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Year 2 LCRS Endocrinology > Endocrinology of food intake > Flashcards

Endocrinology of food intake Flashcards

1
Q

Which signals arrive in the hypothatlamus to ctrontroll food intake

A
  1. Gut Hormones
    • Ghrelin
    • PYY
    • etc.
  2. Neural input
    • periphery (e.g. stomach strech via vagus)
    • other brain regions
  3. Leptin
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2
Q

Which part of the brain processes appetite and food intake?

A

Signals are processed in the Arcuate nucleus in the hypothalamus

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3
Q

What are the neural populations within the arcuate nucleus that process food intake?

A

There are two neural populations

  1. Stimmulatory
    • NPY/Agrp neuron
  2. Inhibitory Neuron
    • POMC neurons
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4
Q

What is the stimmulatory neural population of food intake in the arcuate nucelus?

A

NPY/Agrp neuron

–> stimmulate food intake

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5
Q

What are the inhibitory neural populaitons of the arcuate nucleus in food intake?

A

POMC neurons

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6
Q

What does a deficiency in POMC or MC4-R cause?

A

They cause morbid obesity –> no inhibition of appetite

  • Might be associated with ginger hair/low pigmentation (due to error in Melanocortin systemn)
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7
Q

What is the role of leptin in food control?

A

It

  • decreases food intake
    • ctivates POMC
    • inhibits NPY/AgPR
  • increaseis thermogenesis (burining calories)
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8
Q

When is leptin produced?

A

Leptin is produced by body fat –> high fat content, less appetite, more burning

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9
Q

What are the signs and symptoms in leptin deficiency?

A
  • Increased appetite
  • obesity –> often diabetis
  • reduced body temperature
  • reduced energy expenditure
  • reduced immune function
  • infertility

–> Body thinks it starves to death (not feasable to reproduce)

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10
Q

What is the clinical use of leptin replacement?

A

Obesity

  • No cure for common obesity (individuals get leptin resistant)
  • But in deficiency –> very effective

Hypothalamic amenorrhoea in e.g. athletes with low body fat

  • restores LH pulsatility
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11
Q

What is the main role and function of leptin?

A

It is an anti-starvation hormone, rather than a obesity hormone

–> shows body that there is enough fat for nomal functions (reproduction, immune response)

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12
Q

Explain the relationship between leptin and obesity

A

Leptin deficiency causes reversible obesiy but in Majority of people:

  • Fat people have high leptin levels
  • Develop a leptin resistance over time
  • (if leptin injected in normal-weight people –> effect of weight loss and decreased appetite)
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13
Q

Explain the role of insulin in the control of food intake

A

Insulin reduces food intake

  • normally circulates in levels proportinal to body fat
  • Also has receptors in hypothalamus to decrease appetite
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14
Q

What are the overall ways gut hormones can controll food intake and digestion?

A

The can e.g. controll

  1. Secretions (of secretes and other hormones)
  2. appetite
  3. gut mortility
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15
Q

How/when are gut hormones secreted?

A

Orten: enteroendocrine cells sense parts of food break down via different receptors and release hormones as response

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16
Q

When is Ghrelin released?

A

Ghrelin stimmulates hunger–> secreted during fasting/absence of food

17
Q

What is the neural MOA of Ghrelin?

What is its effect?

A

Ghrelin stimmulates hunger by

  • stimmulation of NPY/Agrp neurons
  • inhibition of POMC neurons

–> increases food intake imn humans

18
Q

Which cells secrete PYY and GLP1?

A

L-cells –> flask shaped enteroendocrine cells

19
Q

When is PYY 3-36 released?

A

Peptide YY 3-36 is released in response to food intake –> proportional to calorie intake

20
Q

What is the effect of PYY and its MOA?

A

It decreases appetite via

  1. Inhibition of NPY/Agpr neurons
  2. Stimmulation of POMC neurons
21
Q

When is GLP (Glucagon like Peptide-1) released?

A

It is released in response to food

increases glucose-stimmulated insulin release

–> decreases food intake

22
Q

What is the effect of GLP-1?

A
  1. It stimmulates glucose-stimmulated insulin release
  2. Decreases appetite–> decreases food intake
23
Q

What are the different types of satiety action of gut hormones?

A
  1. Post-prandial
    • after a meal–> reduced food intake
  2. Chronic
    • in chronic disease –> reduce stress on gut
  3. Acute nausea
    • after toxin ingestion (acute and very high hormone levels)
24
Q

What is the current problem with using gut hormones as therapeutical target for obesity?

A

They have a very short half-life:

  • only short therapeutic effect
  • Other than that: cause nausea or have no effect
25
Q

What are the reasons for the current obesity crisis?

A

It has a genetic component that determine weight in given environment but:

  1. High processed, high calorie foods
  2. Like gene-drift hypothesis: genes are selelcted for putting on body fat (used to be beneficial), now leading to obesity
26
Q

Explain the POMC signaling

A

POMC is cleaved u.g. into alpha-MSH

binds to MC4-receptor

Year 2 LCRS Endocrinology (15 decks)

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