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Endo/Repro: Week 2 > Skildum: glucose Metabolism Review > Flashcards

Skildum: glucose Metabolism Review Flashcards

1
Q

The insulin receptor acts as a….

A

TK receptor

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2
Q

A 44 y/o M ate a 1200 calorie meal taht was 50% carb, 30% fat and 20% protein. He then fasted for 30 hrs. What is the source of C for his blood glucose.

A

FA beta oxidation

Fasted entering into starved

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3
Q

What is the most important source of blood glucose?

A

LIVER

supplies fasted and starved states through gluconeogenesis and glycogenolysis

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4
Q

What regulates glucose homeostasis?

A

Insulin and glucagon

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5
Q

What acts in opposition to insulin?

A

glucagon
catecholamines
cortisol
GH

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6
Q

What leads to an INCREASE in glycogenolysis, gluconeogenesis, and lipolysis but a DECREASE in liver glycolysis?

A

Decrease in blood glucose>
glucagon release>
promotes GENERATION of glucose from storage forms

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7
Q

What leads to an INCREASE in glycogen synthesis, TG synthesis, FA synthesis and liver glycolysis?

A

Increase in blood glucose>
insulin release>
acts on tissues to REDUCE generation of glucose

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8
Q

What promotes hepatic gluconeogenesis?

A

Glucagon

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9
Q

What is required for gluconeogenesis?

A

PEP-CK

G6Pase

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10
Q

Why is PEP-CK impt?

A

gluconeogensis w/ ALANINE or LACTATE

*you can do gluconeogenesis w/out if glycerol is available

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11
Q

Why is G6Pase impt?

A

allows glucose to EXIT the hepatocyte

or else glucose would be trapped in the liver

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12
Q

What PROMOTES gluconeogensis?

A

PKA phosphorylates PFK-2

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13
Q

What happens when PKA phosphorylates PKF-2 and how does this ultimately promote gluconeogenesis?

A

PKA phosphorylates PFK-2 →
activates phosphatase function & inactivates kinase function
→ decreases F-2,6-BP*
→ promotes gluconeogenesis & downregulates glycolysis

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14
Q

What is an allosteric inhibitor of F-1,6-BPase and allosteric activator of Phosphofructokinase-1?

A

F-2,6-BP

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15
Q

Describe how how high concentrations of glucose cause Beta cells to secrete insulin.

A
  1. As extracellular glucose concentrations increase → glucose enters cells
  2. Glucose converted to pyruvate & goes thru TCA to make ATP
  3. ATP blocks K+ channels → depolarization
  4. VG Ca2+ channels open → [Ca2+] in cytoplasm
  5. Ca2+ dependent proteins mediate fusion of insulin containing vesicles w/ plasma membranes → insulin release
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16
Q

Describe the insulin signaling pathway that promotes glucose storage.

A

Insulin binds receptor TYROSINE KINASE
→ Phosphatidyl inositol 3-kinase makes phosphatidyl inositol-3,4,5-trisphosphate.
→ PDK1 and PKB are recruited to the plasma membrane.
→ PDK1 phosphorylates PKB, activating it.
→ PKB phosphorylates Protein Phophatase-1 & Glycogen synthase kinase-3

  • Phosphorylated PP1 is ACTIVATED
  • Phosphorylated GSK-3 is INACTIVATED

Net effect: ACTIVATE GLYCOGEN SYNTHASE

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17
Q

What is the dominant mediator of metabolism in the FASTED state?

A

Glucagon

18
Q

How does glucagon signal for the formation of PEP-CK and G6Pase?

A

Glucagon →
activates PKA → phosphorylates CREB →
activates transcription of PGC1a (transcriptional co-activator) →
liver →
CREB + PGC1a activate transcription of PEP-CK and G6Pase

**both are required for gluconeogenesis

19
Q

How does insulin block hepatic gluconeogenesis?

A

Insulin →
activates PKB (Akt) → blocks transcription factor FOX01 by phosphorylating it>
NO production of genes necessary for gluconeogenesis

20
Q

What is FOX01 required for?

A

FOX01 required for gene transcription of G-6-Pase & PEP-CK

21
Q

What hormone controls metabolism in the FED state?

A

Insulin

22
Q

What is the mechanism for maturity onset diabetes of the Young Type 2?

A

Mutation in glucokinase →
less efficient kinase activity
→ β cell can’t rapidly increase ATP
→ don’t get glucose storage

23
Q

What happens when there is a lack of insulin or insulin signaling?

A

don’t get inhibition of glucagon release from pancreastic cells →
increased glucose uptake & hepatic gluconeogenesis→
water wants to leave cells to balance osmotic P →
bad sx: dehydration, coma, death

24
Q

How does the body deal with a pseudostarved state?

A

increased lipolysis→ increased FA in blood→
diabetic ketoacidosis if ketone bodies too great
→ bad sx: coma, death

25
Q

What happens in T1D?

A

no insulin>
dietary fat doesn’t get stored in adipose →
TAG in blood→
Elevated KB, FA & glucose levels

26
Q

What happens in T2D?

A

Insulin made, but not signalling appropriately or made in small amts that isn’t enough to respond to dietary glucose→
Don’t get uptake of glucose into muscle cells →
inappropriate gluconeogenesis.

27
Q

How does Metformin lower blood glucose?

A

activates LKB1→ phosphorylates and activates AMPK→
AMPK phosphorylates TORC2→
TORC2 can’t localize to nucleus→
This prevents transcription of gluconeogenesis genes and lowers blood glucose.

28
Q

What complex doesn’t dissociate leading to constant gluconeogenesis in T2D? How does Metformin conteract this?

A

TROC2-DREB

Metformin PREVENTS TORC2 translocation to the nucleus

29
Q

How does metformin decrease hepatic gluconeogensesis?

A

blocks complex 1 in ETC→
activation of AMP-K →
decreased hepatic gluconeogenesis

30
Q

What affect does Metformin have on F-2,6-BP ?

A

prevents generation of cAMP → which blocks PKA activation
→ higher levels of F-2,6-BP
→ acts as allosteric inhibitor of gluconeogenesis and allosteric activator of glycolysis

31
Q

What does Dinitrophenol do?

A

It’s an Uncoupler that dissipates the proton gradient without generating ATP.

32
Q

What are some of hte SE of dinitrophenol? Why might it be a future diabetes tx?

A

dose dependent fever

improves hepatic insulin sensitivity–> possible diabetes tx in future

33
Q

How does testosterone affect insulin?

A

It ENHANCES insulin’s effects on glucose metabolism by:

  1. increasing insulinR expression
  2. Increasing GLUT4 expression and membrane translocation
  3. Upregulation of key enzymes> store glucose as glycogen
34
Q

How does an increase in adipose tissue affect testosterone production?

A

increased adipose tissue →
increased aromatase activity→
increased conversion of testosterone to estradiol in adipocytes→ negative feedback to hypothalamus → decreased testosterone production

35
Q

What is metabolic coupling?

A

occurs in many tissues of the body, where one cell type converts glucose to other substrate that is then passed on to the other cell type to be used.

36
Q

How is metabolic coupling used in spermatogenesis?

A

Sertoli cells are glycolytic, fermenting glucose to lactate →
lactate is exported through MCT4, and taken up by spermatocytes through MCT2.→ The spermatocytes then oxidize the lactate.

37
Q

How is metabolic coupling used in oocyte maturation?

A

Cumulus cells are glycolytic, fermenting and providing the oocyte substrates for oxidative phosphorylation.

38
Q

A 16 y/o M is brought to the ER after swallowing two bottles of aspirin tablets. His oral temp is 104. Why?

A

Salicylate is a mitochondrial uncoupler

39
Q

Some tissues are comprise of different cell types that are metabolically coupled. In the brain, astrocytes ferment ________and provide ________to neurons.

A 
GLUCOSE> 
pyruvate>
LACTATE>
MCT transporter>
taken up by adjacent neuron
40
Q

How does insulin receptor signaling inactivate gluconeogenesis?

A

Akt phosphorylates FOX01

41
Q

A toxin inhibits PEP-CK. In the presence of this toxin, what can provide carbon for gluconeogenesis?

A

Glycerol

Endo/Repro: Week 2 (11 decks)

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