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YR2 LCRS Endocrinology > 14. Obesity and the endocrine control of food intake > Flashcards

14. Obesity and the endocrine control of food intake Flashcards

1
Q

what does body weight homeostasis refer to?

A

a balance between energy (food) intake and energy expenditure (BMR, exercise)

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2
Q

what inputs does the hypothalamus receive regarding body weight?

A
  • ghrelin, PPY and other gut hormones
  • neural input from the periphery and other brain regions
  • leptin
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3
Q

where is the arcuate nucleus and what is it involved in?

A

at the base of the brain, above the median eminence where lots of hypothalamic releasing factors exist

it is involved in the regulation of food intake

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4
Q

where is the paraventricular nucleus and what is it involved in?

A

above the 3rd ventricle

it is involved in the regulation of food intake

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5
Q

how does the arcuate nucleus detect factors in the blood?

A

it is not completely isolated from the circulation by the BBB and so the incomplete BBB allows access to peripheral hormones so that peripheral and central feeding signals can be integrated

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6
Q

what are the 2 neuronal populations in the arcuate nucleus and what do both sets do?

A
  • stimulatory (NPY/Agrp neurons) increase appetite
  • inhibitory (POMC neurons) decrease appetite

both sets extend to other hypothalamic and extra-hypothalamic regions

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7
Q

how does NPY stimulate food intake and appetite?

A

it binds to Y family receptors in regions like the paraventricular nucleus

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8
Q

how do the POMC neurones work?

A

POMC neurones in the arcuate nucleus are enzymatically cleaved to produce alpha-MSH, which binds to the MC4R receptor in the paraventricular nucleus to decrease food intake

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9
Q

how does Agrp work?

A

Agrp is an endogenous antagonist of MC4R. there is baseline stimulation of the MC4R by alpha-MSH to suppress appetite. if the signal is taken away you feel hungry as Agrp blocks the suppressing signal and increases appetite

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10
Q

how do human cns mutations affect appetite?

A
  • POMC deficiency and MC4R mutations can cause morbid obesity
  • people with POMC deficiency also lose ACTH and can present with paleness and ginger hair
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11
Q

why do people with POMC deficiency also lose ACTH?

A

because POMC is the precursor for ACTH in the pituitary gland

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12
Q

what does the ob gene code for?

A

leptin - a protein hormone released from white adipose tissue which signals to the brain that you are not starving

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13
Q

what happens when leptin is not produced?

A

obese, diabetic, infertile, stunted linear growth, low body temp, low immune function

symptoms are characteristic of starvation except for obese and diabetes - the individual thinks they are starving and continues to eat, the immune system is energetically expensive so is switched off, the reproductive axis is switched off because it is evolutionarily ineffective to reproduce when you are starving

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14
Q

how does leptin influence other neurones?

A

leptin activates POMC

leptin inhibits NPY/Agrp neurones

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15
Q

what can leptin resistance lead to?

A

obesity as the hormone is present (usually leptin circulates in plasma in a proportional concentration to fat mass) but doesn’t signal effectively

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16
Q

why is leptin ineffective as a weight control drug?

A

most fat people have leptin but are just resistant

17
Q

why is leptin a ‘hormone of absence’?

A

the absence of leptin results in hyperphagia, lowered expenditure and sterility

the presence of leptin tells the brain that there are sufficient fat reserves for normal functioning but high leptin has little effect

18
Q

when is leptin useful therapeutically? what are its risks?

A

useful for people who are actually leptin deficient

HOWEVER
patients may develop antibodies towards leptin

19
Q

what are the effects of leptin administration in children and women?

A

restores LH pulsatility in children with leptin deficiency

restores LH pulsatility in women with amenorrhea (driven by stress/low body fat)

20
Q

what is the role of insulin in food intake?

A
  • insulin circulates at levels proportional to body fat
  • obesity leads to insulin resistance
  • central administration of insulin reduces food intake
21
Q

which gut hormones are released by the stomach and what do they do?

A

ghrelin - hunger, growth hormone release

gastrin - acid secretion

22
Q

which gut hormones are released by the duodenum and what do they do?

A

cholecystokinin - gall bladder contraction, GI motility, pancreatic exocrine secretion

secretin - pancreatic exocrine secretion

GIP - incretin activity

motilin - GI motility

23
Q

which gut hormones are released by the pancreas and what do they do?

A

insulin and glucagon - glucose homeostasis

pancreatic polypeptide - gastric motility, satiation

amylin - glucose homeostasis, gastric motility

24
Q

which gut hormones are released by the large intestine and what do they do?

A

GLP-1 - incretin activity, satiation

GLP-2 - GI motility and growth

oxyntomodulin - satiation, acid secretion

PYY(3-36) - satiation

25
Q

how is food intake regulated in the short-term?

A

peptide YY and ghrelin - they are released from the L cells of the small intestine

26
Q

what is the role of peptide YY?

A

tells the brain you are full

peptide YY is released from the intestines proportional to the calorie intake. to become activated the first 2 amino acids of PYY are cleaved off. PYY(3-36) then:

  • inhibits NPY release
  • stimulates POMC release
  • decreases appetite
27
Q

what is the role of glucagon-like peptide (GLP)?

A

satiety

  • coded for by the pre-proglucagon gene and is released post-prandially
  • stimulates insulin release and reduces food intake
28
Q

what is GLP-1 broken down by and how quickly?

A

broken down by DPP4

has a half-life of 1min

29
Q

what is used instead of GLP-1?

A

saxenda - synthetic version of GLP-1 that is a long-acting GLP-1 receptor agonist used to treat diabetes and obesity

30
Q

what is the role of ghrelin?

A

tells the brain when you are hungry

  • released from the stomach and acts on the brain
  • ghrelin increases before a meal then drops when you are full (opposite to PYY)
  • stimulates NPY/Agrp neurones
  • inhibits POMC neurones
  • increases appetite
31
Q

what are the components of ghrelin?

A

ghrelin o-acyltransferase (GOAT) attaches the fatty acid group and activates ghrelin

the fatty acid chain helps ghrelin access the brain where its receptor is

32
Q

what can injecting gut hormones result in?

A

nausea

33
Q

which comorbidities are associated with obesity?

A
  • sleep apnoea
  • depression
  • bowel cancer
  • osteoarthritis
  • gout
  • stroke
  • MI
  • hypertension
  • diabetes
34
Q

what % of the BMI is predicted by your genes?

A

60-80%

35
Q

what is the thrifty gene hypothesis?

A
  • specific genes selected for to increase metabolic efficiency and fat storage
  • it is evolutionarily sensible to put on weight (in case of famine and for insulation)
  • in modern society where there is enough food and little exercise the genes predispose carriers to obesity and diabetes
36
Q

what is the adaptive drift (drifty gene) hypothesis?

A
  • normal distribution of body weight because the fat are eaten (can’t escape predation) while the thin starve in the cold
  • however as humans learnt to defend against predators obesity was not selected against
  • there was genetic drift towards putting on more weight

YR2 LCRS Endocrinology (18 decks)

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