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Endo/Repro Block1 > Pancreas [TRH] > Flashcards

Pancreas [TRH] Flashcards

1
Q

Where is glycogen stored?

A

the majority is stored in liver and sk.m= 500g or approx. 12hrs of energy

**TG stores in adipose= unlimited

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2
Q

When will the brain switch to using ketone bodies instead of glucose for fuel?

what steps happen during fasting/starvation

A

Fasting

  1. Gly stores in liver & muscle must be depleted–> 24hrs
  2. adipose TG’s are catbolized in2 glycerol & free FA’s
    • glycerol –> glu via GluNeo in liver
    • FA’s [acetoacetate & B-hydroxybutyrate] made in liver
  3. ketone bodies are converted to acetylCoA in tissues [brain, muscle]
  4. eventually you would get muscle wasting
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3
Q

What is the role of insulin?

  • inhibits?
  • promotes?
A

inhibits: intracellular lipases –I breakdown of fat/adipose tissue

promotes: facilitates glu entry into fat & liver cells–>TG accumulation in adipose

  • adipose: glu can be used to synth glycerol
  • liver: glu synth into FA’s once glycogen stores are maximal
    • these FA’s are pkged as lipoproteins & secreted as FFA
    • adipose picks up FFA+glycerol = TG
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4
Q

What do B cells of the pancreas secrete?

A

insulin

**in fed state

***also secretes amylin

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5
Q

What do alpha cells of the pancreas secrete?

A

glucagon

**in fasted state

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6
Q

what does the delta [kinda looks like this: oς] cell secrete?

A

somatostatin

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7
Q

what is the overall effect of insulin on metabolism after eating?

A

reduce serum Glu!!!

^^Glu ox

^^Glycogen synth

^^Fat synth

^^protein synth

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8
Q

What is the overall effect of glucagon on metabolism in the fasted state?

A

increase serum Glu!!!!

^^glycogenolysis

^^GNeo

^^Ketogenesis

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9
Q

What is normal blood glu levels?

fasting levels?

A

normal= 70-120 mg/dl

norm fasting = <100 mg/dl

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10
Q

What do E cells secrete?

A

ghrelin!

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11
Q

What effect does the SNS have on the islets of langerhans cells?

A

SNS: inhibit insulin & amylin secretion [fight or flight]

*don;t want to store energy when busy running from a bear & you need it!

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12
Q

What is the PNS effect on islets of lengerhans?

-where does this PNS innervation come from

A
  • PNS via the vagus
    • involved in cephalic phase of insulin secretion
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13
Q

How are both insulin and glucagon secretion regulated?

A
  • plasma glucose levels trigger secretion [depends on if hi or low]
  • negative feedback involves further glu sensing by a & B islet cells
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14
Q

How is insulin processed and what is it’s mature form?

Which part of insulin contains essential info for biologic activity?

A

Preproinsulin–>proinsulin–>*insulin

Mature form: 2 chains

  • alpha chain [acidic]
  • beta chain [basic]
    • 22-26 sequence essential for biologic activity
  • 2 disulfide bridges connact a & B chains

*C-peptide is cleaved here

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15
Q

What is the significance of C-peptide?

A

proinsulin is cleaved into–> C-peptide & insulin

  • It can be measured to determine if the patients insulin is endogenous [made by the pt] or exogenous [medication]
    • present Cp= endogenous
    • low/none= exogenous
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16
Q

What are the pharmokinetics of insulin?

A
  • t1/2 < 10 mins
  • circulates in free plasma
  • metabolized by K & liver
    • via glutathione-insulin transhydrogenase in microsomes
      • proteolytic enzymes
    • 50% on 1st pass
17
Q

What type of R is the insulin R?

A

InsulinR= tyrosine kinase!

  • promotes glu uptake in2 cells & synth into storage molecules, glycogen, & TGs
18
Q

What is amylin?

  • what R does it bind?
  • what is its main fxn(s)?
A

amylin= insulin’s co-conspirator

  • co-pkged & -secreted w/ insulin from B cell [1:1 ratio]
  • t1/2 = mins
  • calcitonin R dimerized w/ R activity-modifying protein
  • **inhibits glucagon secretion **@ level of pancreatic alpha cell
  • role:
    • reduce food intake
    • delay gastric emptying
    • inhibit secretion of digestive enzymes, stom.acid, & bile
19
Q

Glucagon…

  • what form is it made in?
  • when does it ^^ or decrease?
A

Glucagon is made in a cells of pancreas

  • synthesized as proglucagon
  • increases w/ or when:
    • hypoglycemia
    • AA’s
    • SNS & vagal stimulation [latter to temper insulin effects]
  • decreases w/:
    • amylin present
20
Q

What R does glucagon act through/bind?

What does glucagon promote?

A

glucagon ats on Gprotein coupled Glucagon R’s [GCGR]

  • promotes liver GNeo
  • ” “ glycogenolysis
  • ” “ lipolysis
21
Q

Which H’s does Somatostatin affect?

what triggers/inhibits SST?

what are its effects on GI?

A

SST: inhibits insulin [B cells], glucagon [alpha], & ghrelin [e cells] prodxn

  • triggered by ^^insulin
  • inhibited by ^^ghrelin [hunger]

in GI: SST reduces the rate of food absorption

22
Q

What does Ghrelin do to other pancreatic H levels?

A

Ghrelin:

^^glucagon

decreases Insulin & SSt

23
Q

What are Incretins?

A
  • hormones that promote B cell insulin release after eating [intestinal phase]
  • slow gastric emptying–> slows the rate of nutrient absorption in2 blood
    • may also reduce food intake

ex) GLP-1 & GIP

24
Q

WHat is GLP-1?

A

GLucagon like peptide 1

  • AA peptide produced by L cells of the lower SI & colon
  • produced by alt. splicing of proglucagon gene
    • in pancreas = glucagon, SI & colon= GLP-1
  • stimulates insulin in hi glu environment [fed]
  • inhibits glucagon secretion in hypoglycemia
  • degreaded by dipeptidyl-peptidase-4
25
Q

What is GIP?

A

Glucose dependent insulinotropic peptide

[gastric inhibitory peptide is old name]

  • secreted by K cells of duo & jejunum
  • in a type 2 DM, secretion is normal but response to endogenous peptide is impaired
26
Q

What are the 4 phases of insulin secretion?

A
  1. Cephalic phase: PNS info from sight & smell
  2. Oral phase: PNS info & carb/sugar stimulation of sweet R’s
  3. GI Phase: INCRETINS
  • GIP: in response to hyperosm from ^^glu in GI
    • amt of insulin secreted is > if given oral vs IV
  • GLP1: stimulates insulin

​ 4. ​BLood Glu Phase

  • ​^^ blood glu triggers B cell release of insulin
  • decreased blood glu–> a release of glucagon
27
Q

Oral glu vs IV glu, which triggers more insulin secretion?

A

ORAL!!!

due to oral & intestinal phases of insulin secretion [PNS & incretin signals]

28
Q

how do we prevent hypoglycemia & maintain euglycemia?

A

glucagon is the main regulator

  • other nonpancreatic H’s are involved in maintenance of euglycemia by regulating balance of glucagon/insulin & inducing metabolism in extrapancreatic tissues
29
Q

How does glucose get absorbed into gut epithelium?

kidney epithelium?

A

Gut: SGLT1

  • hi affinity for glu
  • low capacity of glu transport

Kidney: SGLT2

  • low affinity for glu
  • high capacity of glu transport

**both couple active transport of glu w/ movement of Na+ down its [] gradient (maintained by Na/K/AtPase) & then glu diffuses into blood via GLUT2 & GLUT1

30
Q

Quick, where are the GLUTs located?

A

GLUT1: RBCs, brain & cornea

GLUT2: [bidirectional] B-islet cells, liver, kidney, SI basolateral membrane, hypothalamus

  • part of glu sensor in pancreas

GLUT3: brain, neurons, placenta, testes

GLUT4: adipose, striated muscle

  • activated by insulin

GLUT5: for Fructose–>so in spermatocytes & GIT

31
Q

What is GLUT 7 used for

A

glu transport in ER

32
Q

How does insulin secretion happen in/o of the B-cell?

A
33
Q

How does insulin act on other tissues [sk.m, fat, cardiac etc]

A
34
Q

What GLUT does insulin promote?

What else does this?

A

INsulin promotes GLUT4 movement to cell membrane [via exocytosis] of muscle & adipose tissue

***exercise also does this!!!

35
Q

What 3 things stimulate intracellular Ca+ levels to increase

[thus releasing insulin from B cells]?

A
  1. phospholipase C–> stimulates release of intracellular Ca+ stores
  2. Adenylate cylase [does same as above]
  3. closure of ATP sensitive K+ channels, opens VG-Ca+ channels

Endo/Repro Block1 (11 decks)

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