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*GIGU I > Lecture 22: Regulation of Food Intake > Flashcards

Lecture 22: Regulation of Food Intake Flashcards

1
Q

Where are the neuronal centers that control feeding and satiety located and what are they?

A
  • Hypothalamus
  • Lateral nucleus (LH)
  • Ventromedial nucleus (VM)
  • Paraventricular nucleus (PV)
  • Dorsomedial nucleus (DM)
  • Arcuate nucleus (Arc)
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2
Q

What type of signals does the hypothalamus receive?

A
  • Neural signals from GI tract
  • Chemical signals from nutrients in blood
  • Signals from GI hormones
  • Signals from adipose tissue
  • Signals from cerebral cortex (sight, smell and taste)
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3
Q

Where does most of the signaling regulating food intake and energy expenditure occur?

A

Arcuate nucleus via 2 pathways: anorexigenic and orexigenic

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4
Q

What is the anorexigenic pathway?

A
  • α-melanocortin (α-MSH) released by pro-opiomelanocortin (POMC) neurons of arcuate nucleus
  • α-MSH binds to MCR-4 present in second-order neurons of paraventricular nuclei
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5
Q

What is the orexigenic pathway?

A
  • Hunger signals stimulate release of Neuropeptide Y from arcuate nucleus
  • NPY binds to Y1R of paraventricular nuclei
  • Agouti-related peptide (AGRP) is also released; antagonist of MCR-4
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6
Q

How do the arcuate nucleus pathways antagonize eachother?

A
  • Peptides that stimulate the α-MSH pathway inhbit the NPY system
  • AGRP is an antagonist of MCR-4
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7
Q

What hormones activate the POMC and what do they do to the AGRP/NPY?

A
  • Insulin, leptin, and CCK all activate the POMC neurons (anorexigenix path)
  • They inhibit the AGRP/NPY (orexigenic path)
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8
Q

What hormone activates the AGRP/NPY neurons?

A

Ghrelin

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9
Q

Mutations in the POMC and MCR-4 genes have been related to what pathology in some cases?

A

Obesity

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10
Q

What is the vagal –> NTS –> hypothalamus circuit?

A
  • Vagal afferents relay info from stomach to NTS via the sensory ganglian of the vagal nerve (Nodose ganglion)
  • Hypothalamus will then use info to produce the appropriate feeding behavior and metabolic responses using vagal efferents
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11
Q

Even in the absence of higher centers’ input what is able to regulate food intake in response to periphera signals?

A

The hindbrain

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12
Q

Where does Ghrelin come from and what does it do?

A
  • Secreted in the stomach by endocrine cells
  • Binds to growth hormone secretagogue receptors (GHSR)
  • Stimulates neurons that release NPY
  • Increases appetite, gastric motility, gastric acid secretion, and adipogenesis
  • Decreases insulin secretion
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13
Q

Where is insulin released from and what does it do?

A
  • Binds to receptors in POMC and NPY systems
  • Inhibits NPY pathway and stimulated POMC pathway
  • Decreases appetite
  • Increases metabolism
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14
Q

In patients w/ DM type I there is an increase in food intake associated w/ a _______ insulin

A

Decreased insulin

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15
Q

Where is CCK released from and what does it do?

A
  • Released by I cells in the duodenum
  • Elicits satiety
  • Acts on vagal –> NTS -> hypothalamus circuit to decrease ghrelin
  • Decreases gastric emptying, which increases gastric distention
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16
Q

Where is PYY released from and what does it do?

A
  • Released by L cell of the ileum and colon following a meal
  • Binds to Y2R in the hypothalamus
  • Inhibits NPY neurons
  • Releases inhibition of POMC neurons
17
Q

Where is Leptin secreted from and what does it do?

A
  • Cells in adipose tissue
  • Inhibits NPY pathway
  • Stimulates POMC pathway
  • Appetite-suppressing hormone: decreases appetite and ghrelin release and increases metabolism
18
Q

Obese children w/ a congenital leptin deficiency can be treated how; what is the outcome?

A
  • Subcutaneous administration of recombinant leptin
  • Reduces fat mass, hyperinsulinaemia, and hyperlipidaemia
19
Q

Obesity in humans is often associated w/ what leptin issue?

A

High levels of leptin and failure to respond to exogenous leptin (leptin resistance)

20
Q

What does Glucagon-like peptide-1 (GLP-1) do, where is it secreted from and when is it secreted?

A
  • Proglucagon derived peptide
  • Co-secreted w/ PYY from L clls in the intestine
  • Incretin (decrases blood glucose levels)
  • Levels rise after a meal and full during fast
  • Reduces food intake, suppresses glucagon secretion, and delays gastric emptying
21
Q

What is Oxyntomoduin, where is it secreted from, and what is its effect?

A
  • Pro-glucagon derived peptide
  • Released from L cells of the intestine in response to ingested food and in proportion to caloric intake
  • Anorectic effect
22
Q

What does Pancreatic peptide (PP) do, where is it secreted from?

A
  • Secreted from cells in the pancreatic islets of Langerhans
  • Decreases food intake directly through Y4R in the brainstem and hypothalamus
  • May also act via the vagus nerve to produce anorectic effects
23
Q

Where is glucagon secreted from and what does it do?

A
  • Secreted by α cells of the pancreatic islets
  • Increases blood glucose levels and insulin secretion
  • Reduces food intake
24
Q

Where is Amylin released from and what are its effects?

A
  • Stored and released with insulin in response to food intake
  • Anorectic effects (inhibition of NPY release)
25
Q

What are the particularly promising gut hormone targets that are candidates for successful obesity therapies?

A

GLP-1, oxyntomodulin, leptin, and peptide YY

26
Q

What are the 3 most commonly performed procedures for bariatric surgery?

A

1) Roux-en-Y gastric bypass (RYGB)
2) Adjustable gastric banding (AGB)
3) Biliopancreatic diversion (with or w/o duodenal switch)

27
Q

How does RYGB alter endogenous gut hormones responses to a meal; which patients had the most weight loss?

A
  • Elevated responses are seen in GLP-1 and PYY as early as 2 days after RYGB and may remain elevated for >10 years after RYGB
  • Patients w/ the most weight loss after RYGB also had the highest levels of these gut hormones
28
Q

Which bacteria has been shown to be increased following RYGB; and what are the effects?

A
  • Proteobacteria
  • Improvement of weight, inflammation and metabolic status after surgery was associated w/ increased bacterial variety
29
Q

How does RYGB affect taste?

A
  • Appears to alter taste through unconditional and conditional mechanisms
  • May be exerting its effects on food selection and preference through any one of the taste function domains such as: sensory discriminative (stimulus identification), hedonic (ingestive motivation), and physiological (digestive preparation)
30
Q

What are the effects of RYGB on the liver, gastric pouch, portal vein, and pancreas?

A

Liver: decreased glucose output

Gastric pouch: increased gastric emptying

Portal vein: altered nutrient and hormonal sensing

Pancreas: increased insulin release

31
Q

What is the effet of RYGB on the Ileum?

A
  • Increased GLP-1
  • Increased PYY
  • Increased OXY
  • Increased Bile acids
32
Q

In anorexia nervosa what are the levels of leptin and adiponectin like?

A

Both are decreased, likely in association with reductions in fat mass!

33
Q

In anorexia nervosa what are the levels of ghrenlin and peptide YY like; why are each of these hormones significant in this disease?

A

Both are increased

  • Ghrelin (orexigenic) resistance appears to be conductive factor to a restrictive diet
  • Elevated PYY (anorexigenic) might contribute to decreased nutrient intake and disordered eating psychopathology
34
Q

Why is elevated CRH in the hypothalamus significant in anorexia nervosa?

A
  • Leads to increased cortisol (stress hormone)
  • Decreased TSH, which leads to decreased T3 (thyroid hormone)
  • Decreases FSH and LH, which decreases testosterone (males/females) and decreased estradiol (females)

*GIGU I (67 decks)

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