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Biochem Exam 2 > Insulin and Glucagon > Flashcards

Insulin and Glucagon Flashcards

1
Q

What are the two sources that blood provides fuel from?

A

–dietary fuels from carb, fat, protein directly from the gut
–stored fuels from glucose, fatty acids, amino acids

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2
Q

Red blood cells rely on what to make ATP?

A

glucose

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3
Q

Most tissues in the body are ______ when it comes to reliance on substances to make ATP.

A

versatile

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3
Q

Tissues that are don’t absolutely require glucose can switch to what for ATP? Why?

A

fatty acids
to allow tissues that require glucose to get the remaining gluose

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4
Q

The brain relies on what to make ATP?

A

mainly glucose but in times of starving ketone bodies

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4
Q

The master controllers of fuel storage, metabolism and switching are:

A

insulin
glucagon/catecholamines

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5
Q

Insulin and glucagon/ catecholamine levels in the blood are regulated by:

A

blood glucose concentrations

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6
Q

Glucagon and stress hormones sends what where?

A

mobilized stored fuels to be used (glucose, fatty acids and amino acids)

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6
Q

Insulin/glucose inhibits _______

A

glucagon release

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7
Q

After eating insulin sends what, where?

A

fuel, to be stored

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8
Q

Actual duration of post-prandial
glucose/insulin pulse depends
on:

A

how fast carbohydrate is
absorbed from the gut

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8
Q

What happens to blood fuel levels after a high protein, no carbohydrate meal?

A
  • small increase in insulin stimulates a.a. uptake and protein synthesis
  • large increase in glucagon controls glucose and fatty acid metabolism
    (glucagon has no effect on a.a. uptake or protein synthesis)
  • balance of insulin and glucagon keeps glucose levels steady
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8
Q

What is the difference between epinephrine and cortisol effects on fuel?

A

ep is more immediate
cortisol is long term

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9
Q

what regulates the release of insulin?

A

Major: high glucose level
low: amino acids, neural input, gut hormones

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9
Q

what regulates the release of glucagon?

A

low glucose/insulin
amino acids
(insulin is the most major effector of glucagon levels)

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9
Q

Why does insulin level slightly rise even after a no carb meal?

A

When the amino acids are being used to make ATP that increase in ATP stimulates the slight release of insulin

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9
Q

What effect does insulin have on the liver?

A

metabolic and enzymatic changes but not change of entry of glucose to the liver

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10
Q

Insulin has no direct effect on

A

glucose transporters in liver cells

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10
Q

Insulin and glucagon are
–both are ________ sustained action depends on continuous secretion
– both act at the ________ of their target cells

A

–both are short-lived in the blood (minutes)
sustained action depends on continuous secretion
- both act at the cell surface of their target cells
-do not enter the target cell (2nd messenger systems)

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11
Q

What are examples of insulin sensitive tissues?

A

muscle, adipose tissue

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11
Q

What effect does glycogen have on muscle tissue

A

none, the muscle does not have a receptor for glucagon

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11
Q

what tissues are sensitive to glucagon?

A

liver and adiposities

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12
Q

insulin and glucagon are what type of hormone?

A

polypeptide

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13
Q

Protein phosphatases ______ ______ from phosphorylated amino acids

A

hydrolyze phosphate

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14
Q

The insulin receptor becomes a ____ _____ _____when it is activated by insulin

A

protein tyrosine kinase

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14
Q

Protein kinases use ATP to ______ amino acids on substrate proteins

A

phosphorylate

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15
Q

when are g protein active?

A

when GTP is bound
(inactive when GDP is bound)

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15
Q

how does glucagon effect messages across cell membrane?

A

2nd messenger

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15
Q

From the point of view of fuel metabolism, the most important
effect of insulin is ________

A

activation of protein phosphatase-1 and AKT

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16
Q

Because the insulin signal transduction also activates protein phosphatase 1, a significant effect is to
________ enzymes that are substrates for protein kinase A

A

dephosphorylate

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17
Q

How does the glucagon receptor signal transduction work?

A

1- glucagon binds to receptor
2- g protein releases alpha
3- alpha triggers the adenylate cyclase to make cAMP
4- cAMP binds to regulatory subunits of protein kinase A
5-they become altered allowing activation of catalytic subunits
6- protein kinase A is adding phosphates to proteins to change cell behavior

17
Q

why is the mechanism of the G protein with GDP AND GTP important biologically?

A

allows a very quick response to a meal (when you do not need glucagon this can be turned off very quickly)

18
Q

how does insulin effect the glucagon signal transduction?

A

prevents the G protein from going from GDP to GTP, therefore preventing the entire cascade following

18
Q

what does insulin stimulate within the cell?

A

protein phosphatase 1 which can remove all the phosphates glucagon put on the proteins through protein kinase A

19
Q

what is the master switch of fuel metabolism?

A

phosphorylating and dephosphorylating enzymes/proteins

20
Q

In summary, glucagon, through protein kinase A causes ______
insulin through protein phosphatase 1 causes ______

A

phosphorylation of proteins
dephosphorylation of those proteins (in essence when insulin is stimulated after a time of fast it goes in and undoes everything glucagon did)

21
Q

why doesn’t insulin impact the liver?

A

needs to import glucose in fed state
needs to export glucose in fed state
(must have glucose transporters in all states)

22
Q

insulin stimulates glucose transport in which tissues?

A

adipose and muscle

23
Q

How does insulin stimulate glucose transport in muscle and adipose?

A

In the fasting state, glucose transporters (GLUT4) are sequestered inside the cell in vesicles so no glucose being taken into cells, AFTER insulins trigger, vesicles come to the surface presenting the GLUT4 transporters to allow glucose to enter WHEN FED

23
Q

The reducing agent ______ electrons to other species

A

donates

23
Q

Where are GLUT 4 receptors when fasting?

A

inside the cell NOT on cell membrane

24
Q

The oxidizing agent _______ electrons from another species.

A

accepts

25
Q

Oxygen accepts 1 electron forms _______.

A

superoxide

26
Q

When superoxide accepts 1 electron it‘s reduced to ______

A

hydrogen peroxide (H2O2)

27
Q

When hydrogen peroxide accepts 1 electron it forms the _____

A

hydroxyl radical

28
Q

How are free radicals depicted?

A

–A free radical is depicted by a superscript dot, HO.
–If the free radical is charged the charge is written after the dot,
HO.-

29
Q

what is a free radical?

A

Free radicals are defined as molecules bearing an unpaired electron and RS are highly reactive

29
Q

Why are antioxidants important?

A

they work to get rid of free radical species

30
Q

IN the electron transport chain where is there a risk for ROS?

A

CoQ, Complex 1-3
when O are moving around
(he emphasized complex II and III)

31
Q

SOD requires _____ to function

A

zinc and copper (deficiency in these can lead to accumulation of ROS)

31
Q

What are NADPH oxidases (NOXs)?

A

ROS made intentionally to kill bacteria
use NADH to transfer electrons to make superoxide’s and HOCl

31
Q

What protective mechanism is in place to reduce the mitochondrial ROS?

A

antioxidants waiting in the intermembrane space and matrix for the ROS, if ROS made the antioxidants will reduce them to H2O

31
Q

what is the mechanism behind macrophages and neutrophils?

A

in the presence of microorganisms they take up O2, which increases release of ROS (respiratory burst)

32
Q

Generated H2O2 is then
rapidly converted to H2O
by

A

Catalase

32
Q

Does complex 4 make ROS in ETC?

A

no

33
Q

Superoxides are
converted to H2O2 by

A

Superoxide dimutases (SODs)

34
Q

what do SODs and CAT do?

A

enzymatic protection, body from ROS by degrading them

35
Q

Glutathione is a _______:
* Made of ___-___-___.
* Present _____ levels in cells.
* Considered the key cellular anti-oxidant in organisms

A

Tripeptide
Glu-Cys-Gly
high

36
Q

what are the forms of non-enzymatic forms of cellular protection?

A

glutathione

37
Q

Glutathione (GSH) is a ______ agent that can _______ neutralize ROS

A

reducing
donate electrons to
(works together with Glutathione Peroxidases (GPx) and NADPH).

38
Q

How does GSH work?

A

2) Once GSH donates an e-, it is oxidized to the GSSG form (2 S-S linked Glutathione).
3) GSSG is reduced to monomeric GSH by Glutathione Reductase (GSR)
4) NADPH from PPP donates e-
5) GPx contains selenium ion

38
Q

Vitamin E is a non enzymatic anti-oxidant that prevents what specifically

A

lipid peroxidation

39
Q

How does Vit E work as a anti-oxidant?

A

–Fat soluble so readily inserts into membranes. Terminates free radical chain- reaction peroxidation of polyunsaturated fatty acids.
–Donates electron to lipid peroxy radical. Resonance stabilizes free
radical vitamin E form. It will accept an electron from vitamin C to return to fully reduced form

40
Q

How does vitamin B3 (niacin) work as a non-enzymatic factor?

A

because its needed in the PPP to make NADPH

41
Q

Non-enzymatic anti-oxidant: Vitamin C (Ascorbic Acid) works by:

A

Free radical scavenger (anti-oxidant) in aqueous compartments.
Deficiency: Scurvy (defect in collagen cross-linking)
Inability to regenerate vit E

42
Q

review Vitamin E, Ascorbic acid (C) and Niacin (B3): Preventing membrane damage SLIDE

A

slide 365

43
Q

In protein oxidation ROS interact with:

A
  • Thiol groups (met, Cys)
  • Pro, Arg, His NH2 groups
43
Q

How can you synthesize vitamin E?

A

Vitamin C reduces vitamin E radicals formed when vitamin E scavenges oxygen radicals.

44
Q

Which macromolecules can be damaged by ROS?

A

DNA, Lipid, Protein

44
Q

What is lipid peroxidation?

A

chain reaction of radical lipids that react with molecular oxygen to form lipid peroxyl radical (this is stopped by vit E)

45
Q

How does ROS impact DNA and RNA?

A

–ROS-induced base
damage is the conversion
of Guanine to 8-oxoG, a
mutagenic lesion (8-oxoG
pairs with A).
–The most well-defined
ROS-induced damage is
DNA double strand breaks

46
Q

What can protein oxidation lead to?

A
  • Cross-links
  • Aggregation
  • Misfolding
  • Proteosome dysfunction
47
Q

What clinical manifestations does lipofuscin formation have?

A

brownish pigment of cells
age spots

48
Q

oxidative stress can cause

A

many diseases all over different systems

49
Q

IN those with periodontal disease what antioxidants were decreased?

A

Cu, Mn, and Zn (allowing a redox environment favoring oxidative stress in saliva causing periodontitis)

Biochem Exam 2 (6 decks)

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