regulation of energy balance Flashcards

1
Q

which GI diseases can cause spontaneous weight loss

A
  • chronic pancreatitis - CF - IBD - parasitic infection
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1
Q

what other than gene mutations can lead to obesity

A

epigenetics - early exposure to high energy diet –> epigenetic changes in genes controlling hunger

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2
Q

what is the association between food and energy expenditure

A

in a normal person - people will increase E expenditure in an effort to prevent weight gain and vice versa

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2
Q

how is leptin transported into the brain

A

by a receptor on the choroid plexus

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4
Q

how the double labeled water method of measuring energy expenditure work

A

label the body water with stable isotopes of oxygen and hydrogen. - O2-18 is lost from the body in the form of water and CO2 - 2H is lost only as water - difference between them reflects the CO2 production (result of fat, carbohydrate and protein oxidation)

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5
Q

what determines how much leptin is made

A

the size of the adipocytes - bigger cell - more leptin

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6
Q

what is the split up of energy expenditure by the body?

A
  • most basal (65-75%)
  • Thermogenesis (15-20%)
  • activity (10-15%)
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7
Q

primary NTs produced in the arcuate nucleus for hunger/satiety and what does each one specifically do?

A

NPY - cause you to eat AGRP - cause you to eat CART - inhibits food intake alpha-MSH - inhibits food intake

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8
Q

if you lack orrexin gene what happens

A

narcolepsy

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8
Q

what is the most common association of leptin and obesity

A

most people who are obese are resistant to leptin signals due to a SNP in the receptor

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9
Q

why does glucose and other nutrients inhibit hunger

A
  • increases LCFA-CoA which inhibits food intake
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10
Q

which main infections can cause spontaneous weight loss

A
  • TB - subacute bacterial endocarditis - amoebic abscess - HIV
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10
Q

which malignancies commonly cause spontaneous weight loss

A
  • bowel - pancreas - liver - lymphoma - leukaemia
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11
Q

if all things equal…. if the amount of leptin increases.. what happens to hunger

A

reduces

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13
Q

what are the NTs produced in the paraventricular nucleus for hunger/satiety and what are their functions?

A

oxytocin CRH both stimulate food intake

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15
Q

which areas of the hypothalamus interact

A

arcuate nucleus Paraventricular hypothalamic nucleus laternal hypothalamus

16
Q

what peripheral signals does the hunger centre of the brain respond to?

A

size of fat stores presence of food int he gut

16
Q

why does a diabetic not respond to leptin injection to stop eating

A

has a mutation in the R for leptin

17
Q

what causes obesity

A

energy in>energy out - only in the weight gain phase

19
Q

why do some people put on weight when over fed and others dont?

A

due to change in energy expenditure - those who put on weight didnt change their activity thermogenesis - those who didnt put on weight have a big change in activity thermogenesis (fidgiting)

19
Q

where is leptin synthesised

A

adipocytes

21
Q

function of leptin

A

signals the size of the fat stores in the body

22
Q

common mutations causing human obesity

A
  • leptin gene - leptin gene R - MSH gene signalling
23
Q

what is the name of the equations used to predict energy expenditure

A

Harris-Benedit equations

24
Q

which endocrine disease can casue spontaneous weight loss

A
  • untreated T1DM - Throtoxicosis - Addison’s disease (lack cortisol)
26
Q

genetic inheritance of leptin gene mutation

A

homozygous

27
Q

2 functions of orrexin

A
  • inhibits food intake - stabilises the arousal system for sleep - wakefullness
28
Q

which part of the brain controls the set point for weight control

A

the hypothalamus

29
Q

what are some methods of measuring energy expenditure

A
  • whole room respiratory chambers - metabolic carts (hood) - double labeled water
30
Q

medical complications of anorexia nervosa

A
  • amenorrhoea - lanugo hair - bradycardia - anaemia
31
Q

what are the names of the neurons that produce the NTs in the arcuate nucleus of the hypothalamus involved in hunger/satiety

A

primary neurons - NPY and AGRP PomC neurons - CART and alpha-MSH

32
Q

approximating energy expenditure is based on what 4 things

A
  • sex - height - weight - age - activity
33
Q

what NTs can modulate the basic pathways in the hypothalamus involved in hunger/satiety?

A

opoids dopamine endocannabinoids