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Year 2 Endocrinology > Obesity and the endocrine control of food intake > Flashcards

Obesity and the endocrine control of food intake Flashcards

1
Q

What is the arcuate nucleus (in rodents) called in humans?

A

Infundibulum nucleus

Usually refer to arcuate nucleus because most test are done on rodents

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2
Q

How is POMC cut up in the arcuate nucleus? How is this different to in the rest of the body?

A

Normally POMC is cut up to MSH and ACTH

But in arcuate nucleus it is cut up differently to make alpha-MSH

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3
Q

What part of the brain balances energy in vs energy out aka body weight homeostasis? How does it do this?

A

Hypothalamus via neural input from the periphery and other brain regions, as well as hormones eg ghrelin, PYY and leptin

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4
Q

Where does the arcuate nucleus sit?

A

Just above the fenestrated capillaries in the median eminence

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5
Q

Why is the arcuate nucleus not completely protected by the blood brain barrier? What does this lead to

A

Due to the capillaries it sits on are fenestrated leading to access to the peripheral hormones

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6
Q

What is the major mechanism for the arcuate nucleus to monitoring and integrating peripheral nucleus state

A

Stimulating - NPY/Agrp neuron

Inhibitory - POMC neuron

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7
Q

How do NPY/Agrp neurons affect appetite?

A

Increase appetite

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8
Q

How do POMC neurons affect appetite?

A

Decrease appetite

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9
Q

What type of CNS mutations can cause morbid obesity?

A

POMC deficiency and MC4-R mutations

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10
Q

What does leptin do?

A

Activates POMC and inhibits NPY/AgRP -> decreasing food intake and increasing thermogenesis

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11
Q

What are levels of leptin like when there are different levels of body fat?

A

Low when there is low body fat and high when there is high body fat - it is coded in body fat

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12
Q

Where does leptin circulate?

A

In plasma in concentrations proportional to fat mass

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13
Q

What happens to leptin in obesity

A

Most fat humans have high leptin - obesity due to leptin resistance: hormone is present but doesn’t signal effectively

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14
Q

What happens to the body if there is no leptin?

A

Hyperphagia, lowered energy expenditure, sterility - body starves itself if you have no leptin - it is an anti-starvation hormone

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15
Q

What does the presence of leptin in the body tell the brain?

A

One has sufficient fat reserves for normal function - but high leptin has little effect

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16
Q

How does insulin regulate food intake?

A

It circulates at levels proportional to body fat via receptors on the hypothalamus.

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17
Q

What happens if you administer insulin centrally into the hypothalamus

A

Reduces food intake

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18
Q

Why does basal insulin correlate accurately with BMI

A

More body weight put on - more tendency for insulin resistance, so pancreas works harder to make insulin and shifts your insulin release during the early stages

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19
Q

Where are insulin receptors particularly found?

A

In the hypothalamus

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20
Q

What is the body’s largest endocrine organ?

A

GI tract

21
Q

What does the GI tract release?

A

It releases more than 20 different regulatory peptide hormones

22
Q

What do gut hormones influence

A

processes including gut motility, secretion of other hormones, appetite and body weight.

23
Q

What influences gut hormone release

A

gut nutrient content - what you’ve eaten, how much, what is it made up of?

24
Q

What does cholecystokinin affect

A

Gall bladder contraction, GI motility, pancreatic exocrine secretion

25
Q

What does secretin affect?

A

Pancreatic exocrine secretion

26
Q

What does GIP affect?

A

Incretin activity

27
Q

What does Ghrelin affect?

A

Hunger - stimulates NPY/Agrp neurons and inhibits POMC neurons

28
Q

What does insulin and glucagon affect

A

Glucose homeostasis

29
Q

What does GLP-1 affect

A

Incretin activity in stimulating glucose stimulated insulin release and causes satiation (reduces food intake)

30
Q

What does gastrin affect

A

Acid secretion

31
Q

What effects do enteroendocrine effects have?

A

Paracrine effects - cells nearby
Modulation of neuronal function - neuronal network in gut (enteric NS) or vagus
Endocrine effects - go around the body

32
Q

What can enteroendocrine cells detect?

A

Lipids - types, lengths of chains
Carbohydrates - transport mechanisms for carbs
Proteins - products of protein digestion

33
Q

What is ghrelin

A

A peptide hormone 28aa long with a special fatty acid group that helps it work that is attached using GOAT (ghrelin o acyltransferase)

34
Q

What does PYY affect

A

Satiation

35
Q

What happens to PYY levels after a meal

A

More calories you eat, more PYY released

36
Q

What are PYY effects on the arcuate nucleus?

A

Inhibits NPY
Stimulates POMC neurons
Decreases appetite

37
Q

What is GLP1 coded for by and how is released

A

Coded for by the preproglucagon gene and released post prandially

38
Q

How is GLP1 inactivated

A

By DP-IV (dipeptidyl peptidase 4) which cleaves a chunk off the end of GLP1 and causes inactivation

39
Q

What are incretins

A

They stimulate glucose release, detect glucose in the gut, are released from the gut and activate the pancreas and in presence of glucose they greatly exacerbate glucose release

40
Q

What is saxenda?

A

Long acting GLP1 receptor agonist (liraglutide) from novo nordisk that can make people less hungry so used for weight loss

41
Q

What are the three types of satiety action that gut hormones do?

A

Post prandial - reduces food intake following a meal
Chronic - gut disease - chronic elevation suppresses appetite
Acute nausea - toxin ingestion at acutely very high levels

42
Q

What is the problem of using gut hormones as drug targets for obesity?

A

All these hormones have very short half lives - big dose needed of the drug and that can cause nausea.

43
Q

How can dietary manipulation be used to treat obesity

A

Synthetic nutrients to stimulate nutrient receptors and deliver nutrients to specific regions of the gut

44
Q

What are comorbidities linked to obesity?

A

Depression, stroke, sleep apnoea, MI, hypertension, bowel cancer, diabetes, osteoarthritis, peripheral vascular disease, gout

45
Q

How heritable is the variability in your body weight

A

60-80%

46
Q

What is the thrifty gene hypothesis?

A

Specific genes selected for to increase metabolic efficiency and fat storage. In the context of plentiful food and little exercise, these genes predispose their carriers to obesity and diabetes. Evolutionarily sensible to put on weight. Thin humans didn’t survive famines so didn’t pass their genes on to modern humans

47
Q

What is the problem with the thrifty gene hypothesis

A

Doesn’t explain why everyone isn’t overweight

48
Q

What is the drifty gene hypothesis

A

Body weight is a normal distribution: the fat get eaten and the skinny starve. 10-20k years ago humans learned to protect against predators, thus obesity not selected against so putting on body fat became a neutral change so the inheritors of those genes become obese

Year 2 Endocrinology (21 decks)

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