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GI Exam 2 > Regulation of Food Intake > Flashcards

Regulation of Food Intake Flashcards

1
Q
  • Neuronal Centers that control satiety and feeding in the hypothalamus
A
  • Lateral Nucleus (LH)
  • Ventromedial Nucleus (VM)
  • Paraventricular Nucleus (PV)
  • Dorsomedial nucleus (DM)
  • Arcuate nucleus (Arc)
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2
Q
  • _% of the vagus carries afferent fibers to the hypothalamus
A
  • 80%
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3
Q
  • What hormone is important for long term control of satiety?
  • What cells secrete it?
A
  • Leptin
  • Adipose cells
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4
Q
  • Where does the hypothalamus receive signals from to maintain energy balance?
A
  • Neural signals from GI tract
  • Chemical signals from nutrients in the blood
  • Signals from GI hormones
  • Signals from adipose tissue
  • Signals from cerebral cortex (sight, smell, taste)
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5
Q
  • What hormones are part of the anorexigenic pathway?
A
  • Leptin
  • CCK
  • Insulin

(Lept CCK in)

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6
Q
  • Describe the anorexigenic pathway
    • ​What does it stimulate
    • What does it inhibit
A
  • Insulin/CCK/Leptin bind to LepR on POMC/CART cell in the arcuate nucleus
  • Alpha MSH is released and binds MCR 4 on neuron of PVN
  • Inhibits food intake
  • *Alpha MSH also inhibits MCR 3 R on AGRP/NPY cells of the orexigenic pathway
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7
Q
  • What are thre orexigenic hormones?
A
  • Ghrelin
  • (H in ghrelin-hunger)
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8
Q
  • How does the orexigenic pathway work?
A
  • Ghrelin released from the stomach binds to AGRP/NPY cell and releases NPY and AGRP
  • NPY binds Y1R in neurons of PVN
  • AGRP released bings and antagonizes MCR-4 receptor on same neuron to inhibit anorexigenic pathway
  • Overall increase in food intake
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9
Q
  • Most of the integration signaling regulating food intake and energy expenditure happens in the _
A
  • Arcuate nucleus (which then sends its signals to the PVN)
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10
Q
  • Mutations in _ and _ genes have been related to some cases of obesity
  • What pathway are these molecules involved in?
A
  • POMC
  • MCR-4
  • Anorexigenic
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11
Q

_ that stimulate satiety decrease feeding activate receptors on vagal afferents

Vagus sends signals to _ which then sends signals to the hypothalamus

What happens if vagal activity is blocked?

A
  • Peptides
  • NTS
  • Amount of material in stomach no longer influences meal size
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12
Q
  • _ is able to regulate food intake in response to peripheral signals even in the absence of higher center input
A
  • Hindbrain
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13
Q
  • Ghrelin
    • ​Where is it secreted?
    • What does it bind to?
    • What does it stimulate?
    • Actions?
A
  • Endocrine cells in the stomach
  • Binds to GHSR (growth hormone secretagouge receptors)
  • Stimulates neurons that release NPY
  • Actions:
    • Increase appetite
    • Increase gastric motility
    • Increase adipogenesis
    • Increase acid secretion
    • Increase and decrease insulin secretion
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14
Q
  • Insulin
    • ​Where does it bind? (does it excite or inhibit these pathways?)
    • Actions
A
  • Binds to NPY system-inhibits
  • Binds to POMC pathway-stimulates
  • Actions:
    • Decrease appetite
    • Increase metabolism
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15
Q
  • In patients with Type I DM, there is an increase in food intake associated with _ insulin
A

Decreased

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16
Q
  • CCK
    • ​What cells release it?
    • Where does it act and what are its effects?
A
  • Released by I cells in the duodenum
  • Elicits satiety by:
    • ​Acting on vagal-NTS-hypothalamic circuit to inhibit ghrelin
    • Inhibits gastric emptying
    • Increases gastric distension
17
Q
  • PYY
    • Where is it released?
    • Where does it bind? (on what receptor)
    • What are its effects?
A
  • Released by L cells of ileum and Colon AFTER LARGE MEAL
  • Binds to Y2R in hypothalamus
  • Actions:
    • Inhibits NPY neurons
    • Releases inhibition of POMC neurons
  • Anorexigenic
18
Q
  • Leptin
    • ​Where is it secreted?
    • What receptors does it bind (does it have stimulatory or inhibitory effects)?
    • Actions
A
  • Secreted by adipose tissue
  • Binds to NPY (inhibits)
  • Binds to POMC (stimulates)
  • Actions: Appetite-Suppressing hormone
    • ​Decreases appetite
    • Increases metabolism
    • Decreases ghrelin release
19
Q
  • Does administration of leptin aid in treatment for obese patients?
A
  • In obese children with congenital leptin deficiency-yes
  • Obesity in most of population-not responsive to exogenous leptin tx
20
Q
  • Summary integration of signals regulating food intake and energy expenditure
A
21
Q
  • GLP -1 (Glucagon like peptide-1)
    • ​What is it derived from?
    • Co-secreted with what molecule in L cells of small intestine
    • Acts as a _
    • _ after a meal and _ during fasting
    • Actions
A
  • Derived from glucagon-like peptide
  • PYY
  • Incretin-works to decrease BGL
  • Increases after meal
  • Decreases during fasting
  • ACTIONS:
    • ​Decreases food intake
    • Suppresses Glucagon Secretion
    • Delays Gastric emptying
22
Q
  • Oxyntomodulin
    • ​Derived from what?
    • Released from _ in intestine in response to ingested food
    • Has _ effect
A
  • Proglucagon
  • L Cells
  • Anorectic
23
Q
  • Pancreatic Peptide
  • Secreted from?
  • Actions and MOA
  • _ effect
  • Can also act on vagus n.
A
  • Islets of Langerhans (endocrine pancreas)
  • Decreases food intake thru Y4R in hypothalamus
  • Anorectic
24
Q
  • Glucagon
    • ​Where is it secreted?
    • Functions?
A
  • Secreted by pancreatic islets
  • Reduces food intake
  • Increases BGL and insulin secretion
25
Q
  • Amylin
    • ​Stored and released with _ in response to food intake
    • _ effects
A
  • Insulin
  • Anorectic ( inhibits NPY release)
26
Q

KEY FEATURES OF ANOREXIA NERVOSA:

  • _ in genes involved in eating attitudes, regulation of eating behavior, motivation and reward mechanisms (EX: AgRP)
  • Basal and pulsatile secretion of _ is REDUCED in association w/ reductions in fat masses
  • _ resistance helps with restrictive diet
  • Elevated levels of _ (contribute to decreased nutrient intake and disordered eating psychopathology)
A
  • Polymorphism
  • LEPTIN (decreased)
  • GHRELIN RESISTANCE
  • PYY (elevated)

GI Exam 2 (14 decks)

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