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Week 1 Basic Sciences > The Molecular Regulation of Energy Intake > Flashcards

The Molecular Regulation of Energy Intake Flashcards

1
Q

Energy intake - energy expenditure =

A

Energy Balance

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2
Q

signals (that say stop eating!) in response to the sensory and cognitive perceptions of the food or drink consumed, and distention of the stomach

A

Satiation

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3
Q

nutrients absorbed in the intestine, Length of time until drive to eat reappears

A

Satiety

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4
Q

Where in the brain are most of the signals relating in energy intakes integrated?

A

Hypothalamus

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5
Q

This type of signal moves away from the location of nervous input towards the CNS.

A

Afferent signal

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6
Q

This type of signal moves back towards the source of nervous input. These types of signals regulate the intensity of hunger and the level of energy expenditure.

A

Efferent

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7
Q

What is the primary purpose of regulating energy intake?

A

Deficiency prevention (evolutionarily to ensure reproduction can occur)

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8
Q

What releases leptin?

A

adipocytes

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9
Q

Fat mass is directly correlated with what hormone?

A

Leptin (levels decrease after weight loss)

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10
Q

What does decreasing leptin levels signify to the brain? (eventually causes energy stores to be replenished reestablishing the energy balance)

A

Diminishing fat storage (negative energy balance)

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11
Q

What receptor is expressed in almost every tissue, has five isoforms, and is a member of the class I cytokine receptor family?

A

Leptin receptor (LepR)

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12
Q

What leptin receptor isoform contains the STAT3 recruitment domain and is expressed specifically in leptin-responsive brain regions?

A

LepRb

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13
Q
  • A sigle transmembrane domain which homodimerizes upon binding of the ligand
  • phosphorylation of the JAK2 receptor-associated kinase (phosphorylates STAT3)
  • Recruitment and phosphorylation of the signal transducer and activator of transcription, STAT3
  • Activated STAT3 dimerizes and translocates to the nucleus, where is activates transcription of target genes
A

mechanism of signal transduction at leptin receptor (LepR)

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14
Q

What three things occur when leptin acts on receptors int eh hypothalamus of the brain

A
  1. counteracts the effects of neuropeptide Y
  2. counteracts the effects of anandamide
  3. promotes the synthesis of alpha-MSH
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15
Q

What is neuropeptide Y?

A

a potent feeding stimulant secreted by cells in the gut and in the hypothalamus

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16
Q

What is anandamide?

A

an endocannabinoid (endogenous cannabinoid neurotransmitter), potent feeding stimulant

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17
Q

How does alpha-MSH affect appetite?

A

Suppresses appetite

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18
Q

What does marijuana give a person the “munchies?”

A

THC, the active ingredient of marijuana binds to the same receptors as anandamide which stimulates the need for feeding

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19
Q

What causes long-term inhibition of food intake?

A

Leptin

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20
Q

What causes short-term inhibition of food intake?

A

Cholecystokinin

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21
Q

This condition has an early onset and results in extreme obesity (however the patient is receiving signals they are starving). The patient experiences hyperphagia, decreased immune function, and hypogonadotropic hypogonadism.

A

Leptin Deficiency

(the hypogonadotropic hypogonadism reflects deficiency of the leptin signal informing the brain that sufficient energy stores are available for reproduction)

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22
Q

What is the main mechanism by which short-term food intake is regulated?

A

“Gut-brain axis” (has both neuronal and hormonal components)

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23
Q

What regulates short-term food intake?

A

“Gut-brain axis” (has both neuronal and hormonal components)

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24
Q

What are the neuronal components of the “gut-brain axis?”

A
  • feeling a sense of fullness in response to mechanical distention of the stomach
  • triggers afferent neural pathways to the hypothalamus or via brainstem centers (eg. nucleus of the solitary tract)
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25
Q

What are the hormonal components of the “gut-brain axis?”

A
  • released in the gut and directly impact GI mobility and function
  • also stimulate GI neural signaling to the hypothalamus
26
Q

What are the anorexigenic (signal to stop food intake) signals of the hormonal component of the “gut-brain axis?”

A

Cholecystokinin (CCK)
Glucagon-like peptide-1 (GLP-1)
Peptide YY

27
Q

What is the orexigenic (stimulates food intake) signal arising from the gut of the “gut-brain axis?”

A

Ghrelin (Grrrr it makes you eat

28
Q

What hormone is secreted by duodenal I cells into the bloodstream under the presence of fat and protein in the duodenum?

A

Cholecystokinin (CCK)

29
Q

What hormone stimulates gut motility, contraction of the gallbladder, pancreatic enzyme secretion, and acid secretion and delay gastric emptying?

A

Cholecystokinin (CCK)

30
Q

CCK acts locally stimulating what nerves through the CCK1 receptor (CCK-1R)? (message signifying the presence of fat and proteins are being processed and will soon be absorbed is conveyed to hypothalamus via hindbrain)

A

Vagal sensory nerves

31
Q

Do circulating CCK levels increase or decrease after meals?

A

increase

32
Q

What effect does a CCK-1R agonist (CCK33) infusion to postprandial levels (meaning after a meal) have?

A

suppresses food intake

33
Q

What effect does infusion of a CCK-1R antagonist have?

A

increases calorie intake

34
Q

What is secreted into the bloodstream by the intestinal L-cells of the ileum and colon in response to the presence of nutrients in the lumen?

A

Glucagon-like peptide 1 (GLP1)

35
Q

What increases insulin secretion in a glucose-dependent manner, decreases glucagon secretion, increases beta cell mass, inhibits gastric emptying, and decrease food intake?

A

Glucagon-like peptide 1 (GLP1)

36
Q

How the GLP1 signal?

A

Thought to signal through the hindbrain via stimulation of the GLP1 receptor (GLP1R) on the vagus nerve

37
Q

Why does only 10-15% of GLP-1 ever enter systemic circulation and has the possibility to reach the pancreas and the brain via the endocrine pathway?

A

First dipeptidyl peptidase IV (DPP-IV) degrades GLP-1 in the lumen. Only 25% is remaining. This enters portal circulation. In the liver an additional 40-50% is destroyed. This leaves only 10-15%.

38
Q

What are the cellular actions of GLP-1 that lead to stimulation of insulin secretion?

A

Binding of GLP-1 to its receptors couple to activation of adenylate cyclase. Intracellular cAMP levels are elevated leading to activation of protein kinase A (PKA) and cAMP-regulated guanine nucleotide exchange factor II (cAMP-GEFII, also know as Epac2). These two proteins are likely to mediate the plethora of molecular mechanisms.

39
Q

What is released into the gut bloodstream by intestinal endocrine L-cells of the distal gut (ileum and colon) and food ingestion and in response to the presence of fat in the lumen.

A

Peptide YY-36 (PYY)

40
Q

What is the major form of circulating PYY that binds to the hypothalamic NPY-Y2 receptor and reduces food intake. (NPY - Neuropeptide Y)?

A

PYY3-36

41
Q

Do obese individuals have higher or lower PYY levels after a test meal than non obese controls.

A

lower

42
Q

What is secreted in to the bloodstream by endocrine cells lining the funds of the stomach?

A

Ghrelin

43
Q

What peptide’s secretion is stimulated by fasting, increases preprandially (before a meal), and is suppressed by food intake?

A

Ghrelin

44
Q

What is orexigenic, increasing food intake when administered peripherally by acting in part by directly modulating the activity of the NPY (neuropeptide Y)/AGRP (agouti-related peptide) neurons in the arcuate nucleus of the hypothalamus?

A

Ghrelin

45
Q

Where are ghrelin receptors located?

A

In areas of the hypothalamus long known to be involved in appetite regulation. Receptors are also found concentrated in other areas of the brain, including the hippocampus and regions known to be involved in rewards system (e.g. tegmental area). Ghrelin appears to activate some of the same circuits that are involved in drug reward, which may also be related to this hormone’s effects on appetite.

46
Q

What are ubiquitous lipid mediators (endogenous arachidonate-based lipids)?

A

Endocannabinoids (ECBs)

47
Q

Anandamide and 2-arachidonoglycerol are example of what?

A

Endocannabinoids (ECBs)

48
Q

What do endocannabinoids act through to cause an effect?

A

Cannabinoid receptors CB1 and CB2 which are G protein-coupled receptors located in the CNS and PNS.

49
Q

Are ECBs metabolic and anabolic?

A

Anabolic. They increase the intake and promote the storage of energy and decrease the expenditure of energy.

50
Q

What enzyme degrade ECBs?

A

fatty acid amide hydrolase and monoacylgylcerol lipase

51
Q

What part of the brain integrates activity from the autonomic nervous system and endocrine glands with input from others centers that give rise to emotions and behaviors?

A

Hypothalamus

52
Q

What part of the brain makes sure an organism responds appropriately to deviations from internal set point (temperature, volume, osmolality, satiety, and body fat content)?

A

Hypothalamus

53
Q

Where is the primary location for the integration of peripheral signals that influence energy balance?

A

Hypothalamus

54
Q

What would be the result of a lesion in the ventromedial hypothalamus?

A

Obesity

55
Q

What would be the result of a lesion in the lateral hypothalamus?

A

Leanness

56
Q

What are the two adjacent groups of neurons (first-order neurons) in the arcuate nucleus of the hypothalamus?

A

AGRP/NPY neurons (orexigenic)

Pro-opiomelanocortin (POMC) neurons (anorexigenic)

57
Q

What neurons of the hypothalamus are inhibited by leptin and also have the activity modulated by GI hormones such as ghrelin and PYY?

A

AGRP/NPY neurons

58
Q

What neurons of the hypothalamus are activated by leptin and produce alpha-MSH?

A

POMC neurons

59
Q

First-order neurons send projections to second-order neurons which are located in what region of the hypothalamus?

A

Paraventricular nucleus (PVN)

60
Q

What acts on the melanocortin-4 receptor (MC4R) expressed on PVN neurons?

A

alpha-MSH and AGRP

  • alpha-MSH binds to and activates the MC4R
  • AGRP inhibits MCR4-bearing neurons by competing with alpha-MSH for the MC4R
  • MC4R neurons then innervate neurons in other areas of the hypothalamus and brain stem to produce an integrated inhibition of appetite and increase in energy expenditure
61
Q

What occurs in the absence of alpha-MSH or the MC4R?

A

Morbid obesity

Week 1 Basic Sciences (4 decks)

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