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GEMS > Insulin & Counterregulatory Hormones > Flashcards

Insulin & Counterregulatory Hormones Flashcards

1
Q

Storage of glucose

A

Processes that generate ATP decrease

Insulin

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2
Q

Mobilization of glucose

A

Needed when we need energy

Glucagon
Epinephrine

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3
Q

Insulin

A

Promote fuel storage

Increase in blood glucose –> insulin signals to tissues –> cells take up excess glucose from blood –> used to make TAG or stored as glycogen

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4
Q

Insulin

Released from…

A

B-cells of the pancreas in response to high blood glucose

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5
Q

Insulin
All actions ultimately increase glycogen synthesis

A

(1) increases glucose transport into cells

(2) decreases cAMP → glycogen synthesis

(3) increase phosphoprotein phosphatase 1 (PP1)

(4) decrease glycogen synthase kinase 3 (GSK3)

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6
Q

Glucagon

A

Mobilize stored fuels

Decrease in blood glucose –> glucagon signals to hepatocytes –> production and restoration of glucose

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7
Q

Glucagon

Released from…

A

a-cells of pancreas in response to hypoglycemia

Glucagon binds GPCR on liver cells –> increase cAMP –> increase PKA –> Glycogen breakdown–> supplies glucose to tissues

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8
Q

Epinephrine

A

Mobilize stored fuels

Decrease in blood glucose –> epinephrine signals to (1) muscle cells to breakdown glycogen & (2) liver to make more glucose

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9
Q

Epinephrine

Released in response to ..

A

Stress

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10
Q

Epinephrine

Muscle

A

Epinephrine binds B-adrenergic receptors → increase cAMP → increase PKA → glycogen breakdown → glucose monomers into glycolysis → generate ATP

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11
Q

Epinephrine

Liver: direct v. indirect

A

D: epinephrine bind a- & B- andrenergic receptors –> increase Ca++, increase cAMP –> glycogen degradation

I: promotes release of glucagon from pancreas

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12
Q

Cortisol

A

Signals stress, including low blood glucose (counterbalance insulin)

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13
Q

Cortisol acts on..

A

Adipose: increase release of fatty acids from TAG –> FAs are fuel & glycerol for gluconeogenesis

Muscle: breakdown of muscle proteins –> amino acids for gluconeogenesis

Liver: stim gluconeogenesis –> glucose stored as glycogen or exported to tissues for fuel

Pancreas: Decrease insulin, increase glucagon

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14
Q

Liver: Glycogen metabolism is controlled by

A

Insulin & glucagon (acting in opposition)

Synth by pancreas in response to conc. of glucose in blood

Increase glucose (fed) –> increase insulin, decrease glucagon

Decrease glucose (fasted) –> decrease insulin, increase glucagon

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15
Q

Muscle

control is exerted by…

A

Insulin & Epinephrine

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16
Q

Increase blood glucose

A
  1. Glucose binds GLUT2 –> glucose enters cell –> phosphorylated to G6P (now trapped in cell) –> citric acid cycle –> oxidative phosphorylation –> increase in ATP –> ATP closes ATP-gated K+ channels –> decrease K+ efflux –> depolarization –> open Ca++ channels –> increase Ca++ w/in cell –> insulin exocytosis
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17
Q

Feedback loop –> limits insulin relase

A

Insulin lowers blood glucose by stimulating glucose uptake by tissues

Reduced blood glucose detected by B-cells

Less glucose –> slows down cascade –> decrease in signal to release insulin (through glucokinase rxn)

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18
Q

Sulfonylurea drugs

Use:
MOA:

A

U: oral medication for type II diabetes

M: binds to & closes K+ channels –> stim insulin release

19
Q

Regulation of glycogen phosphoylase

Function
Regulated

A

F: breaks down glycogen –> glucose 1-phosphate

Catalyze phosphoolysis of glycogen –> bound cleavage by substitution of a phosphate

R: hormonally (phosphorylation/dephosphorylation) & allosterically

20
Q

Hormonal regulation of glycogen phosphorylase

A

Phosphorylation –> activates glycogen phosphorylase (glycogen breakdown)

PKA activated –> phosphorylates phosphorylase kinase making more active –> phosphoylation of glycogen phosphoylase –> breakdown glycogen–> GLUCOSE

21
Q

Glucagon (liver) & epinephrine (muscle)

A

Increase cAMP –> increase PKA–> increases this process

During vigorous muscular activity –> epinephrine increases phosphorylation

22
Q

Hormonal regulation of Glycogen phosphorylase

Dephosphoylation

A

Inactivates phosphorylase kinase & glycogen phosphorylase

Insulin → PP1 → dephosphorylates & inactivates phosphorylase kinase & glycogen phosphorylase → glycogen synthesis

Predominates in resting muscle

23
Q

Calcium influence on Glycogen phosphorylase

A

Acts synergistically w/ hormones to stimulate glycogen breakdown

24
Q

Calcium influence on Glycogen phosphorylase

Increase calcium

A

–>Increase phosphorylase kinase → increase glycogen breakdown → glucose → glycolysis

Stimulates muscle contraction
○ Rate of glycogen breakdown linked to rate of muscle contraction
○ Glycogen breakdown provides fuel for glycolysis to generate more ATP required for muscle contraction

25
Q

In muscle

ATP & G6P

A

Inactivate glycogen phosphorylase

High ATP = high G6P → don’t need to breakdown glycogen → promote inactive form of glycogen phosphorylase

26
Q

In muscle

AMP

A

Activates glycogen phosphorylase

Breakdown ATP → AMP → signals need to fuel → promote glycogen breakdown

27
Q

In Liver

Glucose

A

Inactivates glycogen phosphorylase

			○ High glucose = don’t need more glucose

Increase energy, increase blood glucose (fed state), inhibit glycogen breakdown

28
Q

Glucose 6 phosphate (G6P)

a. in muscle
b. in liver

A

G1P (end product of glycogen phosphorylase) → G6P

a. G6P –> glycolysis
E to support muscle contract

b. G6P –> glucose + P –> blood
Dephosphoylate glucose –> allows to exit hepatocyte

Muscle & adipose do not have G6P, therefore do not contribute glucose to the blood

29
Q

Regulation of PP1

A

“PP1c is protective from glycogen breakdown”

Function: dephosphorylates & inactivates glycogen phosphorylase a & phosphorylase kinase

30
Q

Regulation of PP1 in the muscle

A

Catalytic subunit PP1c is active when bound to glycogen at glycogen binding (GM) subunit

Regulated by phosphorylation of GM

31
Q

Regulation of PP1 in the liver

A

PP1 bound to glycogen through GL

GL not controlled via phosphorylation → binds phosphorylase a → both T & R strongly bind PP1

R-form: active
T-form: inactive

32
Q

In the muscle

Insulin regulation of PP1

A

Insulin-stimulated protein kinase → GM subunit phosphorylated once → active PP1c → decreased phosphorylation → glycogen synthesis

33
Q

In the muscle

Epinephrine regulation of PP1

A

Stimulate PKA → GM subunit phosphorylated twice → inactive PP1c → increased phosphorylation → glycogen breakdown (active glycogen phosphorylase)

34
Q

GL R-form

A

Active

Phosphoryl not accessible → sequesters PP1

35
Q

GL T-Form

A

Inactive

Phosphoryl groups accessible to PP1 hydrolysis

Conformational change → T form → phosphorylation sites accessible → PP1 dephosphorylated → phosphorylase B → PPI & glycogen can dissociate

High glucose levels –> this is favored

36
Q

In the liver GL’s allosteric effector

A

Independent of insulin –> therefore the cell can rapidly response to changes in blood glucose rather then waiting for insulin

37
Q

PP1

A

dephosphorylates & activates glycogen synthase

In the liver, can dephosphorylate after G6P binds to allosteric site on glycogen synthase (better substrate for dephosphorylation)

38
Q

GSK3

A

Phosphorylates & inactivates glycogen synthase

Casein kinase II (CKII) phosphorylates GSK3 → inactivation of glycogen synthase

39
Q

AMPK

A

Inactivates glycogen synthase

Increase AMP (metabolic stress) → inhibit glycogen synthase

40
Q

Insulin

A

Activates glycogen synthase

Promotes PP1; Inactivates GSK3

41
Q

Epinephrine

A

Increases phosphorylation & inactivates glycogen synthase in the muscle

PKA → P1 & P2-GM → inactivate PP1 → decrease glycogen synthesis

42
Q

Von Gierke disease
(glycogen storage type I)

A

AR

Glucose 6-phosphatase deficiency

  • Inadequate conversion of G6-P → glucose in the liver
  • G6P cannot be dephosphorylated → released into the blood → pt requires supply of dietary glucose
43
Q
A

GEMS (20 decks)

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