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Flashcards in regulation of energy balance Deck (33)
1

which GI diseases can cause spontaneous weight loss

- chronic pancreatitis - CF - IBD - parasitic infection

1

what other than gene mutations can lead to obesity

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

2

what is the association between food and energy expenditure

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

2

how is leptin transported into the brain

by a receptor on the choroid plexus

4

how the double labeled water method of measuring energy expenditure work

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)

5

what determines how much leptin is made

the size of the adipocytes - bigger cell - more leptin

6

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

- most basal (65-75%)

- Thermogenesis (15-20%)

- activity (10-15%)

7

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

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

8

if you lack orrexin gene what happens

narcolepsy

8

what is the most common association of leptin and obesity

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

9

why does glucose and other nutrients inhibit hunger

- increases LCFA-CoA which inhibits food intake

10

which main infections can cause spontaneous weight loss

- TB - subacute bacterial endocarditis - amoebic abscess - HIV

10

which malignancies commonly cause spontaneous weight loss

- bowel - pancreas - liver - lymphoma - leukaemia

11

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

reduces

13

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

oxytocin CRH both stimulate food intake

15

which areas of the hypothalamus interact

arcuate nucleus Paraventricular hypothalamic nucleus laternal hypothalamus

16

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

size of fat stores presence of food int he gut

16

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

has a mutation in the R for leptin

17

what causes obesity

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

19

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

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

where is leptin synthesised

adipocytes

21

function of leptin

signals the size of the fat stores in the body

22

common mutations causing human obesity

- leptin gene - leptin gene R - MSH gene signalling

23

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

Harris-Benedit equations

24

which endocrine disease can casue spontaneous weight loss

- untreated T1DM - Throtoxicosis - Addison's disease (lack cortisol)

26

genetic inheritance of leptin gene mutation

homozygous

27

2 functions of orrexin

- inhibits food intake - stabilises the arousal system for sleep - wakefullness

28

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

the hypothalamus

29

what are some methods of measuring energy expenditure

- whole room respiratory chambers - metabolic carts (hood) - double labeled water

30

medical complications of anorexia nervosa

- amenorrhoea - lanugo hair - bradycardia - anaemia

31

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

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

32

approximating energy expenditure is based on what 4 things

- sex - height - weight - age - activity

33

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

opoids dopamine endocannabinoids