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autonomic final > 21+22 > Flashcards

21+22 Flashcards

1
Q

What happens to NE injected into paraventricular nucleus (PVN)

A
  • increases feeding behavior
  • effects mediated by post-syn a2 R (agonist = increase feeding and antagonist = decrease feeding)
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2
Q

what is the role of a1 R in PVN

A
  • activation = decreases feeding
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3
Q

what is the role of a2 R in PVN

A
  • activation = inhibit a1(decrease feeding) (net increase)
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4
Q

what are the main CNS neuropeptides involved in feeding?

A
  • neuropep Y
  • POMC peptide (MSHs)
  • agouti related peptide (AgRP)
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5
Q

what is the role of NPY in feeding (expression/secretion)

A
  • NPY = powerful appetite stim
  • rats injected with NPY exhibit: increased feeding + weight gain
  • expressed in neurons projecting from ARC to PVN
  • expression and secretion is increase by food deprivation
  • hypoglycemic = increase secretion > increased feeding
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6
Q

describe NPY R

A
  • GPCR (Y1R-Y6R)
  • couples to inhibition of AC
  • R1-5 implicated in mediating feeding effects
  • Y5 agonist > increase feeding behavior (increase food intake = directly related to agonist affinity)
  • inhibition of PVN increases feeding behavior
    (basically NPY R expressed at PVN and neuron project from ARC > send NPY to PVN)
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7
Q

describe melanocortin R

A
  • 5 subtypes cloned
  • coupled through Gs to AC
  • MC3R/4R expressed in CNS both involved in feeding
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8
Q

describe the function of melanocortin R

A
  • inhibits feeding
  • mice lacking MC4R increase feeding > obese
  • inhibition of melanocortin R = stimulate feeding
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9
Q

describe the agouti-related peptide (AgRP)

A
  • expressed with NPY in neurons of ARC
  • endogenous inhibitor of MCRs (3/4)
  • agouti mice develop obesity, hyperinsulinemia,
    hyperglycemia, hyperphagia, yellow coat color
  • agouti protein antagonize MCR
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10
Q

describe NPY and POMC neurons and expression of serotonergic R

A
  • NPY neurons express 5HT 1B R
  • inhibit AC > serotonin binding = inhibit neuron act
  • POMC neurons express 5HT 2C R
  • couples with PLC > serotonin binding increases neuron activity
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11
Q

what is lorcaserin

A

5HT 2C agonist > weight lost

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12
Q

describe the role of ghrelin in feeding

A
  • stim feeding
  • synthesized in stomach
  • levels increase with food deprivation and decrease w/ food intake
  • decrease release of insulin + antagonize effects of leptin
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13
Q

describe ghrelin R

A

ghrelin binds to GHS-R1a
- couples to Gq
- expressed in ARC and present on NPY neurons

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14
Q

describe effect of ghrelin at R site

A
  • activates NPY neurons
  • increase release of NPY and AgRP
  • induces feeding behavior
  • increase transcription of NPY and AgRP
  • effects is blocked by NPY antagonist
  • thus effects are mediated by NPY
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15
Q

what’s evidence for ghrelin’s effects

A
  • obese pateints who lost weight dieting > exaggerated peaks of ghrelin before meals
  • obese patients with gastric bypass = reduce levels of ghrelin
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16
Q

what is prader-willi syndrome

A
  • increased ghrelin levels in patients with this syndro
  • pt exhibit voracious app
  • profoundly obese
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17
Q

describe leptin effect on feeding

A
  • inhibit feeding
  • synthesized in white adipose
  • secreted into blood stream
  • levels increase with food intake and decrease with food deprv
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18
Q

describe the evidence for leptin effect

A
  • leptin cloned from obsese mice that do not express functional leptin ob/ob mice
  • mice that do not express functional leptin R increase food intake fa/fa zucker rats
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19
Q

describe the leptin R

A
  • belongs to cytokine superfam of R
  • ligand binding > dimerization = signal transduction
  • activates the Jak-STAT second mess pathway
  • leptin activation of R > tyrosine phos of Jak2
  • phos of Jak2 > tyrosine phos of STAT3 (transcription factor)
  • phos of STAT3 > dimerize and affect transcription
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20
Q

describe leptin effect at R level

A
  • leptin effect both NPY and POMC (both expresses leptin R)
  • activates POMC neurons > increase release of aMSH
  • inhibit NPY neurons > decrease release NPY + decrease levels of NPY in ARC
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21
Q

describe the effect of sleep on feeding

A
  • subjects with sleep deprivation showed
    Leptin decreased 18%
    Ghrelin increased 28%
    Hunger increased 24%
  • Especially for calorie-dense foods
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22
Q

describe insulin effect on feeding

A
  • inhibit feeding
  • expressed in pancreas
  • increase blood sugar > release insulin
    (review insulin release mec)
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23
Q

review insulin release mec

A
  • glucose enter GLUT2 > ATP increase > ATPsensitive Kch opens > depol > calcium ch open > insulin secretion
  • Binding of insulin to its receptor causes
    activation of its tyrosine kinase activity (insulin receptor is a tyrosine kinase receptor)
  • Phosphorylation of insulin receptor activates
    signal transduction pathway
  • Result is translocation of GLUT4 glucose
    transporters to cell surface
24
Q

how does insulin effect at R level

A
  • decrease feeding by inhibiting neurons that expresses NPY
  • synergizes with leptin
  • decrease release of NPY
  • inhibition of NPY relieves inhibition of POMC
  • decrease transcription of NPY
25
Q

how does leptin and insulin work together

A
  • signaling synergize to decrease the release of NPY
  • increase opening of K+ channels to cause
    hyperpolarization of NPY neurons
  • signaling synergize to decrease transcription of NPY and increase transcription of MSHs
  • High insulin levels = Phosphorylation of transcription factor FOX01 leads to inhibition
  • Decreased transcription of NPY and AgRP = High leptin levels > Phosphorylation of transcription factor STAT3 leads to activation> Increased transcription of MSHs
26
Q

what does FOX01 normally do

A
  • increases the expression of NPY and
    AgRP
  • Normally decreases the
    transcription of POMC
27
Q

what does STAT3 normally do

A

STAT3 normally increases the expression of POMC > Normally decreases the transcription of NPY and AgRP

28
Q

review slide 51

A
29
Q

describe how cholecystokinin (CCK) is synthesized and released and how it effects feeding

A
  • synthesized in small intestine and released when food present
  • fats and proteins in intestine are potent stim
  • CCK cells repond to bitter tastants
  • CCK inhibits feeding
30
Q

describe CCK at the R level

A
  • GPCR = CCK1/2
  • KO animals w/o CCK R are obese (OLETF rats)
  • has peripheral and central actions
31
Q

describe peripheral action of CCK

A
  • inhibits gastric emptying, increase release of bile from liver, stim insulin release by pancreas
  • decrease gastric emptying (can synergi with other signals to decrease feeding ie. low doses CCK + gastric distention = satiety)
32
Q

describe central activity of CCK

A
  • increase satiety
  • increases expression of NPY Y2R R in ARC (inhibitory)
  • activation of Y2R decreases release of NPY > inhibition of NPY neurons release inhibition of POMC neurons > increase POMC activities
33
Q

how does CCK interact with regulatory hormones

A
  • CCK increase release of leptin into bloodstream
  • CCK + leptin synergize to decrease feeding
  • full satiety signal from CCK is dependent of leptin R in ARC (leptin may increase reponsiveness of NPY/POMC neurons in ARC to CCK signalling)
34
Q

describe how peptide PYY is synthesized and released and how it effects feeding

A
  • expressed in lower small intestine and colon
  • released into blood steam in relation of caloric content of meal
  • higher secretion when proteins are ingested
  • inhibit feeding
35
Q

describe PYY peripheral and central actions

A

Peripheral activity
- Inhibits gastric emptying
- Inhibits gut motility
- PYY decreases the release of ghrelin
Central activity
- PYY inhibits NPY neurons to decrease feeding
- Binds receptors in arcuate nucleus

36
Q

describe central activity of PYY at R level

A
  • PYY binds NPY Y2R R in ARC (inhib)
  • activation of Y2R > decrease release of NPY > inhibition of NPY neurons relieves inhibition of POMC > increase activity of POMC neurons.
37
Q

describe the role of glucagon-like peptide1 in feeding (express/release)

A
  • expressed in small intestine and colon
  • released in response to ingestion of food from enteroendocrine cell of small intest
  • can be enhanced by concetration of glucose
  • mec of release thought to be similar to glucose-mediated release of insulin from pan B cells
  • decreases feeding
38
Q

describe GLP1 effects at the R level

A
  • GLP1R is GPCR
  • couples to Gs
  • expressed in several tissues
    GI tract, heart, pancreas
39
Q

describe the action of GLP1

A
  • decrease rate of gastric emptying
  • increase production of ANP1 (hypertension common in T2 diabetes)
  • increase the release of insulin from pancreas
  • decrease release of glucagon
  • has short half life in blood stream but analogs can be made resistant to degradation by peptidases
40
Q

describe GLP1 effect on pancreatic function

A
  • enhances release of insulin from beta cells (incretin hormone)
  • decreases glucagon from alpha cells
41
Q

describe evidence for incretin hormones’ effect

A
  • glucose given orally causes a greater increase in insulin release and given IV
  • incretin released from endocrine cells in intestine in response to ingestion of glucose
  • this increase in insulin release anticipates the rise of blood glucose
42
Q

what is exenatide (byetta)

A
  • treatment for T2 diabetes
  • reduce plasma glucose levels and causes weight loss
43
Q

what is victoza

A
  • treatment for T2 diabetes
  • GLP-1 agonist
44
Q

what is trulicity

A
  • treatment for type 2 diabetes
  • GLP1 R agonist
  • subcutaneously injected (slow absorption allows for 1 a week dosing)
  • decreases A1C levels
45
Q

what is ozempic

A
  • GLP1 analog with 3 key amino acid residues changes > decrease proteolysis and renal clearance > extends the half-life
  • administered by injection 1 a weeks
46
Q

what is januvia

A
  • T2 diabetes treatment
  • Dipeptidyl peptidase-4 (DPP-4) inhibitor
  • GLP-1 is a peptide hormone that is degraded rapidly
    after release > DPP-4 inactivates GLP-1 > Januvia inhibits DPP-4 > extend the duration of action of endogenous GLP-1
  • also decreases HbA1C levels
47
Q

what is metformin

A
  • insulin resistance T2 diabetes
  • Metformin activates AMP-Activated Protein
    Kinase (AMPK) > Increases sensitivity to insulin > translocation of GLUT4 vesicles to cell membrane
    (aka insulin independent GLUT4 translocation)
48
Q

what is invokana

A
  • T2 diabetes treatment
  • inhibitor of sodium-glucose co-
    transporter 2 (SGLT2) = SGLT2 is expressed in the proximal renal tubules + responsible for the reuptake of the majority of glucose filtered in the glomerulus
  • Inhibition of SGLT2 reduces the reuptake of
    glucose in the kidneys > Results in loss of glucose (and Na) from the body through urine
  • (more effective than Januvia at reducing HbA1C in T2 pt)
49
Q

what is Jardiance

A
  • approved for pt w/ T2 diabetes
  • SGLT2 inhibitor
50
Q

what is the role of ENS

A
  • regulates function of the GI tract
  • has intrinsic activity
  • May be modulated by input from sympathetic or
    parasympathetic nervous systems
  • The number of neurons in the ENS is similar to
    the number of neurons in the spinal cord
51
Q

what r the functions of the GI tract

A
  • digestion
  • absorption
  • fluid exchange
  • immune function
52
Q

describe the Gl tract

A

Mouth
Esophagus
Stomach
Small intestine
Large intestine (colon)
Rectum
Anus

53
Q

describe the swallowing reflex

A
  • coordinated by brainstem
  • muscles in esophagus move food in an aboral direction
54
Q

describe digestion in the stomach

A
  • stomach stores food and digest food
  • secretory cells produce acidic environment
  • kneads large clumps of food into small particles
  • produce chyme
55
Q

describe digestion and absorption in the small intestine

A
  • pancreas and liver produce and secrete digestive enzymes
  • enterocytes in the small intestine produce enzymes for digestion
  • final step in digestion occurs at the site of transporter on microvilli which absorb nutrients
56
Q

describe gut motility through small intestine

A
  • propulsion and mixing
  • longitudinal and circular smooth muscle fibers
57
Q

describe large intestine functions

A
  • gut motility (separate from defecation reflex)
  • water absorption

autonomic final (8 decks)

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