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Medical Biochemistry Final > Glycolysis and TCA Cycle > Flashcards

Glycolysis and TCA Cycle Flashcards

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USMLE® Step 1 flashcards
1
Q

3 Pathways Glucose-6-P is used in

A

Gluconeogenesis
Glycolysis
PPP

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2
Q

Glucose Transporters

A

Transport via conformational change

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3
Q

Hexokinase vs Glucokinase

A

Glucokinase: Km = 10 mM, NOT inhibited by glucose 6-phosphate. Present in liver and in pancreas b cells.

Hexokinase: Km= 0.2 mM, inhibited by glucose 6-phosphate. Present in most cells.

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4
Q

3 Regulatory Steps of Glycolysis

A

(+) Insulin ; (-) Glucagon

Hexokinase: inhibited by glucose-6-phosphate; least important regulated step

PFK-1: most important regulatory step; requires ATP; committing step; ** UNIQUE to Glycolysis**

Pyruvate Kinase

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5
Q

Glucose-6-P

A

Adding the phosphate traps the glucose in the cell

** inhibits Hexokinase (most tissues)

** does NOT inhibit Glucokinase (liver): enables glycogen synthesis when glucose is abundant

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6
Q

Glycolysis: Net Rxn

A

2 Pyruvate + 2 ATP + 2 NADH

Total of 4 ATP, however 2 used early on-> net of 2 ATP

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7
Q

Anaerobic Glycolysis

A

Occurs when: low O2, when respiration process is impaired (pyruvate dehydrogenase)

Pyruvate is reduced to lactate, regenerating NAD+ to keep the glycolytic pathway going for minimal ATP production

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8
Q

Hexokinase

A
  • present in all tissues
  • provides glucose-6-P for production of ATP when tissue [glucose] is low
    • inhibited by it’s product (feedback inhibition)
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9
Q

Glucokinase

A
  • LIVER enzyme
  • glucose sensor: functions best when [glucose] is high
  • High Km, high Vmax: allows liver to effectively remove glucose delivered by portal blood
    • regulated by insulin
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10
Q

GKRP

A

Glucokinase Regulatory Protein (liver)

  • regulates glucokinase; reversibly binds GK and translocates to nucleus, inhibiting cycle
  • in presence of fructose-6P, GK moved to nucleus and bound tightly by GKRP
  • when blood glucose is high, GK renters cytoplasm and catalyzes synthesis of G-6P
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11
Q

PFK-1

A

Principal site of regulation of glycolysis

Activators:

  • AMP: signifies low energy charge; stimulates glycolysis at PFK1
  • F-2,6,BP: signifies high blood [glucose]

Inhibitors:

  • ATP: high energy charge
  • Citrate
  • H+ (lactate)
  • FA: indicators of adequate nutrition
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12
Q

Pyruvate Kinase

A

Regulatory step in glycolysis

Activator: F-1,6-BP (“feed-forward”)

Inhibitors:

  • ATP: high energy charge
  • Alanine
  • Hormonal: activation of protein kinase A
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13
Q

Fructose 2,6-bisphosphate synthesis is stimulated by

A

insulin

  • insluin signals the well-fed state and stimulates glycolysis, primarily by enhancing PFK-2 catalyzed synthesis of F-2,6-BP, an allosteric activator of PFK-1
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14
Q

Maturity onset of diabetes of the young (Type II)

A

caused by mutations that decrease glucokinase activity

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15
Q

Arsenic poisioning

A

Arsenic resembles Pi and competes with Pi as a substrate for glyceraldehyde 3-P dehydrogenase; less ATP generated as a result

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16
Q

Pyruvate Dehydrogenase Deficiency

A

second most common cause of hemolytic anemia

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17
Q

Lactic Acidosis

A

In low O2 conditions, anaerobic glycolysis serves as a backup and generates ATP when ETC is not possible; LACTIC ACID created decreases blood pH to dangerous levels–> requires Cori cycle to uptake lactate from the blood by liver followed by gluconeogenesis

18
Q

The Cori Cycle

A

Lactate produced in glycolysis during muscle exertion is transported to the liver for resynthesis of glucose by gluconeogenesis

19
Q

Fructose Metabolism (liver)

A
  • enters lower in glycolysis cycle
  • ** bypasses regulation of PFK**
  • does not stimulate the satiety-promotion substance leptin (you don’t feel full)
20
Q

3 Stages of Cellular Respiration

A

1) Carbon from AA, CHO, and Lipids -> Acetyl CoA
2) TCA: oxidation of Carbon to CO2
3) ETC: reduced electron carriers are reoxidized; coupled to ATP synthesis; CHEMIOSMOTIC NOT substrate level phosphorylation

21
Q

Pyruvate Dehydrogenase Complex Net Rxn

A

pyruvate -> AcetylCoA + NADH + CO2
IRREVERSIBLE: Acetyl COA CANNOT regenerate glucose (no going backwards)

Pyruvate shuttled into mitochondrial matrix for rxn

22
Q

Pyruvate Dehydrogenase Complex Enzymes

A
  • decarboxylase : lose C (as CO2)
  • transacetylase: CoA -> Acetyl CoA
  • dehydrogenase: NAD+ -> NADH
23
Q

E1: pyruvate dehydrogenase/decarboxylase: PDC

A

catalyzes pyruvate to acetyl (releases CO2)

COFACTOR: thiamine pyrophosphate (TPP, Vitamin B1) -> no thiamine = lactic acidosis

24
Q

E2: dihydrolipoyl transacetylase: PDC

A

attaches CoA to acetyl

COFACTOR: lipoic acid & coenzyme A

25
Q

E3: dihydrolipoyl dehydrogenase: PDC

A

reduces NAD+ to NADH

COFACTOR: NAD+ & FAD

26
Q

Pyruvate Dehydrogenase

A
  • Active form NOT P
  • when high ATP, phosphorylated to deactivate (occurs when high NADH and acetylCoA)

dephosphorylation occurs when high Mg and Ca

27
Q

Deficiency in E1 Component PDH

E1: pyruvate dehydrogenase

A

congenital lactic acidosis

- pyruvate can’t be converted into acetylCoA and thus is shunted to lactic acid; fix with diet and thiamine supplement

28
Q

Arsenic Poisoning PDC

A

inhibits PDC

29
Q

Isocitrate dehydrogenase mutation

A

defect in gene encoding TCA cycle; leads to cancers (i.e. glioblastomas)

30
Q

Sites for TCA Control

A
  • isocitrate dehydrogenase
  • a-ketoglutarate dehydrogenase
  • malate dehydrogenase
  • citrate synthesis
31
Q

Glycolysis control vs. TCA control

A

Glycolysis Control: kinase rxns

TCA Control: Dehydrogenase rxns

32
Q

TCA Net Rxn

A

(1 GTP + 3 NADH + 1 FADH2) x 2 (because 2 acetylCoA/glucose)

Total: 2 GTP + 6 NADH + 2 FADH2

33
Q

Complete Oxidation of Glucose to CO2

A

36 ATP

-FA oxidation produces less energy?

34
Q

Conversion of pyruvate -> AcetylCoA and CO2 requires

A

Lipoic Acid

35
Q

Insulin vs Glucagon P

A

Insulin Dephosphorylates

Glucagon Phosphorylates

36
Q

PFK II

A

2 Domains: Kinase; Phosphatase

Fructose-6-P -> Fructose-2,6-BiP Stimulates PFK 1

37
Q

Fructose-2,6-Bisphosphatase

A

Fructose-2,6-Bisphosphate -> Fructose-6-Phosphate inhibits PFK1 and glucokinase

38
Q

Glucagon/Insulin PFKII

A

Glucagon Ps: inactivating PFK II ; activating F26BiPase

Insulin DePs: activating PFK II ; inactivating F26BiPase

39
Q

Most powerful regulator of PFK I

A

Fructose-2,6-BisP

- made by PFK II from F6P and stimulates PFK I

40
Q

Fed State

A

Blood glucose levels high -> insulin secretion -> promotes:

  • glycolysis
  • glycogenesis
  • lipogenesis
  • protein synthesis
41
Q

Fasting State

A

Blood glucose levels fall -> glucagon secretion -> promotes:

  • glycogenolysis
  • gluconeogenesis
  • lipolysis
  • ketogenesis

Medical Biochemistry Final (3 decks)

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