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GIGU > Regulation of Food Intake > Flashcards

Regulation of Food Intake Flashcards

1
Q

What are the five areas in the hypothalamus that can control feeding and satiety?

A
  • Lateral nucleus
  • Ventromedial nucleus
  • Paraventricular nucleus
  • Dorsomedial nucleus
  • Arcuate nucleus:
    • has NPY/AgRP and POMC paths
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2
Q

What pathway in the arcuate nucleus decreases food intake?

A
  • a-melanocortin (a-MSH) pathway that secretes POMC and decreases food intake
  • Insulin, Leptin, and CCK stimulates this anorexigenic path that causes release of POMC to the neurons of the PVN
  • In the PVN, POMC will bind to MCR-4 receptors which results in sympathetic activity and energy expenditure
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3
Q

What pathway in the arcuate nucleus increases food intake?

A
  • NPY pathway stimulated by hunger signals such as Ghrelin
  • NPY will bind to Y1R releasing AgRP, an antagonist of the MCR-4 receptor found in the PVN
  • This results in suppression of the anorexigenic pathway and stimulation of food intake
  • Insulin leptin and CCK inhibit this pathway
  • Called orexigenic pathway
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4
Q

What two genes have mutations related to obesity?

A
  • POMC and MCR-4 genes
    • receptor that inhibits food intake
    • POMC also is part of anorexigenic path
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5
Q

What is Prader-Willi-Syndrome?

A
  • partial deletion of chromosome 15 or loss of paternally expressed genes
  • Results in neonatal hypotonia, slow feeding, small hands and feet, mental retardation, hypogonadism, hyperphagia, severe obesity and elevated ghrelin
    • ​obese patients usually have decreased ghrelin
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6
Q

What happens if vagal activity is blocked in regards to the stomach and meal sizes?

A

The amount of food in the stomach doesn’t influence meal size like it normally would

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7
Q

How does the vagal NTS circuit work?

A
  • The vagus nerve sends signals to the Nucleus Tractus Solitarius and gets integrated with information from the hypothalamus to decide the appropriate feeding behaviour and metabolic responses
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8
Q

If there is an absence of higher centers input to regualte food intake, what will occur?

A

The hindbrain takes over regulation of food intake

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9
Q

What does the Lateral hypothalamic area do/have?

A
  • It is the hunger center and it has neurons that project throughout the brain to release orexigenic peptide melanin concentrating hormone (MCH) or orexins A and B
  • Hunger response is generated
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10
Q

What is the ventromedial hypothalamic nucleus?

A

Satiety center

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11
Q

What does the PVN do?

A

Recieves info from Arcuate nucleus and sends axons to cerebral cortex and brainstem

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12
Q

What does Ghrelin result in?

A
  • Increases appetite
  • Increases gastric motility
  • Increases gastric acid secretion
  • Increases adipogenesis
  • Decreases ilsulin secretion
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13
Q

How does Ghrelin work and where does it come from?

A
  • Secreted in stomach by endocrine cells
  • It binds to GH secretagogue receptors and stimulates neurons that release NPY
  • Initiates feeding response
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14
Q

What is insulins role in hunger?

A
  • It will bind to receptors in the POMC and NPY pathways
    • inhibits NPY
    • Stimulates POMC
  • Results in decreased appetite and increased metabolism
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15
Q

How does increased eating relate to insulin and T1 DM patients?

A

there is an increase in food intake associated with decreased insulin secretion as insulin will normallly decrease appetite and increase metabolism

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16
Q

What is CCK’s role in feeding?

A
  • Released from I cells in duodenum
  • Elicits Satiety
    • acts on vagus nerve which sends signals to the NTS and goes to the hypothalamus circuit to decrease ghrelin and decrease gastric emptying and increase gastric distention
17
Q

What releases PYY & what does it do?

A
  • Released by L cells w/n iileum and colon following a meal
  • Binds to Y2R receptors in the hypothalamus and inhibits NPY neurons and releases the inhibition of POMC neurons
  • Net response is to promote anorexogenic pathway
18
Q

Where is leptin released from and what does it do, and what increases its secretion?

A
  • Secreted from adipose and binds receptors in POMC and NPY pathways
    • Inhibits NPY
    • Stimulates POMC
  • Appetite suppression hormone!
    • increases metabolism and decreases ghrelin release
  • As fat stores increase or intake of meal occurs more leptin is released
19
Q

Obesity is associated with ___ levels of ___. and failure to respond to exogenous versions of this.

A

High Leptin

20
Q

What signals are involved in long term regulation of energy balance?

A

Adiposity signals

21
Q

What modulates food intake on a meal by meal basis?

A

Gut peptides

22
Q

Where is GLP-1 released from & what deoes it do? Describe the levels when eating and fasting.

A
  • Reduces food intake suppresses glucagon secretion and delays gastric emptying
  • Co secreted with PYY from L cells int he intestine
  • Levels rise after meal and fall during fasting
23
Q

What does Oxyntomodulin do and where is it released from?

A
  • Anorectic effect
  • Released from L cells of intestine in response to ingested food and in proportion to caloric intake
24
Q

What does PP do and where is it from?

A
  • Secreted from pancreatic islets of langerhans
  • Decreases food intake by binding Y4R in hypothalamus
  • Can also act on vagus nerve to produce anorectic effect
25
Q

Glucagon function? Where is it released from?

A
  • Reduces food intake
  • Inicreases blood glucose levels and insulin secretion
  • Alpha cells of pancreatic islets
26
Q

What does Amylin do and where is it released from?

A
  • Anorectic effects, inhibits NPY release
  • Stored and released with insulin in response to food intake
27
Q

What is Anorexia Nervosa? What hormones & systems are impacted?

A
  • Self starvation and excessive weight loss
  • Patients are severely malnourished and significantly emaciated leading to endocrinological and cardiological dysfunctions as well as abnormalities in the digestive, skeletal and reproductive systems
    • increased cortisol
    • decrease testosterone and estradiol
    • decreased T3
    • decrease adiponectin and leptin
    • increased ghrelin and PYY
28
Q

With anorexia nervosa, what happens to the secretion of leptin?

A

Basal and pulsatile secretion is reduced correlating with a reduction in fat mass

29
Q

What happens with Ghrelin in AN?

A
  • Ghrelin resistance occurs due to a restrictive diet
30
Q

In AN, what can elevated levels of PYY contribute to?

A

Could contribute to nutrient intake and disordered eating psychopathology

GIGU (17 decks)

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