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NPLEX 1 > Biochemistry - Metabolism > Flashcards

Biochemistry - Metabolism Flashcards

1
Q

Pathways with metabolism site occurring in the mitochondria

A

Fatty acid oxidation (b-ox)
Acetyl CoA production
TCA cycle
Oxidative phosphorylation

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2
Q

Pathways with metabolism site occurring in the cytoplasm

A 
Glycolysis
FA synthesis
HMP shunt
Protein synthesis (RER)
Steroid synthesis (SER)
Cholesterol synthesis
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3
Q

Pathways where metabolism occurs in both mitochondria and cytoplasm

A

HUGs take TWO (i.e., both)
Heme synthesis
Urea cycle
Gluconeogenesis

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4
Q

Hexokinase

A

all tissues other than liver and b-cells of pancreas
Km and Vmax - lower (increased affinity, decreased capacity)
Not induced by insulin
Feedback inhibited by glucose 6-P

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5
Q

Glucokinase

A

Liver and b-cells in pancreas
Km and Vmas - higher (decreased affinity, increased capacity)
Induced by insulin
Feedback inhibited by fructose 6-P

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6
Q

First step of glycolysis?

A

Glucose to glucose 6-P

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7
Q

Where is glucose stored at low concentrations? high concentrations?

A

Tissue (low) and liver (high)

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8
Q

Rate limiting step of glycolysis?

A

PFK 1

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9
Q

What is occurring in the fed state during regulation by F2,6BP?

A

Increase insulin, decreased cAMP, decreased protein kinase A, decreased FBPase 2, increased PFK 2, more glycolysis, less gluconeogenesis

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10
Q

What is occurring in the fasting state during regulation by F2,6BP?

A

Increased glucagon, increased cAMP, increased protein kinase A, decreased PFK 2, increased FBPase 2, more gluconeogensis, less glycolysis

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11
Q

What are the enzymes in the pyruvate dehydrogenase complex? what are their cofactors?

A

Pyruvate dehydrogenase - TPP (B1 thiamin)
Dihydrolipoyl transacetylase - lipoate, CoA
Dihydrolipoyl dehygrogenase - NAD+, FAD

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12
Q

What happened when there is a pyruvate dehydrogenase complex deficiency?

A

Causes a buildup of pyruvate that gets shunted to lactate (via LDH) and alanine (via ALT)

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13
Q

What is the conversion that the pyruvate dehydrogenase complex is apart of?

A

Pyruvate -> Acetly CoA

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14
Q

How do you treat pyruvate dehydrogenase complex deficiency?

A

Increase intake of ketogenic nutrients (high fat content or increase lysine and leucine)

Lysine and Leucine - the onLy pureLy ketogenic amino acids

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15
Q

Findings in pyruvate dehydrogenase complex deficiency?

A

neurologic defects, lactic acidosis, Increased serum alanine starting in infancy

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16
Q

Pyruvate -> Acetyl CoA produces what products? and how many?

A

1 NADH

1 CO2

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17
Q

Where do TCA cycle rxns occur?

A

Mitochondria

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18
Q

What products and how many of each are produced by the TCA cycle?

A

3 NADH, 1FADH2, 2 CO2, 1 GTP per acetyl CoA = 10 ATP/acetyl CoA (2x everything per glucose)

19
Q

What substrates are in the Krebs cycle?

A

Citrate Is Kreb’s Starting Substrate For Making Oxaloacetate

Citrate
Isocitrate
alpha-Ketoglutarate
Succinyl-CoA
Succinate
Fumarate
Malate 
Oxaloacetate
20
Q

NADH electrons from glycolysis enter the mitochondria via what shuttle?

A

Malate-aspartate shuttle or glycerol 3-P shuttle

21
Q

How many reactions occur in the Kreb’s cycle?

A

8 reactions

22
Q

Where does the electron transport chain occur?

A

Inner membrane of the mitochondrion

23
Q

How many types of electron carriers comprise the ETC?

A 
4
FMN
Fe-S clusters
CoQ10
Cytochromes
24
Q

Which of the electron carriers in the ETC are mobile?

A

CoQ10 and Cytochrome C

25
Q

What occurs in Complex I: NADH Dehydrogenase of the ETC?

A

NADH transfers ions and electrons to FMN. The reduced FMNH2 forms, while NADH is deoxidized to NAD+, which returns to oxidative pathways such as TCA cycle oxidize more substrates

Within complex I, the electrons are transferred to the Fe-S clusters and then to CoQ10

26
Q

What occurs in Complex II: Succinate Dehydrogenase of the ETC?

A

Used when FADH2 is generated from the conversion of succinate -> fumarate in the TCA cycle
Electrons from FADH2 are transferred to CoQ10 to yield QH2
This complex has a lower energy level than Complex I so FADH2 enters at a lower energy level here then NADH in complex I

27
Q

What occurs in Complex III: Coenzyme Q10-Cytochrome c Reductase of the ETC?

A

The mobile carrier QH2 transfers electrons it has collected from NADH and FADH2 to an Fe-S cluster and then to cytochrome b, the first cytochrome in complex III

From cut b, the electron is transferred to an Fe-S cluster and then to cut c1 and tgeb ti cut c. Each time an Fe3+ ion accepts an electron, it is reduced to Fe2+ and then oxidized back to Fe3+ as the electron is passed on along the chain. Cyt c is another mobile carrier, it moves the electron from complex III to complex IV

28
Q

What occurs in Complex IV: Cytochrome c Oxidase of the ETC?

A

electrons are transferred from cytochrome c to cytochrome a, and then to cytochrome a3, the last cytochrome. In the final step of electron transport, electrons and hydrogen ions combine with oxygen (O2) to form water

4H+ + 4e- + O2 -> 2H20

29
Q

What enzyme converts pyruvate to oxaloacetate in gluconeogenesis? Where does this occur?

A

Pyruvate carboxylase

Occurs in the mitochondria

30
Q

What enzyme converts oxaloacetate to phosphoenolpyruvate (PEP)? Where does this occur?

A

PEP carboxykinase

Occurs in the cytosol

31
Q

What enzyme converts fructose-1,6-BP to fructose 6-P in gluconeogenesis? Where does this occur?

A

Fructose 1,6-Bisphosphatase

Occurs in the cytosol

32
Q

What enzyme converts Glucose 6-P to Glucose in gluconeogenesis? Where does this occur?

A

Glucose 6-phosphatase

33
Q

What organ does gluconeogensis primarily occur in?

A

Liver

34
Q

From what substrate to substrate is repeated in gluconeogenesis from glycolysis?

A

PEP to fructose 1,6-P

35
Q

Odd-chain vs even-chain FAs as a glucose source

A

odd chain FAs cab enter TCA cycle, undergo gluconeogenesis and serve as a glucose source

even chain FAs cannot produce new glucose, since they yield only acetyl CoA equivalents

36
Q

What tissue cannot participate in gluconeogenesis and why?

A

Muscle bc it lacks glucose 6-phosphatase

37
Q

What is the enzyme responsible for the oxidative reaction for the HMP shunt (pentose phosphate pathway)?

A

glucose 6-P dehydrogenase

38
Q

What does the HMP shunt provide a source of?

A

NADPH from abundantly available glucose 6-P and ribose for nucleotide synthesis and glycolytic intermediates

39
Q

Where does the HMP shunt occur?

A

Cytoplasm

40
Q

What is NADPH necessary for?

A

It keeps glutathione reduced, which in turn detoxifies free radicles and peroxides

41
Q

What does decreased NADPH in RBCs lead to?

A

Hemolytic anemia due to poor RBC defence against oxidizing agents

42
Q

Essential fructosuria

A

defect in fructokinase
autosomal recessive
benign, asxs since fructose is not trapped in the cells
fructose appears in blood and urine

43
Q

Fructose intolerance

A

hereditary deficiency of aldolase B
autosomal recessive
Fructose-1-P accumulates, causing a decrease in available phosphate, which results in inhibition of glycogenolysis and gluconeogenesis
Symptoms present following consumption of fruit, juice, or honey
Sxs: hypoglycemia, jaundice, cirrhosis, vomiting
Tx: decrease intake of both fructose and sucrose (glucose + fructose)

44
Q

Galactokinase Deficiency

A

Hereditary deficiency of galactokinase
Galactitol accumulates if galactose is present in diet
Relatively mild condition
autosomal recessive, metabolic dz
Sxs: galactose appears in blood and urine, infantile cataracts. May initially present as failure to track objects or to develop a social smile

NPLEX 1 (10 decks)

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