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Medicine 3 > 7 obesity 2: control of appetite > Flashcards

7 obesity 2: control of appetite Flashcards

1
Q

what factors affect the control of food intake?

A

hunger (desire/ need) for food

appetite (psychological desire to eat food)

satiation (feeling of fullness that terminates meal)

satiety (feeling of repletion that inhibits further meals)

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2
Q

is appetite more powerful than hunger?

A

yes

rats given palatable foods gain weight

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3
Q

which part in the brain controls food intake?

A

hypothalamus

arcuate nucleus ARC

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4
Q

describe what happens in ARC in terms of food control

A

NPY and AgRP stimulate orexigenic neurones-> stimulate food intake

POMC and CART stimulate anorexigenic neurones-> inhibit food intake

POMC undergoes post translational modification to generate melanocortins-> act on melanocortin receptors (inhibit food intake)

AgRP is antaognist to melanocortin-4-receptor

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5
Q

dsecribe the role of peripheral body signals on ARC

A
  • leptin stimulates release of POMC and inhibit NPY AgRP
  • PYY- directly acts n ARC or stimulate insulin- inhibiting appetitie
  • CCK- directly acts on brain or vagal inputs
  • grehlin stimulates appetite
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6
Q

how are gut peptides involved in regulation of food intake?

A

gastric distention leads to release of number of hormones from enteroendocrine cells:

inhibit food intake:

cholecystokinin (CCK)

glucagon-like-peptide 1 (GLP 1)

oxyntomodulin

Peptide YY (PYY 3-36)

apolipoprotein A-IV

enterostatin

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7
Q

Leptin:

where is it secreted from?

what stimulates/ inhibits secretion?

correlation?

mutations?

A

adipose tissue

decreased food intake decreases leptin secretion

  • reversed by refeeding or insulin

Production of leptin correlates with amount of adipose tissue- ie energy stores

Mutations causing absence of leptin leads to severe obesity

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8
Q

Grehlin:

where/when is it secreted?

where does it act?

A

produced from GIT

secreted on anticipation of food

acts centrally at ARC or brain stem to stimulate food intake through NPY and AgRP

hunger at certain times of the day is due to Grehlin (eg. mealtimes)

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9
Q

PYY

where is it secreted?

stimulations?

mechanism?

actions?

A

secreted from distal GIT dependent on nutrient intake (eg protein> fat or CHO).

Also stimulated by CCK, gastric acid, bile

PYY1-36 cleaved to PYY3-36- acts at NPY Y2 receptor: negative feedback mechanism

Inhibits food intake. Possibly through vagal inputs

PYY levels stay elevated for 12 hours post meal.

Decreases food intake in lean and obese (no resistance)

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10
Q
A
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11
Q

reward centres in the brain:

A

Appetite linked to reward processes in the brain.

eg opioid receptors (endorphins)

Cannabinoid receptors

Dopamine

Reinforcement of motivation to find and consume foods of high incentive/energy content?

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12
Q

dopamine and reward

A

Feeding is associated with dopamine release in the dorsal striatum.

Degree of pleasure correlates with the amount of dopamine released.

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13
Q

how can the dopamine mechanism be used for weight loss?

A

dopamine reuptake inhibitor: bupropion

inhibition of reuptake increases amount of dopamine in synpase- prolonged activity of dopamine receptor

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14
Q

effects of nicotine on appetite?

A

supressor- those who quit gain weight

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15
Q

current prescription medications for obesity

A

Orlistat

Liraglutide - 2017

Sibutramine- Suspended Jan 2010

Rimonabant- marketing authorisation suspended Oct. 23rd 2008.

Dexfenfluramine, fenfluramine and phentermine associated with valvular heart disease (obesity already has increased CV risk) and pulmonary hypertension.

No longer recommended.

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16
Q

orlistat

A
  • Inhibits Gastric and Pancreatic lipase
  • minimal absorption (most action in GI tract)
  • Needs to be taken before each main meal
  • ~ 30% inhibition of lipases at normal therapeutic doses (lose 200kcal per day)
  • Needs to be combined with a low fat diet – reinforces the need to restrict fat intake
17
Q

side effects of orlistat

A

Steatorrhea- fatty, foul smelling faeces

  • may actually help to reduce fat intake (more fat more steatorrhea)

In reality, patients will give up taking orlistat

Reduced absorption of fat therefore need to monitor fat soluble vitamin status- supplements?

18
Q

prescribing guidelines of orlistat

A

To be combined with reduced calorie diet.

BMI > 30 kg/m2 or

BMI > 28 kg/m2 if other risk factors eg type 2 diabetes, hypercholesterolaemia, hypertension

Should only be continued after 12 weeks if weight loss exceeds 5%

Treatment > 12 months should only be done after discussion potential benefits and risks with patient.

Dose

120 mg taken immediately before, during or 1 hr after each main meal

Max. 360 mg daily (only 3 meals a day)

Miss dose if meal contains no fat (small liklihood)

19
Q

OTC orlistat

A

Reduced dose- 60mg tds

Max 6 months

Combined with reduced fat diet

BMI > 28

Review after 12 weeks to see if beneficial

Dietary approaches and physical activity should be tried before OTC Orlisat

Still need calorie reduced diet

20
Q

saxenda (Liraglutide) - GLP1 agonist

approved 2017

A

s.c. injection

Appetite suppression- increased secretion of POMC/ CART- anorexigenic neurons

GLP-1 can also reduce high fat food intake by suppressing dopamine signalling- effect on reward pathways.

orlistat is cheaper

Treatment Guidelines similar to orlistat

ie BMI> 30 or lower if concurrent disease

NB care with type 2 diabetes- is patient already on a GLP-1 agonist?

Monitor after 12 weeks- stop if less than 5% weight loss

21
Q

mysimba

A

Combination of naltrexone & bupropion

Effects on reward pathway.

Similar efficacy as orlistat.

Not recommended by NICE- cost effectiveness not clear

22
Q

Sibutramine

A

Combined NA and 5HT uptake inhibitor. (similar to anti depressant)

cf antidepressants.

Appetite suppressant.

No longer used- increase bp and hr. (increase CV risk)

Originally thought weight loss outweighed CV risk (CV risk lowers with weight loss) but risk outweighs benefits

23
Q

Rimonabant (Acomplia)

A

CB1 receptor antagonist (CB1 stimulates appetite)

Complaints of CNS side effects like depression

Licensed for use in EU July 2006

NICE guidelines issued June 2008

European Medicines Agency suspended marketing authorisation Oct. 23rd 2008.

Review found that benefits do not outweigh the risks.

Severe side effects

24
Q

Phentermine- US

A

Not licensed in UK.

Increases catecholamine levels in brain.

Also peripheral effects- increase hr, bp, palpitations.

Qsymia - phentermine + topiramate

42% > 10% weight loss

Approved by FDA

Refused by EMEA October 2012 due to increased CV risk

Medicine 3 (31 decks)

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