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Year 2 - endocrinology > Endocrine control of food intake > Flashcards

Endocrine control of food intake Flashcards

1
Q

Where inputs does the hypothalamus receive to regulate food intake?

A
  • Ghrelin, PPY and other gut hormones
  • Neural input from the periphery and other brain regions
  • Leptin
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2
Q

Where is leptin released from and what does it tell the hypothalamus?

A

From body fat - it tells the brain how much fats store there is

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3
Q

Which nucleus is found above the median eminence?

A

The arcuate nucleus

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4
Q

Where does the paraventricular nucleus sit?

A

Above the 3rd ventricle

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5
Q

Which two nuclei are important in food intake regulations?

A

The arcuate and paraventricular nucleus

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6
Q

Is the arcuate nucleus completely enclosed by the BBB and why?

A

NO - it allows them nucleus to access peripheral hormones (it is a circumventricular organ that can detect things in the blood to integrate peripheral and central feeding signals)

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7
Q

What are the two neuronal populations in the arcuate nucleus?

A

stimulatory (NPY/Agrp)

inhibitory (POMC)

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8
Q

What does NPY/Agrp neurones do?
What about POMC neurones?

Where do these neurones extend to?

A

increase appetite

reduce appetite

other hypothalamic and extra-hypothalamic regions

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9
Q

What is the melanocortin system?

A
  • NPY binds to Y family receptors (particularly in regions like the paraventricular nucleus)
  • Downstream from that, NPY stimulates food intake and appetite
  • The POMC neurones work via alpha-MSH, which binds to the MC4R receptor and suppresses food intake
  • Agrp is an endogenous antagonist of the MC4R
  • There is baseline stimulation of the MC4R by alpha-MSH to suppress appetite
  • If this signal is taken away, you feel hungry (Agrp blocks the suppressing signal and increases appetite
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10
Q

What does alpha-MSH act on and what happens if this stimulation is removed?

A

MCR4 receptor

You feel hungry as normally it would suppress food intake.

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11
Q

What are some mutations that can affect appetite?

A
  • No known NPY or Agrp mutations in humans associated with food intake
  • POMC deficiency and MC4-R mutations can cause morbid obesity
  • People deficient in POMC also lose ACTH -> you no longer have the hypothalamo-pituitary-adrenal axis
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12
Q

How is POMC deficiency spotted?

A 
Obesity
Pale
Ginger
Lack of ACTH
Lack of cortisol
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13
Q

What is an ob gene deficiency?

What happens if this exists in someone?

A
  • ob gene codes for leptin that signals to the brain that you are not starving
  • It is released from white adipose tissue
  • If this gene is missing, the body thinks it is starving and has to keep eating
  • The immune system is energetically expensive, so this switches off ‘in starvation’
  • The reproductive axis switches off because it is evolutionarily stupid to reproduce when starving
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14
Q

What are the characteristics of ob gene deficiency?

A

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

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15
Q

What happens in leptin deficient children?

A
  • They think that they are starving to death, because their brains are signalling this to them
  • They will eat virtually anything
  • Starvation rewires the brain and makes people behave differently
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16
Q

How much leptin is released in obese and slim people?

A

Leptin is released from body fat, so if you are not very fat, leptin is low. In obese people, leptin is high (because of high body fat).

17
Q

Which neurones does leptin activate/inhibit?

A

Leptin activates POMC and inhibits NPY/Agrp neurones

18
Q

What is leptin resistance?

A
  • Leptin circulates in plasma in concentrations proportional to fat mass
  • Most fat humans have high leptin – but they are not responding to it very well
  • Obesity due to leptin resistance: the hormone is present but doesn’t signal effectively
19
Q

Why is leptin ineffective as a weight control drug?

A

Most fat people have leptin

20
Q

What is the effect of leptin absence?

A

hyperphagia, lowered expenditure and sterility

21
Q

How can leptin be used in people who are deficient and what are some issues that may occur?

A
  • Leptin therapeutical treatment
  • Patients sometimes develop antibodies towards leptin – keep increasing the dose
  • Leptin administration restores LH pulsatility in leptin deficient children
  • Leptin administration restores LH pulsatility in women with amenorrhea (driven by stress/low body fat
22
Q

What is the role of insulin in food intake?

A
  • Insulin circulates at levels proportional to body fat
  • When you are obese, you get insulin resistance
  • There are receptors in the hypothalamus
  • Central administration of insulin reduces food intake
23
Q

What is the body’s largest endocrine organ?

A

GI Tract - releases hormones to influence gut motility, secretion and appetite

24
Q

Which hormones are involved in short term regulation of food intake and where are they made?

A

Peptide YY and GLP-1 are released from L cells of the small intestine
(enteroendocrine cells -side facing the lumen senses whilst other side has secretory granules)

25
Q

What is the role of peptide YY?

A
  • Peptide YY is released from the intestines – 36 AA
  • Released in proportion to the calorie intake
  • To become activated, the first two amino acids of PYY are chopped off -> PYY3-36
  • PYY3-36 directly modulates neurones in the arcuate nucleus:
    1. Inhibits NPY release
    2. Stimulates POMC release
    3. Decreases appetite
  • PYY consistently suppresses feelings of hunger
  • Released after you have eaten
26
Q

What codes for GLP-1?

What is the role of glucagon like peptide (GLP-1)?

A
  • Gut hormone coded for by the pre-proglucagon gene and released post-eating
  • Reduces food intake
  • It stimulates glucose stimulated insulin release
  • Animals stop eating and fall asleep after an ICV injection
27
Q

How does the glucagon gene product modification vary in different cells?

A
  • It is chopped up in different ways depending on the tissue its present in
  • E.g. in alpha cells in the pancreas (glucagon) or in the L cells of the intestine (GLP-1)
28
Q

How are GLP-1 based drugs used in therapeutics?

A

GLP-1 based drugs are now a really big class of anti-diabetic medications

  • Peripheral GLP-1 inhibits food intake in humans
29
Q

What breaks down GLP-1?

What does this mean?

A

DPP4 - has a very short half life, around a minute, hence drugs are synthetic and have a long half life

30
Q

Give an example of A GLP-1 agonist and its use

A

saxenda - to treat diabetes and obesity

31
Q

What is ghrelin?

A
  • Peptide hormone (28aa) that has a fatty acid chain stuck on it at the serine at the 3 position
  • GOAT attaches the fatty acid group and activates ghrelin
  • Released from the stomach, acts in the brain
32
Q

What is the role of ghrelin?

A
  • Ghrelin increases before a meal, then it drops when you are full (opposite to PPY)
  • It makes you hungry
33
Q

What does ghrelin act on?

A

Directly modulates neurones in the arcuate nucleus:

  • Stimulates NPY/Agrp neurones
  • Inhibits POMC neurones
34
Q

Why is injecting gut hormones a bad idea?

A

It can cause nausea as you get a bug sudden spike

35
Q

What are the co-morbidities associated with obesity?

A

Sleep apnoea, depression, bowel cancer, osteoarthritis, gout, stroke, MI, hypertension, diabetes

36
Q

Is obesity genetic?

A
  • Obesity is genetic – your hypothalamus decides how much weight you put on in a given environment
  • 60-80% of the body mass index is predicted by your genes
  • In twin studies, identical twins are similar in body weight
  • Non-identical twins have a lot more discrepancy when comparing their weight
37
Q

What is the thrifty gene hypothesis?

A
  • Specific genes selected for to increase metabolic efficiency and fat storage
  • Where there is plentiful food and little exercise the genes predispose their carriers to obesity, diabetes
  • It is evolutionarily sensible to put on weight
  • Thin humans didn’t survive famines, so didn’t pass their genes on to modern humans

But then why isn’t everyone obese in an obesogenic environment?

38
Q

What is the adaptive drift hypothesis?

A
  • Here, there is a normal distribution of body weight
  • The fat are eaten (can’t escape predation), whilst the thin starve in the cold
  • However years ago, humans learned to defend against predators; so obesity was not selected against
  • Putting on body fat then a neutral change
  • In current context, the inheritors of these genes become obese
  • When you look at people who are genetically prone and genetically resistant to obesity, in a healthy environment, there wouldn’t be much difference between them
  • In an obesogenic environment, those genetically predisposed would put on weight

Year 2 - endocrinology (18 decks)

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