The Endocrine Control of Food Intake Flashcards

1
Q

Describe the hypothalamus structure

A

Paraventricular nucleus -> 3rd ventricle
lateral hypothalamus beside the paraventricular nucleus
Ventromedial hypothalamus beside the 3V
Arcuate nucleus alongside the bottom of 3V

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2
Q

Describe the arcuate nucleus

A

Key in regulation of food intake
Incomplete blood brain barrier - allows access to peripheral hormones
Integrates peripheral and central feeding signals

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3
Q

What are the neuronal populations of the acute nucleus

A

Stimulatory - NPY/Agrp neuron Inhibitory - POMC neuron

Both extend to other hypothalamic and extra-hypothalamic regions

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4
Q

Which CNS mutation affect appetite

A

POMC deficiency and MC4-R mutations -> morbid obesity

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5
Q

What brain regions are involved in appetite regulation

A
Prefrontal cortex
Cortex
Amygdala
Nucleus Accumbens
Brainstem
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6
Q

When are leptin levels high and low

A

Low in low body fat

High in high body fat

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7
Q

What is the action of leptin

A

Activates POMC and inhibits NPY/AgRP neurons.

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8
Q

What is the effect of central or peripheral administration of leptin

A

Decrease in food intake and increase in thermogenesis

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9
Q

How is leptin associated with obesity

A

Leptin resistance
Most fat humans have high leptin
Leptin is ineffective as a weight control drug

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10
Q

What are the effects of an absence of leptin

A

Hyperphagia
Lowered energy expenditure
Sterility

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11
Q

What are the associations between insulin and food intake

A

Insulin circulates at levels proportional to body fat
Receptors in the hypothalamus
Central administration reduces food intake
May co-ordinate glucose and energy homeostasis

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12
Q

How many hormones does the gut release and what are the processes influenced by

A

> 20 regulatory peptide hormones

Gut motility, secretion of other hormones, appetite

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13
Q

What is the release of gut hormones regulated by

A

Gut nutrient content

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14
Q

Which hormones are released by the stomach and what do they stimulate

A

Ghrelin - hunger, growth hormone release

Gastrin - acid secretion

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15
Q

Which hormones are released by the duodenum and what do they stimulate

A

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

Secretin - pancreatic exocrine secretion

GIP - Incretin activity

Motion - GI motility

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16
Q

Which hormones are released by the pancreas and what do they stimulate

A

Insulin + glucagon - glucose homeostasis

Pancreatic polypeptide - Gastric motility, satiation

Amylin - glucose homeostasis, gastric motility

17
Q

Which hormones are released by the colon and what do they stimulate

A

GLP-1 - incretin activity, satiation

GLP-2 - GI motility and growth

Oxyntomodulin - satiation, acid secretion

PYY 3-36 - satiation

18
Q

Describe the structure of ghrelin and its daily levels

A

28 amino acids

Fluctuates throughout the day and is highest at breakfast, lunch and dinner

19
Q

Explain how ghrelin achieves its affect on food intake

A

simulates NPY/Agrp neurons (arcuate nucleus)
Inhibits POMC neurons
Increases appetite
Increased food intake

20
Q

Which cells secrete PYY and GLP-1

A

L cells in the colon

21
Q

Explain how PYY 3-36 achieves its affect on food intake

A

Inhibits NPY release
Stimulates POMC neurons
Decreases appetite
Decreased food intake

22
Q

Describe GLP-1

A

Glucagon-like-peptide-1
Characterised incretin role to stimulate glucose-stimulated insulin release
Reduced food intake

23
Q

Describe the processing of pro-glucagon in intestinal L-cells

A

Gut hormone coded for by the preproglucagon gene and released post-prandially
Prohormone convertase 1 converts GLP-1 to the active agonist
After half life (1min) it becomes inactive (DP-IV)

24
Q

What is saxenda

A

Long-acting glucagon-like-peptide-1 receptor agonist (liraglutide)
Double the dose used for T2DM

25
Q

What are the 3 types of satiety action

A

Post-prandial - reduces food intake after a meal

Chronic - gut disease - chronic elevation to suppress appetite

Acute nausea - toxic ingestion - acutely very high levels

26
Q

What are the comorbidities associated with obesity

A
Depression 
Stroke
MI
Sleep apnoea
Hypertension 
Diabetes 
Bowel cancer 
Osteoarthritis 
Peripheral vascular disease
Gout
27
Q

Describe the thrifty gene hypothesis

A

Specific genes are selected to increase metabolic efficiency and fat storage
Plentiful food and little exercise -> the genes predispose the carrier to obesity and diabetes

28
Q

Describe the adaptive drift hypothesis

A

Following a normal distribution of body weight - fat are eaten, thin starve
Humans then learned to defend against predators so the obese were not selected against
Putting on fat led to a genetic drift
Those who inherit this gene put on weight

29
Q

What can leptin administration restore

A

LH pulsatility in leptin deficient children

LH pulsatility in women with amenorrhoea

30
Q

What is the association with PYY and calories

A

More calories -> more PYY