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PDAT2 > 8 - DM Endocrinology > Flashcards

8 - DM Endocrinology Flashcards

1
Q

Insulin effect on

Liver

A
  • *Glycogen Synthesis**
  • inhibition of glycogen breakdown*
  • *FA + TG synthesis**
  • inhibition of LIPOLYSIS* (TG->FFA)

Celular RESIPIRATION

  • *Protein Synthesis**
  • inhibition of protein/AA degredation*
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2
Q

IGF-1

Synthesis

insulin-like growth factor 1

A

70AA acids -> folds into tertiary structure similar to insulin

Mainly by the LIVER,
also by bone / connective tissue / muslce / kidney

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3
Q

GLP-1

Synthesis

A

30 AA’s w/ a C-terminal

part of the PROGLUCAGON peptide, released by proteolytic processing along with Glucagon

Mainly from the Endocrine L-Cells in SMALL INTESTINE
pancreas alpha cells with glucagon is NOT main source

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4
Q

How is the signaling of Insulin

INTERRUPTED/INTERFERRED?

A

There are also SER/THR residues on the beta chains that can be phosphorylated

this can interfere with the normal TYROSINE Phosphorylation* and proper *Signal Transduction

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5
Q

Insulin Signal Transduction Photo

A
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6
Q

Insulin Receptor Activation Steps

RTK

A
  • Insulin -> a-subunit -> b-subunits come together
  • Autophosphorylation of tyrosine residues on B-chains INSIDE cell
    • Can cause conformational change
    • or serve as a docking site
      • for Adaptor proteins (SH2 Domains)
  • Further phosphoralation of signaling can occur: CASCADE
    • IRS-1,2,3,4
      • ​RAS -> MAP Kinase -> gene expression
      • PI3K -> PIP3 -> PKB/AKT
    • CBL (also with PKB)
      • ​upregulate GLUT4 to membrane –> glucose uptake
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7
Q

Insulin Receptor

A
  • Transmembrane Receptor = RTK
  • Heterodimer w/ 2 subunits:
    • α-subunit
      • ​​extracellular with hormone-binding domain
    • β-subunit associates with α-subunit;
      • it spans the membrane; cytosolic region has ATP-binding and tyrosine kinase (TK) domains
  • Disulfide bonds stabilize dimer
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8
Q

GLP-1

Release is stimulated by what and what are its ACTIONS?

A

mainly from endocrine L-cells in small intestine, secretion is stimulated by FOOD INTAKE

ENHANCES INSULIN RELEASE

in a fasting state, Supress Glucagon Levels

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9
Q

What is added to Injected Insulin to help PROLONG its effects?

A

PROTAMINE (basic protein) + ZINC ions

Proteolytic tissue enzymes degrade the protamine first then allow for the absorption of insulin

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10
Q

Amylin

Actions

A

After a meal, promotes GLUCOSE CONTROL

  • a NEUROPEPTIDE*
  • Reduces* Glucagon Secretion
  • SLOWS* Gastric Emptying (vagus nerve effect)
  • Decreases* Appetite
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11
Q

Glucagon Functions

A

Glycogenolysis + inhibits glycogenesis in liver

Gluconeogenesis

Lipolysis
(TG–>FFA)

Ketone Formation

AA Uptake

(Glycogen -> Glucose)

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12
Q

Insulin Release Kinetics

A

1st Phase = Acute, short

2nd Phase = ~5 minutes -> Sustained Phase

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13
Q

Insulin Cleavage / Formation

A
  • Preproinsulin
    • cleaved in ER
      • remove 22 AA’s from N-TERMINUS
  • ​​Proinsulin
    • folds over –> forms 3 disulfide Bridges
  • ​Insuli​n
    • ​C-Peptide cleaved in the Golgi
      • also 4 more AA’s are removed
  • ​​Mature insulin = A + B chain held by 3 disulfide bridges
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14
Q

What DEGRADES Insulin and what is it’s Half Life?

A

In BLOOD Insulin T1/2= 3-5 min

INSULINASE cleaves the DISULFIDE links
(glutathione-insulin transhydrogenase)

Liver + Kidney
are the main 2 organs that remove insulin

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15
Q

Which Insulin effects affect ALL 3 ORGANS?

Liver & Muscle & Fat

A

Cellular Respiration

Stimulation of Protein Synthesis

inhibition of _Protein & AA degradation_

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16
Q

3 Effects of INTURRUPTING

Insulin Signals

A

Can be from phosphorylation of ser/thr residues on beta chains INSTEAD of the tyr-residues

Insulin Resistance
HYPERinsulinemia

Apparent Starvation

Increased FA Metabolism –> KETOSIS
FA –> Ketone bodies

17
Q

Glucagon Receptor Signaling

A
  • Low Glucose –> pancreas alpha cells –> GLUCAGON release
  • IN LIVER, Glucagon binds GPCR
    • (Adenylate Cyclase) AC produces cAMP
  • cAMP** (second msger) –> activates **PKA
    • Glucogenolysis
      • Glycogen -> Glucose
    • Gluconeogenesis
18
Q

Amylin

Synthesis

AKA Islet amyloid polypeptide = IAPP

A

CO-SECRETED w/ INSULIN
from B-cells from pancreas

Is a NEUROPEPTIDE

19
Q

Insulin Release Photo

20
Q

Insulin effect on

FAT

A

Lipoprotein uptake

Glucose Uptake

  • *FA + TG Synthesis**
  • inhibition of LIPOLYSIS* (TG–/–>FFA)

Cellular Respiration

Stimulation of Protein Synthesis
inhibition of Protein & AA degradation

21
Q

Somatostatin

ACTIONS

A

Generally INHIBITORY_,_ inhibits secretion of:

Insulin + Glucagon + ITSELF (paracrine)

Gut Hormone Secretion
(gastrin + secretin + cholecytokinin…)

blocks secretion of Pituitary Hormones
(TSH / ACTH / GH)

  • Reduces* Salivary Secretion / Acid + Pepsin in stomach
  • reducs motility of the* GI Tract
22
Q

IGF-1

Actions

A

Binds to 2+ receptors, Insulin Receptor & 1 distinctly for IGF-1

potency is only 1/10 that of Insulin

overall effects/actions are the same as insulin

23
Q

Glucagon Synthesis

A

Peptide hormone synthesized from ProGlucagon,
from single gene proteolytic processing:

From A-Cells in pancreas –> Glucagon

ALSO from Small+Large Intestine –> GLP-1

Several functions, mainly to increase Glucose concentration in plasma

Glycogenolysis (glycogen->glucose)

24
Q

Stimulation of Insulin Release

A
  • High Glucose –> GLUT2 on pancreatic beta cell
    • Glycolysis -> ATP production
      • Ligand gated K+ Channels CLOSE
        • MEMBRANE DEPOLARIZATION
  • Voltage Gated Ca2+ channels OPEN
    • ​Calcium -> Activated Phospholipase C
      • –> cleaves PPD4,5BP into:
        • IP3 & DAG
          • ligands for the ER Calcium Channel
  • ​​​Cytosolic Calcium increases
    • -> Secretory vesicle Exocytosis to release INSULIN
25
Q

What type of IONS improve the stability of INSULIN and HOW?

A

Insulin is normally a monomer @ phys concentration <0.1um
dimerizes at HIGHER concentrations

in the presence of ZINC ions, insulin dimers –> hexamers
(Oligomerization, storage form in B-cells)

Hexamers diffuse poorly –> delayed absorption after subQ injection

Zinc improves the stability of insulin

26
Q

Insulin Structure Photo

27
Q

Somatostatin

SYNTHESIS

A

“Feedback from glycogen / insulin”

DELTA CELLS of pancreas + Gut Cells** + **NEURONS

made as a pre-pro-hormone, 2 active forms, cleaved in alternate ways, depending on source tissue & cell type

28
Q

Insulin Storage

A
  • Zinc help stabilize & protect the stored insulin
    • from proteolytic cleavage
  • Insulin is stored in vesicles for later secretion
    • C-Peptide is also stored in here
29
Q

Insulin effect on

MUSCLE

A

Amino Acid UPTAKE

Glucose Uptake

  • *Glycogen Synthesis**
  • inhibition of Glycogen breakdown*

Cellular Resipration

  • *Protein Synthesis**
  • Inhibition of Protein / AA degradation*

PDAT2 (22 decks)

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