lecture 9 Flashcards by Aneeka Phadnis

sources of glucose to support life phases

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

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when is exogenous

absorptive

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when is glycogen peaking

post absorptive

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when is gluconeogenesis peaking

early to intermediate starvation

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gluconeogenesis

is the synthesis precursor of glucose from non-carbohydrate precursors

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glucose stores

are depleted during periods of starvation beyond a day

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brain relies on glucose

120g/d for energy

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glucose must be synthesized

from molecules other than carbs

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pyruvate becomes

glucose

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

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

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any molecule that can be converted to pyruvate

gluconeogenic

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examples of glucogenic molecules

lactate, several amino acids, glycerol

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reactions that overcome high negative free energy of irreversible glycolysis reactions

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

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enzymes in common btw glycolytic and glucogenic pathways

phosphoglucose isomerase
aldolase
trios phosphate isomerase
GAP dehydrogenase
phosphoglycerate mutase
enolase

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irreversible glycolytic enzymes

hexokinase
phosphofructokinase
pyruvate kinase

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gluconeogenesis enzymes

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

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pyruvate carboxylase

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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Phosphoenolpyruvate carboxykinase (PEPCK)

Synthesis of PEPCK increases in fasting
Takes place in cytosol

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pyruvate is

carboxylated in the mitochondria by pyruvate carboxylase

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oxaloacetate

can’t pass out of mitochondria

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what happens to OAA instead

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

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where is oxaloacetate decarboxylated and phosphorylated

in the cytosol by phosphoenolpyruvate carboxykinase

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

A metabolically irreversible reaction

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

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Glucose 6-phosphatase

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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Glucose 6-P is a precursor for

glycogen synthesis glucose synthesis

g6P is the starting spot for

pentose phosphate pathway

glucose 6- phosphotase is present only in

tissues responsible for maintaining blood glucose levels in LIVER AND KIDNEY

in liver

glucose 6-phosphatase is highly regulated

it takes 6 ATP to make glucose

but only 2 are generate in glycolysis

how many more ATP are needed to drive unfavorable gluconeogenesis pathway

flux through pathway

is controlled at rate limiting steps

rate determining steps are altered by several mechanisms

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

high amp indicates

that energy charge is low and signals for need ATP

high ATP and citrate

the energy charge is high and intermediates are abundant

why do we care about AMP

prevents both pathways from operating together

refer back to 18 and try to understand it later

carl and gerty cori

Nobel prize in physiology and medicine 1947

cori cycle

interaction of glycolysis and gluconeogenesis

lactate from peripheral tissues

goes to liver and is made into glucose

glucose can go

back to the peripheral tissues

liver

uses lipid for energy

placement of the liver in the circulation

first pass at removing nutrients absorbed from the intestine

liver in circ

can make nutrients available to other major tissues

liver participates in interconversions of all types of metabolic fuels

carbs, amino acids, fatty acids

liver regulates

distribution of fuels and supplies fuel from its own reserves

Pentose Phosphate Pathway

Hexose phosphate Shunt

Production of NADPH

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

NADPH also important in

in elimination of oxygen radicals

Formation of ribose 5-phosphate for ribonucleotides

RNA, DNA, certain coenzymes

where in the body is pentose ribose pathway

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

enzymes of pentose phosphate pathway are

cytosolic

2 stages of Pentose Phosphate Pathway:

oxidative and non oxidative

oxidative phase

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

Pentose Phosphate Pathway: Nonoxidative Phase

Disposes excess pentose phosphates by converting to glycolytic intermediates

Series of C-C bond cleavage and formation reactions

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

Transketolase and transaldolase

catalyze the exchange of two- and three-carbon fragments between sugar phosphates one substrate is an aldose, one substrate is a ketose

NADPH functional roles biosynthetic pathways

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

NADPH functional roles

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

regulation

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

role of NADPH in RBC

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

Both O2-. & H2O2 can produce

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

lecture 9 Flashcards

(61 cards)