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FOO > ATP PRODUCTION FROM NUTRIENTS > Flashcards

ATP PRODUCTION FROM NUTRIENTS Flashcards

1
Q

ANABOLISM VS CATABOLISM: WHICH ONE IS REDUCTIVE AND WHICH ONE IS OXIDATIVE REACTION AND WHAT DOES THAT MEAN’

A

ANABOLISM IS REDUCTIVE; ELECTREONS AND H+ ARE GAINED

CATABOLISM IS OXIDATIVE; RELEASE OF ELECTRONS AND H+

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2
Q

WHAT ARE THE MAIN ELECTRON CARRIERS FOR OXIDATIVE PROCESSES?

A

NAD+, NADP+, FAD+

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3
Q

OXIDATION OF WHICH MOLECULES GIVES DRIVE TO MAKE ATP IN THE MITOCHONDRIA?

A

NADH and FDH2

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4
Q

DOES CATABOLISM USE OR PRODUCE ATP?

A

IT PRODUCES ATP

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5
Q

3 CATABOLIC REACTIONS:

A

GLYCOLYSIS, BETA-OXIDATION, AMINO ACID CATABOLISM

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6
Q

WHICH METABOLITES DO ALL METABOLIC REACTIONS CONVERGE TO:

A

PYRUVATE AND ACETYL-CoA

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7
Q

WHAT IS PRODUCED FROM THE METABOLITES (ACETYL CoA) FROM THE END OF CATABOLIC REACTIONS?

A

NADH AND FADH2

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8
Q

WHAT IS THE MAIN SITE OF THE NADH AND FADH2 PRODUCTION?

A

THE CITRIC ACID CYCLE, LOCATED IN THE MATRIX OF THE MITOCHONDRIA

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9
Q

CATABOLIC PROCESSES MAKE MINORITY OR MAJORITY OF ATP ENERGY IN CELLS?

A

MINORITY

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10
Q

WHICH REACTION DOES THE MOST ATP COME FROM?

A

OXIDATIVE PHOSPHORYLATION

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11
Q

WHICH CELLS HAVE NO MITOCHONDRIA?

A

ERYTHROCYTES

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12
Q

HOW MANY MITOCHONDRIA ARE THERE IN THE CYTOPLASM OF EACH CELL?

A

CCA 2000

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13
Q

WHAT PERCENTAGE OF THE CELL VOLUME DO MITOCHONDRIA OCCUPY?

A

25%

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14
Q

EXAMPLES OF CELLS THAT HAVE A LOT OF MITOCHONDRIA BECAUSE OF HIGH ENERGY DEMAND?

A

LIVER, MUSCLE, SPERM CELLS, OOCYTE (MORE THAN 300 000)

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15
Q

WHAT ARE CRISTAE:

A

FOLDINGS ON INNER (OUT OF THE TWO) MITOCHONDRIAL MEMBRANE. THAT’S WHERE ATP IS LOCATED.

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16
Q

WHAT ARE THE 2 STEPS OF OXIDATIVE PHOSPHORYLATION AND THEIR BRIEF EXPLANATIONS:

A

1) THE CITRIC ACID CYCLE; PROVIDES A LOT OF NADH, FADH2 AND NADPH MOLECULES AND THESE ELECTRON CARRIERS WILL BE OXIDIZED BY DIFFERENT COMPONENTS OF THE INNER MEMBRANE
2) THE PHOSPHORYLATION; ATP WILL BE FORMED BY ADDING A PHOSPHATE TO THE ADP MOLECULE (DONE BY THE ATP SYNTHASE); ADP is phosphorylated to ATP by using the electrochemical gradient established by the redox reactions of the electron transport chain.

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17
Q

WHERE IS NADH PRODUCED AND AS A RESULT OF WHICH PROCESS?

A

IN THE CELL CYTOPLASM, GLUCOSE DEGRADATION

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18
Q

¸HOW ARE NADH AND FADH2 GENERATED IN THE MITOCHONDRIA?

A

BY FATTY ACID OXIDATION AND ENTRY OF ACETYL CoA IN THE CITRIC ACID CYCLE

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19
Q

WHERE IS THE NEWLY SYNTHESIZED ATP FIRST RELEASED TO?

A

MITOCHONDRIAL MATRIX

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20
Q

WHICH ANTIPORT MOVES ATP FROM THE MATRIX INTO THE CYTOSOL AND WHAT IS TAKEN IN EXCHANGE?

A

ADENINE NUCLEOTIDE TRANSLOCASE, ADP TAKEN INTO THE MATRIX

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21
Q

WHICH SYMPORT MOVES PHOSPHATE INTO THE MATRIX TO ENABLE THE ATP SYNTHESIS AND WHAT DOES IT BRING ALONGSIDE PHOSPHATE?

A

PHOSPHATE TRANSLOCASE, A PROTON

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22
Q

WHERE DOES GLYCOLYSIS OCCUR?

A

CYTOPLASM OF THE CELL

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23
Q

FOR WHICH CELLS IS GLYCOLYSIS THE ONLY WAY TO MAKE ATP?

A

ERYTHROCYTES

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24
Q

HOW MANY ATP MOLECULES ARE PRODUCED AT THE END OF GLYCOLYSIS?

A

2 (ACTUALLY 4, BUT 2 ARE USED DURING THE PROCESS)

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25
Q

WHAT MOLECULE IS THE START AND WHAT MOLECULE IS THE END OF GLYCOLYSIS AND WHAT HAPPENS TO IT?

A

START IS GLUCOSE, END PRODUCT IS PYRUVATE WHICH GOES INTO THE CITRIC ACID CYCLE FOR MORE NADH PRODUCTION.

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26
Q

RBC CAN CONVERT PYRUVATE INTO WHAT AND WHAT KIND OF CHANGE IS IT?

A

LACTATE, REVERSIBLE (GLUCONEOGENESIS)

27
Q

WHAT ARE THE MAIN ENZYMES IN THE GLYCOLYSIS PATHWAYS?

A

HEXOKINASE, PHOSPHOFRUCTO KINASE 1 AND THE PYRUVATE KINASE

28
Q

WHAT IS THE HEXOKINASE CALLED IN THE LIVER?

A

GLUCOKINASE

29
Q

GLYCOLYSIS CAN SCHEMATICALLY BE DIVIDED INTO 2 PARTS:

A

1) INVESTMENT OF ENERGY; ATP USED

2) ATP AND NADH ARE PRODUCED

30
Q

WHAT ARE KINASES?

A

ENZYMES THAT PHOSPHORYLATE THEIR SUBSTRATES

31
Q

STEPS IN PART 1 OF GLYCOLYSIS:

A
  • GLUCOSE PHOSPHORYLATED TO GLUCOSE-6-PHOSPHATE BY HEXOKINASE (IRREVERSIBLE, USES ATP)
  • G6P CONVERTED INTO FRUCTOSE-6-P BY ISOMERASE (REVERSIBLE)
  • F6P PHOSPHORYLATED TO FRUCTOSE 1,6 BISPHOSPHATE (F-1,6-bP) BY PHOSPHOFRUCTO KINASE (PFK) (IRRIVERSIBLE, USES ATP)
32
Q

WHY IS GLUCOSE CONVERTED INTO G6P?

A

BECAUSE G6P CAN’T DIFFUSE ACROSS THE MEMBRANE BILAYER OF THE CELL BECAUSE OF THE PHOSPHATE GROUP. ALSO, THE REACTION DECREASES THE CONCENTRATION OF FREE GLUCOSE, FAVOURING ADDITIONAL IMPORT OF THE MOLECULE

33
Q

WHAT IS THE INVERSE MEASURE OF ENZYME AFFINITY?

A

MICHAELIS CONSTANT, Km

34
Q

WHAT ARE THE DIFFERENCES BETWEEN ISOFORMS OF HEXOKINASE?

A

THEY DIFFER BY THEIR TISSUE EXPRESSION AND TYPE OF GLUCOSE TRANSPORTERS THEY HAVE

35
Q

WHAT ARE THE CHARACTERISTIC OF HEXOKINASE 1?

A

IT IS EXPRESSED EVERYWHERE, INCLUDING THE BRAIN AND IT HAS VERY HIGH AFFINITY FOR GLUCOSE, INHIBITED BY G6B

36
Q

WHAT ARE THE CHARACTERISTICS OF HEXOKINASE 2?

A

IT IS EXPRESSED IN INSULIN SENSITIVE TISSUES (ADIPOSE TISSUE, SKELETAL MUSCLE, HEART) + ALSO HIGHLY EXPRESSED IN CANCER CELLS. LOWER GLUCOSE AFFINITY THAN HK1, INHIBITED BY G6P

37
Q

WHAT ARE THE CHARACTERISTICS OF HK4?

A

EXPRESSED IN LIVER AND CALLED GLUCOKINASE, AND IT HAS A LOW AFFINITY FOR GUCOSE

38
Q

HOW IS NADH FORMED IN PART 2 OF GLYCOLYSIS?

A

FRUCTOSE 6 PHOSPHATE WILL BE BROKEN DOWN (BY ALDOLASE) AND IT WILL GIVE TO MOLECULES OF GLYCERALDEHYDE 3 PHOSPHATE (G3P). EACH G3P MOLECULE WILL GIVE RISE TO ONE NADH.

39
Q

WHAT IS THE FIRST METABOLITE PRODUCED IN GLUCONEOGENESIS PATHWAY?

A

PHOSPHENOLPYRUVATE (PEP)

40
Q

WHAT IS THE LAST STEP OF GLYCOLYSIS?

A

PEP IS CONVERTED INTO PYRUVATE BY THE PYRUVATE KINASE (IRREVERSIBLE)

41
Q

WHAT STIMULATES AND WHAT INHIBITS PYRUVATE KINASE?

A

STIMULATION: PEP, FRUCTOSE 1,6 BIPHOSPHATE
INHIBITION: HIGH LEVELS OF ATP

42
Q

OVERALL, WHAT IS PRODUCED DURING GLYCOLYSIS?

A

2 MOLECULES OF PYRUVATE, 4 MOLECULES OF ATP (BUT 2 ARE CONSUMED DURING THE PROCESS), 2 NADH (WILL BE TRANSPORTED TO MITOCHONDRIA TO MAKE MORE ATP)

43
Q

WHAT ARE THE POSSIBLE OPTIONS FOR THE FUTURE OF THE PYRUVATE PRODUCED DURING GLYCOLYSIS?

A
  • IN MOST CELLS IT IS FURTHER CONVERTED INTO ACETYL CoA TO PRODUCE MORE ELECTRON CARRIERS THAT WILL BE USED TO MAKE MORE ATP IN THE MITOCHONDRIA
  • CAN BE CONVERTED INTO LACTATE BY LACTATE DEHYDROGENASE (ESP IN RBC) EITHER TO PREPARE CELLS FOR THE OPPOSITE PATHWAY, GLUCONEOGENESIS, AS LACTATE IS PRECURSOR FOR GLUCOSE PRODUCTION OR TO REGENERATE NAD+ MOLECULES IF NEEDED
44
Q

WHAT IS THE ENTRY POINT IN THE GLYCOLYSIS PATHWAY FOR FRUCTOSE?

A

IT IS CONVERTED INTO FRUCTOSE 6 PHOSPHATE AND THE PATHWAY CONTINUES FROM THERE

45
Q

WHAT WILL HAPPEN TO THE GLYCOLYSIS PATHWAY IF LEVELS OF FRUCTOSE THAT ARE INGESTED ARE VERY HIGH, E.G. FROM A FRUCTOSE SYRUP?

A

FRUCTOSE WILL BYPASS THE FRUCTOSE 1,6 BIPOSPHATE STEP, AND THE PYRVATE KINASE FROM THE LAST STEP OF THE PATHWAY WON’T BE FULLY ACTIVATED, SO THE GLUCOSE BREAKDOWN WILL BE SLOWER AND PLASMA LEVELS HIGHER FOR LONGER

46
Q

HOW DO PYRUVATE AND NADH ENETR THE MITOCHONDRIA?

A

NADH CAN CROSS THE MITOCHONDRIAL MEMBRANE BUT PYRUVATE NEEDS A TRANSPORTER

47
Q

DO PHOSPHORYLATIONS USUALLY ACTIVATE OR DEACTIVATE ENZYMES?

48
Q

WHAT HAPPENS TO PYRUVATE INSIDE MITOCHONDRIA?

A

IT IS DECARBOXYLATED AND OXIDIZED BY THE PDH COMPLEX (THE PYRUVATE DEHYDROGENASE) TO GIVE 1 MOLECULE OF ACETYL CoA

49
Q

WHERE DOES THE NAME ‘CITRIC ACID CYCLE’ COME FROM?

A

BECAUSE THE FIRST STEP OF THE CYCLE IS CONVERSION OF ACETYL CoA INTO CITRIC ACID BY THE CITRATE SYNTHASE

50
Q

WHAT IS PRODUCED IN THE CITRIC ACID CYCLE AND WHAT HAPPENS WITH THE PRODUCTS?

A

NADH AND FADH2 MOLECULES WHICH WILL GO AND BE USED IN THE ELECTRON TRANSPORTER CHAIN TO PRODUCE ATP

51
Q

WHEN SAYING THAT THE CITRIC ACID CYCLE IS ANAPLEROTIC, WHAT DOES THAT MEAN?

A

THAT IT SUPPLIES INTERMEDIATES OR PRECURSOR MOLECULES TO PATHWAYS

52
Q

IS MORE ACETYL CoA PRODUCED FROM GLUCOSE OR FATTY ACIDS?

A

FATTY ACIDS

53
Q

WHAT IS THE NAME OF THE PROCESS WHICH PROVIDES ACETYL CoA FROM FATTY ACIDS AND WHERE DOES IT OCCUR?

A

BETA-OXIDATION, IN THE MITOCHONDRIA

54
Q

GLUCOGENIC VS KETOGENIC AMINO ACIDS?

A

GLUCOGENIC: PRODUCE INTERMEDIATES IN THE GLYCOLYSIS PATHWAY
KETOGENIC: PRODUCE INTERMEDIATES OF ACETYL CoA

55
Q

ROLE OF AMINO ACID ALANINE IN STARVATION?

A

ALANINE IS ONE OF THE MAIN ENDOGENOUS PRECURSORS FOR BODY TO PRODUCE GLUCOSE AFTER A FASTING PERIOD OR DURING STARVATION, AS IT CAN BE CONVERTED INTO PYRUVATE

56
Q

DO PROTEINS HAVE ANAPLEROTIC PROPERTIES?

A

YES (THEY CAN FEED THE CITRIC ACID CYCLE)

57
Q

WHAT IS THE POTENTIALLY TOXIC (FOR THE BRAIN) PRODUCT OF AMINO ACID DEGRADATION?

A

AMMONIA, NH3

58
Q

HOW IS AMMONIA DEALT WITH IN THE BODY?

A

VIA THE UREA CYCLE THAT HAPPENS IN THE LIVER, BUT THE FINAL PRODUCT (UREA) WILL BE EXCRETED BY THE KIDNEYS

59
Q

WHY IS UREA DANGEROUS?

A

BECAUSE IT CAN EASILY CROSS THE BLOOD BRAIN BARRIER AND IT IS AN INHIBITOR OF THE CITRIC ACID CYCLE SO IT IMPAIRS ATP PRODUCTION?

60
Q

WHAT PERCENTAGE OF THE WHOLE BODY ENERGY SPENT/ NEEDED IS ATTRIBUTABLE TO THE CNS?

61
Q

WHICH TISSUES CAN’T USE FATTY ACIDS TO PRODUCE ATP?

A

BRAIN AND ERYTHROCYTES

62
Q

WHICH SUBSTANCES CAN BE USED BY ALL TISSUES FOR ATP PRODUCTION?

A

GLUCOSE AND AMINO ACIDS

63
Q

WHAT IS THE SITE OF OXIDATIVE PHOSPHORYLATION?

A

ELECTRON TRANSPORT CHAIN

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