lecture 9 Flashcards

1
Q

sources of glucose to support life phases

A

1-absorptive
2-post absorptive
3-early starvation
4-intermediate
5-prolonged starvation

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2
Q

when is exogenous

A

absorptive

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3
Q

when is glycogen peaking

A

post absorptive

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4
Q

when is gluconeogenesis peaking

A

early to intermediate starvation

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5
Q

gluconeogenesis

A

is the synthesis precursor of glucose from non-carbohydrate precursors

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6
Q

glucose stores

A

are depleted during periods of starvation beyond a day

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7
Q

brain relies on glucose

A

120g/d for energy

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8
Q

glucose must be synthesized

A

from molecules other than carbs

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9
Q

pyruvate becomes

A

glucose

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10
Q

2 Pyruvate + 2NADH + 4ATP + 2 GTP + 6 H2O + 2H+

A

glucose + 2NAD + 4 ADP + 2 GDP + 6Pi

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11
Q

any molecule that can be converted to pyruvate

A

gluconeogenic

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12
Q

examples of glucogenic molecules

A

lactate, several amino acids, glycerol

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13
Q

reactions that overcome high negative free energy of irreversible glycolysis reactions

A

Glucose 6 phosphatase
Fructose 1,6 Bisphosphotase
Phosphoenol pyruvate carboxykinase
pyruvate carboxylase

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14
Q

enzymes in common btw glycolytic and glucogenic pathways

A

phosphoglucose isomerase
aldolase
trios phosphate isomerase
GAP dehydrogenase
phosphoglycerate mutase
enolase

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15
Q

irreversible glycolytic enzymes

A

hexokinase
phosphofructokinase
pyruvate kinase

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16
Q

gluconeogenesis enzymes

A

pyruvate carboxylase
phosphoenolpyruvate carboxykinase
Fructose 1,6-bisphosphatase
Glucose 6-phosphatase

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17
Q

pyruvate carboxylase

A

Metabolically irreversible
- Uses biotin as a cofactor
- Allosterically activated by acetyl-CoA
- Anaplerotic for the TCA cycle – replenishes OAA
- Takes place in mitochondria

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18
Q

Phosphoenolpyruvate carboxykinase (PEPCK)

A
  • Synthesis of PEPCK increases in fasting
  • Takes place in cytosol
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19
Q

pyruvate is

A

carboxylated in the mitochondria by pyruvate carboxylase

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20
Q

oxaloacetate

A

can’t pass out of mitochondria

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21
Q

what happens to OAA instead

A

it is converted to malate which is then converted to OAA in cytosol

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22
Q

where is oxaloacetate decarboxylated and phosphorylated

A

in the cytosol by phosphoenolpyruvate carboxykinase

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23
Q

Fructose 1,6-bisphosphatase (F1,6BPase)

A

A metabolically irreversible reaction

F1,6BPase is allosterically inhibited by AMP and fructose 2,6-bisphosphate (F2,6BP)

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24
Q

Glucose 6-phosphatase

A

Metabolically irreversible hydrolysis reaction
Glucose-6-phosphatase found only in liver and kidney (pancreas and small intestine)
Only those tissues can serve as source of glucose from gluconeogenesis.

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25
Q

Glucose 6-P is a precursor for

A

glycogen synthesis
glucose synthesis

26
Q

g6P is the starting spot for

A

pentose phosphate pathway

27
Q

glucose 6- phosphotase is present only in

A

tissues responsible for maintaining blood glucose levels in LIVER AND KIDNEY

28
Q

in liver

A

glucose 6-phosphatase is highly regulated

29
Q

it takes 6 ATP to make glucose

A

but only 2 are generate in glycolysis

30
Q

how many more ATP are needed to drive unfavorable gluconeogenesis pathway

A

4

31
Q

flux through pathway

A

is controlled at rate limiting steps

32
Q

rate determining steps are altered by several mechanisms

A
  1. Allosteric control
  2. Covalent modifications
  3. Substrate cycles - Futile cycles
  4. Genetic control - Enzyme concentrations
33
Q

high amp indicates

A

that energy charge is low and signals for need ATP

34
Q

high ATP and citrate

A

the energy charge is high and intermediates are abundant

35
Q

why do we care about AMP

A

prevents both pathways from operating together

36
Q

refer back to 18 and try to understand it later

A
37
Q

carl and gerty cori

A

Nobel prize in physiology and medicine 1947

38
Q

cori cycle

A

interaction of glycolysis and gluconeogenesis

39
Q

lactate from peripheral tissues

A

goes to liver and is made into glucose

40
Q

glucose can go

A

back to the peripheral tissues

41
Q

liver

A

uses lipid for energy

42
Q

placement of the liver in the circulation

A

first pass at removing nutrients absorbed from the intestine

43
Q

liver in circ

A

can make nutrients available to other major tissues

44
Q

liver participates in interconversions of all types of metabolic fuels

A

carbs, amino acids, fatty acids

45
Q

liver regulates

A

distribution of fuels and supplies fuel from its own reserves

46
Q

Pentose Phosphate Pathway

A

Hexose phosphate Shunt

47
Q

Production of NADPH

A

the pyridine nucleotide used for reductive biosynthesis
Fatty acids
Cholesterol
nucleic acids

48
Q

NADPH also important in

A

in elimination of oxygen radicals

49
Q

Formation of ribose 5-phosphate for ribonucleotides

A

RNA, DNA, certain coenzymes

50
Q

where in the body is pentose ribose pathway

A

Not in brain and muscle
Mammary glands, liver, adrenal glands, adipose

51
Q

enzymes of pentose phosphate pathway are

A

cytosolic

52
Q

2 stages of Pentose Phosphate
Pathway:

A

oxidative and non oxidative

53
Q

oxidative phase

A

production of 2 NADPH and ribulose-5-phosphate from glucose-6-phosphate

54
Q

Pentose Phosphate Pathway: Nonoxidative Phase

A

Disposes excess pentose phosphates by converting to glycolytic intermediates

55
Q

Series of C-C bond cleavage and formation reactions

A

Ribulose 5-P ->Ribose 5-P or Xylulose 5-P
2 Xylulose 5-P + Ribose 5-P ->2 Fructose 6-P + GAP

56
Q

Transketolase and transaldolase

A

catalyze the exchange of two- and three-carbon fragments between sugar phosphates

one substrate is an aldose, one substrate is a ketose

57
Q

NADPH functional roles biosynthetic pathways

A

FA synthesis (liver, adipose, mammary)
Cholesterol synthesis (liver)
Steroid hormone synthesis (adrenal, ovaries, testes)

58
Q

NADPH functional roles

A

Detoxification (Cytochrome P-450 System) – liver
Reduced glutathione as an antioxidant (RBC)
Generation of superoxide radicals (neutrophils): microbicidal activity

59
Q

regulation

A

occurs with G6P dehydrogenase
-First step
-Rate limiting
Allosteric Regulation
-Feedback inhibited by NADPH
enzyme induced by insulin

60
Q

role of NADPH in RBC

A

Production of superoxide
Hb-Fe2+-O2 -> Hb-Fe3+ + O2-.
Spontaneous rxn, 1% per hour

61
Q

Both O2-. & H2O2 can produce

A

produce reactive free radical species, damage cell membranes, and cause hemolysis