people are NPY are significantly elevated?

A

people with diabetes, starved, undergone hugely intense exercise- in strong negative energy balance- NPY levels go up to protect us- trying to turn off thermogenesis to lead to weight gain- an anti-starvation factor

37
Q

what is a- MSH?

A

a member of the melacortin peptide family. deprived from a large precursor molecule- pro-opiomelanocortin. POMC producing neurones are located in the ARC (ie a-MSH is produced in the ARC). a-MSH containing pathways project throughout the brain. two receptors have been identified within the hypothalamus: MCR-3 and MCR-4. body is configured so that one group of neurones only produce POMC ect- each group produces one peptide

38
Q

what does a-MSH do?

A

decreases food intake, increases thermogenic activity and decreases fat cell mass

39
Q

what study shows the effects of a-MSH

A

williams et al 2002- intracerebroventricular injection of MT-II and examine ingestive behaviorual effects at the microstructural level using a licking model. findings: meal size was redcued bby MT-II in a dose dependent manner, licking parameters associated with taste evaluation were not altered by MT-II. conclusion: MT-II acts to modulate satiety, reductions in food intake are not due to altered taste evaluation. MT-II is an artificial version of a-MSH- not broken down easily so can investigate effects more easily. a-MSH is a satiety signal. mightve reduced food intake due to inducing nausea however there was no adverse taste so must be due to satiation

40
Q

what is other evidence that a-MSH is a satiety signal

A

levels of POMC mRNA are reduced by fasting (mizuno et al 1998- hypothalamic POMC mRNA was decreased >60 % after a single day’s fast. also administration of melanocortin receptor antagonist block administration blocks inhibition of food intake- fan et al 1997- co-administration of MT-II and shu9199 blocks MT-II induced inhibition of feeding. administration of SHU9119 alone enhanced feeding

41
Q

how does a- MSH repsond to nutritional status?

A

the antagonist is AGRP- made by same neurons that make NPY- these neurons signal to the same places the a-MSH signal to. MSH released binds to MC4 receptors and AGRP released. need to consider regulation of a-MSH and AGRP when looking at MCR-4 system (melanocortin)

42
Q

mizuno et al 1998- what is decreased in both db/db and ob/ob mice?

A

POMC mRNA - this is because they are resistant to leptin hence POMC neurones are not stimulated

43
Q

what does treatment of ob/ob mice with leptin do?

A

stimulates hypothalamic POMC mRNA

44
Q

levels of what are lowered in obese Zucker rats?

A

ARC POMC mRNA and PVN a-MSH peptide levels - zucker rats cant repsond to leptin so a-MSH levels will lower

45
Q

30% of POMC neurones express what?- cheung et al 1997

A

OB-Rb

46
Q

what does leptin stimulate?- Cheung et al 1997

A

POMC neurones

47
Q

what is POMC for?

A

all melanocortin signals

48
Q

what study showed the regulation of ARC AGRP neurones?

A

Ebihara et al 1999- design: examine the effect of AGRP on the satiety effect of leptin- study leptin’s regulation of AGRP expression. findings: leptin-induced inhibition of food intake was reversed by co-injection of AGRP in a dose dependent manner, hypothalamic AGRP mRNA expression was upregualted in leptin deficient ob/ob mice. central injection of leptin reversed the increased AGRP levels

49
Q

what study is evidence that alpha MSH has a role in obesity in humans?

A

yeo et al 1998- rare cases of morbid obesity in humans are associated with specific mutations affecting components of the melanocortin system - this confirms that alpha msh operates in the melanocortin system to regulate appetite in humans

50
Q

what study suggests melanocortins could be used as treatment for obesity if it is a satiety factor?

A

horst et al 2001. design: 36 normal weight students divided into 3 groups: 1) ACTH(4-10) 2) Desacetyl- MSH 3) placebo. findings: decreased body weight, body fat and plasma leptin levels in subjects treated with ACTH(4-10). No significant changes in group treated with desacetyl- MS.conclusion: there is an essential role for hypothalamic melanocortins in body weight control in humans

51
Q

what study shows that levels of peripheral AGRP are regulated by the dyanmics of the changes in plasma leptin?

A

hoggard et al 2004. design: 11 lean and 18 obese healthy males. baseline measures after 4-6 days fast (rapid loss of 5% body weight) after very low calorie diet (less rapid loss of 5% body weight). findings: alpha MSH and AGRP elevated in obese- correlated with fat mass and leptin. fasting increased AGRP but a-MSH did not change. VLCD did not alter levels or either peptide

52
Q

how does leptin exert some of its satiating effects?

A

by acting at receptors in the ARC

53
Q

what does leptin inhibit?

A

NPY/AGRP neurones, suppressing their feeding effects

54
Q

what does leptin activate?

A

POMC neurones- consistent with a role for both factors in modulating satiety

55
Q

what interacts directly to directly modualte each others activity

A

NPY and POMC neurones

56
Q

how do NPY and POMC neurones also interact indirectly?

A

also interact indirectly at the level fo MCH and orexin neurones in the LHA to regulate appetite

PSYCH310 (9 decks)

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