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Glycolysis/Gluconeogenesis (Bikman) > Glycolysis > Flashcards

Glycolysis Flashcards

1
Q

Glucose uptake occurs from?

Glucose recovery occurs from?

A

uptake–>GI tract/gut

recovery–> kidneys

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2
Q

glucose is transported ____ the concentration gradient by ____ in epithelial cells of the gut and kidneys.

A

against the concentration gradient

by SGLTs (sodium-glucose symport)

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3
Q

what do SGLTs utilize as the energy source for glucose transport?

A

the sodium gradient, this is active transport.

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4
Q

A sodium free diet might cause?

A

disruption to SGLTs, so glucose would remain in the gut, causing the osmotic gradient to increase and cause diarrhea.

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5
Q

There are __ types of Glucose transporters (GLUTs).

Which GLUT is regulated by insulin? Found in what tissues?

A

13 total GLUTs.

GLUT-4 is insulin dependent, found in skeletal MM, Cardiac MM, and Adipocytes

(All other GLUTs are NOT regulated by insulin, and are found in RBCs, Brain, kidney, liver, intestines….)

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6
Q

glucose transporters move glucose ____ (up/down?) its concentration gradient. Is this active or passive?

A

Down its concentration gradient, Passive.

move glucose into and out of all cells in the body

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7
Q

Insulin is a peptide hormone that is synthesize by ______?

What is also produced with insulin that can determine if someone has type 1 diabetes?

A

pancreatic B cells.

C peptide is also produced with insulin.

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8
Q

What is the optimal blood glucose level?

A

75-110 mg/dl

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9
Q

insulin causes a ___ in blood glucose levels, via uptake in gut, recovery in kidneys, and release in the liver.

A

decrease

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10
Q

Muscles can uptake glucose without insulin by?

A

By muscle contraction, which signals GLUT4 to increase glucose uptake.

Both insulin and muscle contractions can increase GLUT4 activity=increase glucose uptake in skeletal muscle.

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11
Q

Insulin also regulates glucose clearance, which is?

Which insulin dependent tissue would the most glucose go to?

A

how glucose gets OUT of the cell (in adipose, cardiac MM and skeletal MM)

-Whatever tissue has the most mass, Skeletal MM

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12
Q

Two types of insulin “highs”?

A

acutely & chronically

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13
Q

True or False:

Insulin goes into the cell.

A

False, insulin binds to receptors on the cell membrane, then degrades.

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14
Q

When is insulin acutely high? (3 times….)

A
  • after a meal
  • when anticipating a meal
  • when you wake up (dawn phenomenon)
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15
Q

When would insulin levels be highest? (Breakfast, lunch, or dinner)

A

breakfast=highest insulin levels

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16
Q

The Dawn Phenomenon is associated a surge of which hormones?

A

Growth hormone and cortisol

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17
Q

Chronically high insulin is also called?

A

insulin resistance (pre-diabetes) or diabetes.

With chronically high insulin, if insulin is always high = diabetes.

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18
Q

The sympathetic nervous system and stress causes what to happen to insulin & glucagon ?

A

Sympathetic NS-

increases glucagon, decreases insulin.

(if you increase glucagon, you will have more glucose in your blood stream to be used as an energy source needed for fight-or-flight responses via sympathetic NS)

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19
Q

Parasympathetic nervous system and thinking about food/relaxation causes what to happen to insulin & glucagon ?

A

Para- Increases insulin, decreases glucagon.

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20
Q

Where would insulin and glucose go to first, second, and third?

(Liver ? Adipose? Skeletal MM? )

A

1st skeletal MM
2nd liver
3rd adipose

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21
Q

When insulin binds to muscles, what two events occur?

A
  • glucose uptake

- anabolism

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22
Q

when insulin binds to liver, what 3 events occur?

A
  • inhibition of ketogenesis
  • activation of lipogenesis
  • activation of glycogenesis
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23
Q

when insulin binds to adipose, what three events occur?

A
  • glucose uptake
  • activation of lipogenesis
  • activation of adipogenesis
24
Q

So overall, insulin reduces blood levels of what three things?

A

glucose
fats
ketones

^all reduced in blood by insulin because they are taken up into cells.

25
Q

What is the only hormone that promotes fat storage and inhibits fat use?

A

insulin
cant gain fat without insulin
(need functional pancreas)

26
Q

What counteracts insulin?

A

-Glucagon (mainly)

Also

  • Epinephrine/Norepinephrine
  • Catecholamines
  • Cortisol
  • Growth Hormone

^ these all do catabolism

27
Q

What is the primary regulator of insulin and glucagon release?

A

plasma glucose concentration

28
Q

Insulin effects muscles, liver, and adipose, while glucagon only effects?

A

liver and adipose

NOT muscles, because they lack receptors

29
Q

In the liver, glucagon has what effects?

A

tells liver to make glucose
out of anything available!

activates keteogensis,
activates glycogenolysis

catabolism^

30
Q

If you have a high blood glucose level, insulin will be ? Glucagon will be?

A

insulin- high
glucagon-low

with high blood glucose levels

31
Q

In adipose cells, glucagon will cause ?

A

lipolysis,

fat to break down (catabolism).

32
Q

Glucagon causes increase of blood levels of?

A
  • glucose
  • fat
  • ketones
33
Q

What are the end products of glycolysis?

A

2 ATP
2 NADH
2 Pyruvate

34
Q

Once glucose is in the cell, what is the fate?

A

glycolysis

35
Q

What are the three irreversible steps of glycolysis?

What are the starting and ending products of those three steps and the enzymes that catalyze them?

A

Step 1.
D-glucose –> glucose 6 P

via hexokinase (in Muscles) or glucokinase (in liver)

^^^ this step requires ATP, and commits glucose to metabolism within the cell, because g-6-p can’t escape cell

Step 3.
fructose 6 phosphate –> fructose 1-6 bisphosphate

via PFK-1
^^^ requires ATP

Step 9.
phosphoenolpyruvate –> pyruvate

via pyruvate kinase
^^ creates 2 ATP, second example of substrate level phosphorylation

36
Q

Skeletal muscles use glycolysis primarily for production of?

A

ATP, but they can store a limited amount as glycogen

37
Q

What are the two steps of glycolysis that include substrate level phosphorylation ?

What are the starting and ending products of those steps and the enzymes that catalyze them?

A

Step 6.
1,3 bisphosphoglyercate–>
3-phosphoglycerate

via phosphoglycercate kinase

Step 9.
phosphoenolpyruvate –> pyruvate

via pyruvate kinase

Both create two ATPs per 1 glucose

38
Q

Which step of glycolysis produces 2 NADHs with the addition of two organic phosphates ?

What are the starting and ending products of that step and the enzymes that catalyze it?

A

Step 5.
glyceraldehyde 3 phosphate
1,3 bisphoglycerate

via glyceraldehyde-3-phosphate dehydrogenase

39
Q

Where does glycolysis occur ?

Where does the pyruvate dehydrogenase reaction occur?

A

in cytosol

in mitochondria (inner matrix)

40
Q

What are the starting and end products of pyruvate dehydrogenase reaction?

A

2 pryuvate –>

2 acetyl-coA
2 NADH
2 ATP

41
Q

What inhibits the pyruvate dehydrogenase reaction?

A

-Acetyl-coA
-ATP
-NADH
^ which are the products

& the phosphorylation of pyruvate dehydrogenase kinase

all inhibit the pyruvate dehydrogenase reaction

42
Q

Dephosphorylation of pyruvate dehydrogenase phosphatase ___ the pyruvate dehydrogenase reaction.

A

Activates it.

43
Q

T or F:

The liver is capable of glucose catabolism and anabolism depending on hormonal and non-hormonal signals.

A

true

44
Q

Liver uses glycolysis primarily to convert glucose into ___ and ___, but can use glucose for its own energy is glucose levels are high.

A

glycogen and fat

45
Q

Non hormonal regulators of glycolysis in the liver?

A

ATP and AMP.

Also glucokinase because it has a high Km.

46
Q

In the liver,
if ATP is low, and/or AMP is high,
is glycolysis activated or deactivated?

A

activated

47
Q

What are the 2 hormonal regulators of glycolysis in the liver?

A
  • fructose 2,6 bisphosphate, stimulates PFK-1, even if ATP levels are high
  • pyruvate kinase phosphorylation/ dephosphorylation

(pyruvate kinase phosphorylation inhibits PK activity )

48
Q

Insulin represses or induces synthesis of GK, PFK-1, and PK in the liver?

Glucagon represses or induces synthesis of GK, PFK-1, and PK in the liver??

A

Insulin induces,

Glucagon represses

49
Q

insulin does what to PK?

A

dephosphorylates it!

PK must be dephosphorylated to be active

50
Q

Insulin inhibits fructose 2,6 biphosphatase, causing an ____ of fructose 2,6 bisPhosphatate.

A

increase, which in turn increases fructose 2,6 bisPhosphate (which activates PFK-1)

(insulin activates products of glycolysis)

51
Q

Glycolysis non hormonal regulators (3)

A

Glucokinase

phosphofructokinase-1

pyruvate kinase

(GK, PFK-1, PK)

52
Q

PFK-1 is activated by? (2 things)

deactivated by?

A

activated - AMP (cAMP) & fructose 2,6 bisphosphate

deactivated by ATP

53
Q

Pyruvate kinase activated by? (2)

deactivated by (3)?

A

activated by fructose 1,6 bisphosphate (the prod of step 3) and
dephosphorylation

deactivated by phosphorylation, ATP, Alaine

54
Q

What is significant about Fructose 2,6 bisphosphate ?

A

regulates glycolysis by

stimulating PFK-1, even if ATP levels are high

55
Q

What is the significance of fructose 1,6 bisphosphate (the product of step 3) in regards to pryuvate kinase?

A

it activates it pyruvate.

Glycolysis/Gluconeogenesis (Bikman) (2 decks)

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