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GI Final > Regulation of Food Intake > Flashcards

Regulation of Food Intake Flashcards

1
Q

What is hunger?

A

internal state of an animal seeking food

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2
Q

What is satiety?

A

feeling of fulfillment or satisfaction

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3
Q

What brain region has complete control of appetite?

A

-No single brain region has complete control

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4
Q

What does the hypothalamus regulate?

A
  • metabolic rate
  • food intake
  • body weight
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5
Q

What is the dual-center hypothesis?

A
  • 2 appetite centers in hypothalamus (outdated due to oversimplification)
  • one signals hunger (anorexic)
  • one signals satiety (orexigenic)
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6
Q

What does the hypothalamus process?

A

-signals that modulate food intake and energy expenditure

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7
Q

What are the regions of the hypothalamus?

A
  • arcuate nucleus (ARC)
  • paraventricular nucleus (PVN)
  • dorsomedial nucleus (DMN)
  • ventromedial nucleus (VMN)
  • lateral hypothalamic area (LHA)
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8
Q

What signals does the hypothalamus receive and from where?

A
  • neural signals from GI tract (stomach filling/distention)
  • chemical signals from nutrients in blood (glucose, amino acids, fats)
  • signals from GI hormones (ghrelin, CCK, peptide YY)
  • signals from adipose tissue itself (leptin)
  • signals from cerebral cortex (sight, smell, taste)
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9
Q

____ is best-characterized region related to feeding behaviors

A

arcuate nucleus of hypothalamus

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10
Q

What are anorexic signals for the arcuate nucleus of hypothalamus?

A

-pro-opiomelanocortin (POMC) neurons
-cocaine and amphetamine related transcript (CART)
(+)

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11
Q

What are orexigenic signals for the arcuate nucleus of the hypothalamus?

A

-neuropeptide Y (NPY)
-agoutirelated peptide (AgRP) neurons
(-)

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12
Q

What do peripheral signals in the arcuate nucleus do?

A

cause release of specific neuropeptides from subpopulations of these neurons

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13
Q

What does the anorexigenic pathway do?

A
  • reduces food intake and increases EE
  • POMC/CART neurons release alpha-melanocyte stimulating hormone (alpha-MSH)
  • alpha-MSH binds to MCR-3 on NPY/AgRP neurons to inhibit their activity
  • Leptin is a well-characterized stimulator of POMC/CART anorexigenic pathways while inhibiting AgRP/NPY orexigenic pathways leading to reduced food intake
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14
Q

What does the orexigenic pathway do?

A
  • increases food intake and decreases EE
  • NPY/AgRP neurons release NPY
  • NPY binds to Y1Rs on second order neurons to stimulate food intake
  • AgRP is an MCR-4 antagonist, blocking the action of alpha-MSH
  • Ghrelin is released from the stomach and activates NPY/AgRP neurons to stimulate food intake (stimulate weight gain)
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15
Q

Long-term metabolic regulation of energy balance or meal by meal basis: adiposity signals

A

long-term metabolic regulation of energy balance

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16
Q

Long-term metabolic regulation of energy balance or meal by meal basis: gut peptides

A

modulate food intake on meal by meal basis

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17
Q

What are the types of obesity genes?

A
  • disruptions in leptin-melanocortin pathway
  • SNPs in fat mass and obesity-associated gene
  • developmental delay syndromes
  • chromosomal rearrangements
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18
Q

What are examples of disruptions in leptin-melanocortin pathway?

A
  • leptin- homozygous frameshift, nonsense, and missense mutations involving LEP and LEPR
  • POMC deficiency
  • MCR-4 - heterozygous mutations
  • Prohormone convertase-1-deficiency, Albright’s Hereditary Osteodystrophy, SRC homology 2B (SH2B1) 1 deficiency
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19
Q

What is the SNPs in fat mass and obesity associated gene?

A

FTO

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20
Q

What is a developmental delay syndrome associated with obesity?

A

Prader-Willi

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21
Q

What is the vagal mediated reflex in satiety and feeding?

A

control energy homeostasis in short-term (homeostatic) and long-term (hedonic)

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22
Q

What is the NTS crucial for?

A

interpretation and relaying of peripheral signals

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23
Q

What is Ghrelin?

  • secreted by
  • binds to
  • stimulates
  • actions
  • initiates
  • peak
A
  • secreted by oxyntic cells of stomach
  • binds to growth hormone secretagogue receptors (GHSR)
  • stimulates neurons that release NPY
  • actions: increase appetite, gastric motility, gastric acid secretion, adipogenesis; decreases insulin secretion
  • appears to initiate feeding response
  • levels peak right before meals
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24
Q

What is insulin?

  • binds
  • actions
  • disease
A
  • binds to insulin receptors in NPY/AgRP (inhibitory) and POMC/CART (activates) systems
  • actions: decreases appetite; increases metabolism
  • influence of type 1 diabetes - increased appetite due to loss of insulin
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25
Q

What is peptide YY (PYY)?

  • released by
  • binds to
  • releases
A
  • released by L cells of the ileum and colon following a meal
  • binds to Y2R on NPY/AgRP neurons to inhibit
  • releases inhibition of POMC neurons
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26
Q

What is leptin?

  • secreted by
  • binds to
  • actions
A
  • secreted by adipocytes
  • binds to POMC/CART (stimulates) and NPY/AgRP (inhibits) neurons
  • actions: decreases appetite and ghrelin release; increases metabolism
27
Q

What can congenital leptin deficiency cause?

A

obese children

-can by treated by sc administration of recombinant leptin

28
Q

What is adult obesity often associated with?

A

elevated leptin and failure to respond to exogenous leptin (leptin resistance)

29
Q

What is CCK?

  • released by
  • elicits
  • acts via
A
  • released by I cells in duodenum
  • elicits satiety
  • acts via vagal –> NTS –> hypothalamic circuit
30
Q

What is glucagon-like peptide-1 (GLP-1)?

  • derived from
  • secretion
  • when do levels change
  • action
A
  • proglucagon derived peptide
  • co-secreted with PYY from L cells of intestine
  • incretin molecule
  • levels rise during meal and decrease during fasting
  • action: reduces food intake, suppresses glucagon secretion, delays gastric emptying
31
Q

What is oxyntomodulin (OXM)?

  • derived from
  • released
  • action
  • increase is proportional to
A
  • proglucagon derived peptide
  • released from L cells of intestine in response to ingested food
  • action: decrease gastric motility and secretions
  • increase is proportional to caloric intake
  • anorexic effect
32
Q

What is the anorexic effect?

A

-systemic administration of OXM can reduce food intake and body weight (maybe by suppressing ghrelin)

33
Q

What is pancreatic peptide (PP)?

  • secreted from
  • decreases
  • acts via
A
  • secreted from cells in pancreatic islets of langerhans
  • decreases food intake via Y4R in brainstem and hypothalamus
  • may also act via vagus N
34
Q

What is amylin?

  • stored and released
  • inhibits
  • what effect?
A
  • stored and released with insulin from pancreatic beta cells in response to food intake
  • inhibits NPY release
  • anorexic effect
35
Q

What is glucagon?

  • secreted by
  • increases
  • reduces
A
  • secreted by pancreatic alpha cells
  • increases blood glucose levels and insulin secretion
  • reduces food intake
36
Q

What hormones are released during feeding or just before?

A

CCK, amylin, insulin, glucagon

37
Q

What hormones are released after feeding?

A

PYY, GLP-1, oxcyntomodulin

38
Q

What hormone is released with hunger?

A

ghrelin

39
Q

What hormones target vagal afferents?

A

CCK, amylin, insulin, glucagon

40
Q

What hormones target brainstem?

A

PYY, GLP-1, OXM, leptin

41
Q

What hormones target hypothalamus?

A

PYY, GLP-1, OXM, ghrelin

42
Q

What hormone targets the arcuate nucleus?

A

leptin

43
Q

What hormone targets the vagus N?

A

CCK, amylin, insulin, glucagon, ghrelin

44
Q

What hormones limit size of meal?

A

CCK, amylin, insulin, glucagon

45
Q

What hormones postpones need for next meal?

A

PYY, GLP-1, OXM

46
Q

What hormone has a longer-term regulation of food intake?

A

leptin

47
Q

What hormone increases food intake by increasing size and number of meals?

A

ghrelin

48
Q

What hormones are from the pancreas?

A

amylin, insulin, glucagon

49
Q

What hormones are from the ileum and colon?

A

PYY

50
Q

What hormones are from the stomach?

A

ghrelin

51
Q

What cells produce CCK?

A

I cells

52
Q

What does obesity increase the risk for?

A
  • cardiometabolic disease
  • dementia/Alzheimer’s
  • kidney disease
  • certain cancers
  • respiratory disease
  • osteoarthritis
53
Q

What are the treatments for obesity?

A
  • lifestyle interventions
  • bariatric surgery
  • drug therapies
54
Q

What are the 4 most common bariatric surgeries in the US?

A
  1. adjustable gastric band (“lap band”)
  2. Roux-en-Y gastric bypass
  3. duodenal switch (DS)
  4. vertical sleeve gastrectomy (“gastric sleeve”)
55
Q

What is adjustable gastric band bariatric surgery?

A

“lap band”

  • adjustable band around upper portion of stomach, restricts stomach’s capacity for filling
  • can be adjusted upon weight loss/gain via small access port located just under skin
  • patient’s lose 40-50% of excess weight
  • diabetes resolves in 50-60% of patients
56
Q

What is sleeve gastrectomy?

A
  • left lateral portion of stomach is removed
  • leaves banana shaped and sized stomach behind
  • patients lose 50-75% of excess weight and diabetes resolves in 60% of patients
57
Q

What is biliopancreatic division with duodenal switch (BPD-DS or DS)?

A
  • sleeve gastrectomy is performed and large portion of small intestine bypassed
  • decrease absorption of nutrients
  • weight loss better than gastric bypass
  • diabetes resolves in >90% of patients
58
Q

What is Roux-en-Y gastric bypass?

A
  • involves creating a small stomach pouch and bypassing 3-5 ft of small intestine
  • used for >40 yrs
  • stomach becomes size of egg
  • restricts amount of food that can be consumed
  • patients lose 50-75% of excess weight with good maintenance of weight loss
  • diabetes resolves in 80% of patients
59
Q

What are the effects of Roux-en-Y gastric bypass?

A
  • reduced activity of mesolimbic reward pathway and other reward centers - especially when shown pictures of high caloric density food (decreased desire to eat)
  • altered taste through changes in palatability and condition mechanisms
  • increased gut hormones (GLP-1 and PYY increase as early as 2 d after RYGB surgery and remain elevated for 10 yrs)
  • improved gut bacteria colony - related to improved inflammatory status
60
Q

What is anorexia nervosa (AN)?

A

-characterized by self starvation and excessive weight loss

DSM-5 criteria

  • persistent restriction of energy intake leading to significantly low body weight (in context of expected)
  • either an intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain
  • disturbance in the way one’s body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight
61
Q

Describe the gut-brain axis in anorexia nervosa

A
  • polymorphisms of genes involved in eating attitudes, regulation of eating behavior, motivation, and reward mechanisms (AgRP)
  • basal and pulsatile secretion of leptin reduced
  • ghrelin resistance (fasting, so chronically elevated)
  • elevated levels of PYY
62
Q

What is bulimia nervosa?

A

characterized generally by binge-purging episodes (purging not necessarily self-induced vomiting)

  • swollen parotid glands
  • upper GI acid reflux, dysfunctional LES
  • esophagitis and barrett’s esophagus (Barrett’s sign on hand)
  • Mallory Weiss tear - life threatening
  • heart and electrolyte disturbances
63
Q

What hormones are released from the small intestine?

A

GLP-1

Oxcyntomodulin

GI Final (15 decks)

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