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endo - yr2 > endocrine control of food intake > Flashcards

endocrine control of food intake Flashcards

1
Q

draw a diagram to illustrate how the hypothalamus regulates appetite *

A

–

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2
Q

what are the 2 factors in body weigt homeostasis

A

food intake and energy expenditure

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3
Q

what are the factors that influence the body weight homeostasis that act on the hypothalamus *

A

ghrelin, PYY and other gut hormones

neural input from the periphery and other brain regions

leptin

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4
Q

how is the hypothalamus involved in food regulation *

A

integrates lots of inputs

eg vagal nerve from GI to brainstem tell hypothalamus how much stomac has stretched

hypothalamus determines whether you should feel hungry

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5
Q

what is te arcuate nucleus, where is it and what does it do *

A

key brain area involved in regulation of food intake

at base of brain below the circle of willis

as incomplete blood brain barrier ie is a circumventricular organ - so has access to peripheral hormones - as idea of the peripheral feeding state

it integrates peripheral and central feeding signals

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6
Q

what are the neuronal populations in the arcuate nucleus and what do they do *

A

NPY/Agrp neurons are stimulatory- increase appetite

POMC neurons - decrease appetite - POMC is chopped into alpha MSH wich suppresses food intake

both neurons extend to other hypothalamic and extra-hypothalamic regions - circuits to higher centres

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7
Q

explain how mutations in neuronal pathways controlling food intake affect weight balance *

A

no NPY/Agrp mutations - in mice when induce in development - brain adjusts accordingly

POMC deficiency and MC4-R mutations = morbid obesity, also pale skin and red hair because of lack of other POMC products also POMC codes for ACTH so stress axis doesnt work. if have melanocortin receptor deficiency - just have problems with food regulationn

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8
Q

are mutations in neuronal pathways responsible for obesity epidemic *

A

no - obesity is polygenic

if you have monogenic mutation causing obesity - you are obese from a very young age

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9
Q

what kind of mutation is the ob/ob mutation *

A

recessive

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10
Q

characteristics of the ob/ob mouse *

A

obese

diabetic

infertile

stunted linear growth

decreased body temp

decreased energy expenditure

decreased immune func - immune system energetically expensive - sut down if you are staving

similar abnormalities to starved animals - thinks starving to death so eats loads

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11
Q

what is leptin *

A

protein hormone

made form fat tissue to tell the brain you’re not starving

it is what is missing in the ob/ob mouse

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12
Q

describe leptin’s role in food intake *

A

low levels when body fat is low

igh wen body fat is high

central/peripheral admin = reduced food intake and increased thermogenesis

activats POMC and inhibits NPY and Agrp neurons

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13
Q

why is leptin ineffective as a weight control drug *

A

fat people develop leptin resistance - it is present at igh levels just doesnt signal effectively

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14
Q

wy is leptin considered a ‘hormone of absence’ *

A

when it is missing, there are profound effects

hyperphagia, lowered enrgy expenditure and sterility (switces off the reproductive axis)

antistarvation hormone rather than an anti-obesity one

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15
Q

what is the effect if your body as never seen leptin *

A

dont go through puberty - reproductive axis has been switched off

obese

when give recombinant leptin = reactivation of the system = lose weight and begin puberty - not resistant, yiu’re just missing leptin

leptin also restores LH pulsitility in people with ypothalamic amenorrhoea

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16
Q

why is puberty earlier in teh developed world

A

people are better nourised so have higher leptin

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17
Q

what time frame signal is leptin and insulin with regard to reducing food intake

A

long term

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18
Q

describe insulin’s role in food intake 8

A

circulates at levels proportional to fat - tis is the basal insulin - more weight means pancreas works harder to produce basal insulin = insulin resistance

receptors for insulin are in the hypothalamus

central administration reduces food intake

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19
Q

describe gut hormones *

A

there are >20 regulatory peptide hormones

influence gut motility, secretion of other hormones abd appetite

their release depends on the nutrient level in the gut

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20
Q

where is ghrelin released from *

A

the stomach

21
Q

describe how and when gut hormones are released *

A

enterendocrine cells can detect fats - see if they are short chain or long chain, carbs - transporter mech tat takes glucose into cell changes electrical state and uses downstream signalling, and protein products

then releases combinatioon of gut hormones from the basal side of the cell

hhormones have an endocrinbe effect acting on panc or brain, paracrine effect altering secretions or effect neuronal function of enteric nervous system or vagus

22
Q

what is ghrelin *

A

28aa gut hormone

has fatty acid chain - necessary for receptor binding and movement in the circulation

ghrelin o-acyltransferase - attach FA chain

23
Q

what is the role of ghrelin *

A

it increases appetite and drives when you want to eat by acting on the arcuate nucleus

it stimulates nPY/Agrp neurons

inhibits POMC neurons

increases food intake

24
Q

what is satiation *

A

stop eating present meal

25
Q

what is satiety *

A

how long you fell full - controls pattern of food intake

26
Q

what do L cells release *

A

PYY and GLP-1

27
Q

describe how the structure of an L cell relates to function *

A

it is flask shaped - open cell

has end near lumen with all the sensory machinary

signal modulates teh release of the secretory granules from the broad base on a capillary

also have neuro/pseudopods that communicate directly with the neurons by releasing tracers that synapse with the neurons so propagate a neuronal signal that way

28
Q

what is PYY and whatbdoes ot do *

A

it is a 36 chain aa

directly modulates neurons in the arcuate nucleus

inhibits NPY

stimulates POMC neurons

decreases appetite

eat less - brain thinks tat you have just eaten

29
Q

wat is GLP-1 *

A

gut hormone coded for by the preproplucagon gene and released post-prandially

pre-proglucagon gene is in L cells

chopped into GLP-1 used to treat diabetes and obesity

GLP-2 involved in gut growth perhaps treatment for intestinal disease

the end og GLP-1 is quickly cleaved so GLP-1 is turned off - has a short half life

it has the incretin role - stimulate glucose stimulated insulin release

incretins are hormones tat detect glucose form the gut, released from the gut and detected by the pancreas

reduces food intake

30
Q

how can we use GLP-1 therapeutically *

A

modulate it

GLP1 agonists that bind to GLP1 receptor but ave a longer half life

and DPP4 inhibitors - suppress the breakdown of endogenous GLP1

31
Q

what is saxenda *

A

it is a long acting GLP-1 receptor agonist

ave fatty acid attached to help it move through the circulation

have arg aa so that it is not broken down

use double the dose you would use for t2dm and it can cause weight loss to help with cardiovasscualr disease

32
Q

other than glp1 and 2 what does pre-proglucagin get converted into and where

A

glucagon in a cells of the pancreas

33
Q

what are the 3 types of satiety action caused by gut hormones 8

A

post-prandial - reduces food intake following a meal - pyy and glp-1

chronic - gut disease, chronic elevation suppresses appetite - reduce stress in gut and give it a chance to recover

acute nausea - toxic ingestion, acutely very high levels - toxins bind to receptors and cause surge in hormones - signal that you shouldnt be eating it so it makes you sick

34
Q

what is the possibility of using gut hormones as drugs *

A

use a combination to reduce food intake by suppressing appetite

35
Q

what is the difficulty of using gut hormones as drugs 8

A

have to inject a high amount for it to have an effect

if inject too much = nausea

level rapidly decrease because have short half life

only in the anorexigenic range for a short period of time

have to alter the pharmacokinetics of the drugs so they last longer

36
Q

what is the possibility of dietry manipulation to alter food intake 8

A

understand how the gut detects food and hijack these systems

eg use synthetic nutrients to stimulate nutrient receptors - spark enteroendocrine cells to fire - feel like get calories but dont have to eat as much

or get food to target the lower gut, because the bigger the meal the lower the food goes down to the gut, therefore have longer satiety - if you can get smaller meals to lower end of gut you drive satiety without eating too much

37
Q

what are the comorbiditiees assoiciated with obesity *

A

depression

sleep apnoea

bowel cancer

osteoarthritis

gout

stroke

mi

hypertension

dm

peripheral vascular disease

38
Q

how do genetics influence weight gain *

A

in given env genetics determine how much weight you put on

monozygotic twins have a higher concordance than dizygotic twins

ie if one monozygotic twin is obese the other has a higher chance of being obese than if they were dizygotic twins

39
Q

what is teh thrifty gene hypothesis 8

A

specific genes are selected for to increase metabolic efficiency and fat storage when cavemen - thin humans didnt survive famines so didnt pass their genes on

in context of plentiful food these genes predispose obesity

populations previously prone to starvation become most obese when exposed to western diet

40
Q

what is the drifty gene hypothesis *

A

in the past there was a normal distribution of body weight - the fat are eaten and the thin starve

but now obesity is not selected against

genetic druft is putting on body weight and there being a neutral change ie inheriting genes that mean you put on weight

however in current context the people who inherit these genes put on weight

in a toxic environment those who are genetically prone will put on more weight

41
Q

what time frame do gut peotides prevent food intake over

A

short term

42
Q

effect of leptin on hypothalamo-gonadal axis *

A

leptin is permissive of it - ie hig leptin means axis works

43
Q

wat does POMC split into that is involved in food regulation *

A

aMSH

44
Q

where are POMC neuronal cell bodies *

A

te arcuate nucleus

45
Q

name for arcuate nucleus in humans *

A

infundibular nucelus

46
Q

what is teh role of a melanocyte stimualting hormone *

A

endogenous agonist of melanocortin 4 receptor

47
Q

what neurons does ghrelin stimulate

A

orexigenic agrp

48
Q

where is glp-1 produced

A

from the pre-proglucagon gene in l cells in the gut

endo - yr2 (24 decks)

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