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Endocrine Midterm > Biochem > Flashcards

Biochem Flashcards

1
Q

Define and correctly use the following terms:

Anaerobic and aerobic glycolysis

A

Anaerobic glycolysis–>Lactate (fast 2 ATP)
Aerobic glycolysis–>Pyruvate–>CAC—>ETC (slow)

Differences: Speed and amount of ATP produced, lactate can be toxic (removed by gluconeogenesis)

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2
Q

Define and correctly use the following term:

Rate limiting enzyme

A

Controls the overall flux of the pathway and activity of the pathway, independent of substrate and product concentration

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3
Q

Define and correctly use the following term:

Allosteric and covalent regulation

A
  • Covalent regulation is via a +/- chemical bond…phosphorylation of an enzyme to reduce its activity (ex: glucagon on PFK-2)
  • Allosteric regulation is by binding reversibly an effector molecule at a site other than the protein’s active site (ex: NADH, acetyl CoA, ATP, and FA on PDH)
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4
Q

What tissues are dependent on glucose as their primary energy source? (3)

A
  • Red blood cells (anaerobic)
  • Active skeletal muscle (anaerobic short-term, aerobic long-term)
  • Brain
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5
Q

What are the key regulatory enzymes and committed steps in glycolysis? (3)

These enzymes catalyze reactions that are highly exergonic, and therefore, irreversible and rate-limiting.

A

Key enzymes:

  • Hexokinase & Glucokinase (liver, B-cells of pancreas, lower affinity)
  • Phosphofructokinase-1 (PFK-1): MOST IMPT, catalyzes the committed step
  • Pyruvate kinase (PK): final step of glycolysis–>lactate or acetyl-CoA
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6
Q

What are the key regulatory enzymes and committed steps in the citric acid cycle? (4)

A
  • Pyruvate dehydrogenase
  • Citrate synthase
  • Isocitrate dehydrogenase
  • Alpha-ketoglutarate dehydrogenase
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7
Q

What is the effect of fructose 2,6-bisphosphate (F-2,6-BP) on glycolysis?

A
  • Activator of PFK-1 (incr glycolysis)

- Produced by PFK-2

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8
Q

What is the effect of glucagon on glycolysis? What is this an example of?

Hint: released by pancreas when blood glucose is low

A 
Blocks glycolysis via cAMP-dep protein kinase-->
Phosphorylation of PFK-2-->
Decr PFK-2 activity-->
Decr F-2,6-BP-->
Decr PFK-1

Ex of COVALENT regulation

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9
Q

T/F:

ATP and NADH reduce the activity of both glycolysis and the CAC

A

TRUE!

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10
Q

Describe the effects of NAD+ on the activity of the citric acid cycle

A
  • CAC activity depends on the avail. of NAD+ (co-substrate for many of the dehydrogenases)
  • Amount of NAD+ is determined by the rate of NADH oxidation
  • NAD+ also activates PDH phosphatase
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11
Q

How does insulin promote glycolysis and the citric acid cycle?

(high glucose)

A 
Glycolysis:
Insulin reverses effects of glucagon by activating a protein phosphatase--> 
Dephosphorylates PFK-2-->
Incr PFK-2 activity-->
Incr PFK-1
CAC:
Activates PDH phosphatase-->
Dephos. PDH-->
Incr PDH activity-->
Incr production of acetyl-CoA from glucose, lactate, and alanine
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12
Q

Describe the effects of NADH, acetyl CoA, ATP, and FA on the activity of the citric acid cycle

A

*Allosterically inhibit PDH:

Stimulate PDH kinase–>
Phosphorylates PDH–>
Decr PDH activity

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13
Q

Citrate synthase activity is limited by avail. of what 2 substrates in the CAC?

A

-Acetyl-CoA and oxaloacetate

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14
Q

Accumulation of NADH inhibits what 2 enzymes in the CAC?

A
  • Isocitrate dehydrogenase

- Alpha-ketoglutarate dehydrogenase

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15
Q

ATP inhibits what 2 enzymes in the CAC?

A
  • Citrate synthase
  • Isocitrate dehydrogenase

(allosteric inhib)

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16
Q

Calcium activates what 3 enzymes in the CAC?

A
  • Isocitrate dehydrogenase

- Alpha-ketoglutarate dehydrogenaseq

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17
Q

How are glycolysis and the CAC linked?

A

PDH

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18
Q

Define and correctly use the following term:

Second messenger

A

cAMP

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19
Q

Define and correctly use the following term:

Reversible phosphorylation

A

Hormones (epi, glucagon, insulin) control reversible phosphorylation via cAMP

Ex: glycogen phosphorylase, and glycogen synthase

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20
Q

Define and correctly use the following term:

Fructose 2,6-bisphosphate

A
  • Synthesized by PFK-2/F-2,6-BPase bifunctional enzyme
  • PFK-2 catalyzes formation of F-2,6-BP
  • F-2,6BPase catabolizes F-2,6-BP
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21
Q

Define and correctly use the following term:

Reciprocal regulation

A

Interlocking mechanisms that ensure that separate pathways of synthesis and degradation do not operate at the same time

Ex: pyruvate carboxylase and pyruvate dehydrogenase in gluconeogenesis

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22
Q

What are the key enzymes of glycogen degradation (glycogenolysis)? (5)

A
  • Glycogen phosphorylase
  • Transferase and debranching enzyme (alpha-1,6-glucosidase)
  • Phosphoglucomutase (G1P to G6P)
  • Glucose 6-phosphatase (G6P to Glucose) in the ER of liver, kidney, and intestine and requires G6P transporter to enter ER
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23
Q

What are the key enzymes of glycogen synthesis (glycogenesis)? (3)

A
  • UDP-glucose pyrophosphorylase (G1P + UTP–>UDP-glucose)
  • Glycogen synthase (a-1,4)
  • Branching enzyme (a-1,6)
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24
Q

What are the effects of cAMP on glycogen metabolism?
ie, what are the sequence of events involving protein kinase, phosphorylase kinase, glycogen phosphorylase, and glycogen synthase?

A

Epinephrine and glucagon mediate actions through cAMP (2nd messenger)–>
cAMP activates protein kinase A–>
PKA phosphorylates glycogen synthase & phosphorylase kinase–>
Phosphorylase kinase phosphoylates glycogen phosphorylase–>
G1P

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25
Q

What is the effect of glucagon and epinephrine on glycogen metabolism?

A

-Trigger phosphorylation and stimulate glycogen breakdown
HOWEVER:
-Glucagon stimulates breakdown in the liver
-Epinephrine triggers breakdown mostly in skeletal m.

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26
Q

What is the effect of insulin on glycogen metabolism?

A

Triggers dephosphorylation and stimulates glycogen synthesis in liver and muscle

Activates protein phospatase 1–>
Dephos. glycogen synthase, phosphorylase kinase, & glycogen phosphorylase

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27
Q

What are the key enzymes in regulation of gluconeogenesis? (4)

Hint: All by-lass the irreversible kinase reactions of glycolysis

A
  • Pyruvate carboxylase
  • Phosphoenolpyruvate (PEP) carboxykinase
  • Fructose 1,6-bisphosphatase (most impt!)
  • Glucose 6-phosphatase
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28
Q

Explain how fructose 2,6-bisphosphate affects the key enzymes in gluconeogenesis

A

Allosterically inhibits F-1,6-BPase, therefore inhibiting gluconeogenesis.

F-2,6-BP promotes glycolysis.

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29
Q

Explain how FA oxidation affects the key enzymes in gluconeogenesis

Ex of reciprocal regulation!

A

Incr FA oxidation in liver–>
Incr acetyl CoA–>
Allosteric activation of pyruvate carboxylase–>
Inhibits pyruvate dehydrogenase–>
Blocks glycolysis and promotes glyconeogenesis

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30
Q

Explain how glucagon affects the key enzymes in gluconeogenesis

A

Promotes gluconeogenesis through phosphorylation of PFK-2/F-2,6-BPase via signal transduction:
Phosphorylation decr PFK-2 and incr F-2,6-BPase activity–>
Decr F-2,6-BP–>
Stimulates F-1,6-BPase–>
Incr gluconeogenesis &
Blocks PFK-1

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31
Q

Explain how insulin affects the key enzymes in gluconeogenesis

A

Reverses glucagon’s effects by dephosphorylation of enzymes

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32
Q

What are the 2 key enzymes in the regulation of glycogen metabolism? How are they regulated?

A
  • Glycogen phosphorylase (phosphorylation incr. activity)
  • Glycogen synthase (phosphorylation decr. activity)

Regulated by reversible phosphorylation w/ opposite effects

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33
Q

Ex of allosteric regulation in glycogen metabolism?

A

Glycogen synthase is allosterically activated by high levels of G6P

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34
Q

Dx and deficiency?

  • Pts have hepatomegaly, elevated liver glycogen
  • Hypoglycemia
  • Hyperlipidemia
  • Elevated serum lactate and urate
  • Decr. serum pH
A

Von Gierke (GSD 1)

Deficiency in glucose 6-phosphatase OR glucose 6-phosphate transporter in liver

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35
Q

Dx and deficiency?

  • Pts have limited ability to exercise and painful muscle cramps
  • No buildup of serum lactate following exercise
A

McCardle (GSD 5)

Deficiency of glycogen phosphorylase in muscle

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36
Q

Dx?

  • Deficiency of glycogen phosphorylase in muscle
  • Pts have similar symptoms to GSD 1 but are milder
A

Hers (GSD 6)

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37
Q

Dx?

  • Deficiency of phosphorylase kinase in liver
  • Pts have mild hepatomegaly and hypoglycemia
A

GSD 9

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38
Q

Dx?

  • Deficiency of protein kinase A (cAMP dependent) in liver
  • Symptoms similar to GSD 6
A

GSD 10

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39
Q

Dx?

  • Deficiency of glycogen synthase in liver
  • Pts have fasting hypoglycemia and ketosis
  • Increased serum lactate and glucose after eating
A

GSD 0

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40
Q

Overview of FA synthesis (lipogenesis). 5 steps:

A
  1. Glucose&raquo_space; Acetyl CoA
  2. Acetyl CoA&raquo_space; Malonyl CoA
  3. FA synthase complex
  4. Elongation of FA
  5. Desaturation of FA
41
Q

How is FA synthesis hormonally regulated in the fed state (high carbs/low fat)?

Start with the action of insulin on protein phosphatase.

A
  • Insulin induces protein phosphatase
  • Activates acetyl CoA carboxylase (ACC) (dephosphorylated)
  • FA synthesis proceeds
42
Q

How is FA synthesis hormonally regulated in the starvation state (high fat diet/fasting)?

Start with the action of glucagon / epinephrine increasing cAMP.

A
  • Glucagon / epinephrine increases cAMP
  • Activates protein kinase A
  • Inactivates acetyl CoA carboxylase (ACC) (phosphorylated)
  • FA synthesis stopped
43
Q

What is the key regulatory enzyme in FA synthesis?

A

Acetyl CoA carboxylase (ACC)

44
Q

Dephosphorylated ACC is the rate-limiting enzyme which catalyzes the conversion of acetyl CoA to what?

A

Acetyl CoA&raquo_space; Malonyl CoA

45
Q

What is the major building block for TAG synthesis?

How is it formed in adipose tissue? What enzyme is used?
How is it formed in liver and kidney? What enzyme is used?

A

Glycerol 3-phosphate

In adipose tissue:
Glucose&raquo_space; DHAP&raquo_space; Glycerol 3-phosphate
The DHAP to glycerol 3-phosphate conversion uses NADH»NAD+ and glycerol phosphate dehydrogenase.

In liver and kidney:
Glycerol&raquo_space; Glycerol 3-phosphate
The glycerol is converted to glycerol 3-phosphate by glycerol kinase (only in liver and kidney).

46
Q

The storage of FA in adipose tissue only occurs when glycolysis is activated in the ___ state.

A

The storage of FA in adipose tissue only occurs when glycolysis is activated in the FED state.

47
Q

Where does TG formation occur?

What is the process? 4 steps:

A

TG formation occurs in the cytosol.

1) Formation of glycerol 3-phosphate
2) Activation of FA to form acyl CoA
3) Formation of phosphatidic acid (phosphatidate)
4) Formation of TG (major storage form of bio-fuel).

48
Q

The common aspect of TG synthesis in adipocytes, hepatocytes, and intestinal cells is:

A

Fatty acyl CoA

49
Q

You may choose to inhibit TG synthesis in only the liver by selectively inhibiting which enzyme?

A

Glycerol kinase

Glycerol&raquo_space; Glycerol 3-phosphate

50
Q

In order to release FA, TG’s must be hydrolyzed.

What are the 3 main lipases in adipocytes and what does each hydrolyze?

A

1) Hormone-sensitive lipase (HSL) – hydrolyzes TG&raquo_space; DG + FA (initial liberation of FA)
2) Lipoprotein lipase – hydrolyzes DG&raquo_space; MG + FA
3) Monoglycerol lipase – hydrolyzes MG&raquo_space; Glycerol + FA

51
Q

Why do we need 3 different enzymes for TG hydrolysis?

A

Because substrate solubility at emulsion surface might modulate rates of hydrolysis.

i.e., monoacyl glycerol lipase is less hydrophobic than diacyl glycerol lipase (aka lipoprotein lipase)

52
Q

Which of the 3 TG hydrolyzing enzymes is the most active in the fasting state?

A

Hormone-sensitive lipase (HSL)

53
Q
  • Hormone that is predominately secreted by adipose tissue in direct proportion to fat mass
  • Acts through its specific receptor and is highly expressed in hypothalamus
  • Results in release of neuropeptides that signal cessation of eating (anorexigenic factors)
  • Regulates body weight by: 1) Inhibiting food intake, and 2) Stimulating energy expenditure.

Which fat hormone is described?

A

Leptin = “stop eating”

54
Q

Failure of adipose tissue to produce leptin leads to:

A

Obesity and abnormal increased appetite

55
Q
  • Most abundantly secreted hormone from adipocytes
  • Secretion is reduced as adipocyte gets larger, leading to obesity
  • Reduced secretion may be linked to development of insulin resistance in obesity

Which fat hormone is described?

A

Adiponectin

56
Q

Acetyl CoA is synthesized in:

A

Mitochondria

57
Q

FA synthesis takes place in:

A

cytosol

58
Q

TGs are released into the blood via:

A

VLDL (shuttles for TG)

59
Q

The rate of lipolysis is controlled by the activity of which enzyme?

A

Hormone-sensitive lipase (HSL)

60
Q

Explain FA activation.

Where does it occur?
What is the full reaction, including enzyme?

A

FA activation:

Occurs in cytosol.

Fatty acid + CoA&raquo_space; Fatty acyl-CoA
Formation of a thioester linkage, which is carried out by acyl CoA synthetase, assoc wit outer mitochondrial membrane.

61
Q

TQ
Malonyl CoA inhibits which enzyme in the carnitine shuttle?

Outer or inner mitochondrial membrane?

A

Malonyl CoA inhibits CPT-I

located on outer membrane

62
Q

TQ

What are the 4 steps of ß-oxidation?

A

1) 1st oxidation
2) Hydration
3) 2nd oxidation
4) Thiolysis

63
Q

TQ (know how to calculate amt of ATP)

What is the ATP yield from the ß-oxidation of palmitate (16C FA)?

A 
NADH = 2.5 ATP
FADH2 = 1.5 ATP
GTP = 1 ATP

7 reps of ß-ox spiral ((2.5+1.5)*7) = 28 ATP
8 acetyl CoA = 80 ATP

ATP generated = 28 + 80 - 2 = 106

64
Q

Availability of FAs can be stimulated by which 2 hormones?

A

Glucagon and epinephrine

65
Q

Availability of FAs can be inhibited by which hormone?

A

Insulin

66
Q

High mitochondrial acetyl CoA (stimulates/inhibits) ketothiolase of ß-oxidation (step 4).

A

High mitochondrial acetyl CoA INHIBITS ketothiolase of ß-oxidation (step 4).

i.e., high amounts of the product (acetyl CoA) means that you don’t need to make any more of it!

67
Q

The oxidation of odd number chain FAs produces which molecule?

From there, what is the 3-step process of entry into the TCA?

A

Propionyl CoA (3C fatty acyl CoA)

Propionyl CoA&raquo_space;
Methylmalonyl CoA&raquo_space;
Succinyl CoA&raquo_space;
TCA

68
Q
  • Inherited defect in transport of LCFAs into mitochondria&raquo_space; toxic accumulation
  • Hypoketotic hypoglycemia*
  • Hyperammonemia
  • Weakness

What disorder of FA metabolism is described?

A

Carnitine metabolism deficiency

aka “systemic 1° carnitine deficiency”

69
Q
  • AR disorder of FA oxidation
  • Decr ability to break down FAs into acetyl-CoA&raquo_space; accumulation of 8- to 10-carbon fatty acyl carnitines in the blood and hypoketotic hypoglycemia
  • May present in infancy or early childhood with vomiting, lethargy, seizures, coma, and liver dysfunction

What is the disorder?
How is it treated?

A

Medium-chain acyl-CoA dehydrogenase deficiency (MCAD)

Tx:

  • Avoid fasting
  • Frequent feeding
  • Carnitine supplement
70
Q
  • Caused by a lack or reduction of peroxisomes
  • Characterized by accumulation of LCFAs, pristanic acid in plasma and tissues
  • Affects infants 6-12 months
  • Results in death
A

Zellweger syndrome

aka “cerebrohepatorenal syndrome”

71
Q
  • Inborn error of metabolism
  • When ß-oxidation is impaired, FAs are oxidized 1C at a time from the omega-C by microsomal cytP450-dependent hydroxylases and dehydrogenases
  • These dicarboxylic acids are substrates for peroxisomal ß-oxidation, which continues to the level of 6-10C dicarboxylic acids… excreted into urine

What disorder of FA metabolism is described?

A

Dicarboxylic aciduria

72
Q
  • Deficiency in a single peroxisomal enzyme (phytanoyl CoA hydroxylase)
  • Retinitis pigmentosa
  • Cerebellar ataxia
  • Chronic polyneuropathy

What disorder of FA metabolism is described?
What is the treatment?

A

Refsum disease

Tx: low-phytanic acid diet

73
Q

What are the 3 forms of ketone bodies?

A
  • Acetoacetate
  • ß-hydroxybutyrate
  • Acetone
74
Q

In early stage of starvation, heart and skeletal muscle will consume ______ ______ to preserve glucose for use by the brain.

A

In early stage of starvation, heart and skeletal muscle will consume KETONE BODIES to preserve glucose for use by the brain.

75
Q

In prolonged starvation, brain switches to use ______ ______ and __ (protein) for fuel.

A

In prolonged starvation, brain switches to use KETONE BODIES and AAs (protein) for fuel.

76
Q

Where does the metabolism of ketone bodies (ketogenesis) take place?

What is the rate-limiting step in the metabolism of ketone bodies?

A

Produced in liver mitochondrial matrix.

Acetoacetyl CoA&raquo_space; HMG CoA
Enzyme = HMG CoA synthase

77
Q

Succinyl CoA:acetoacetate CoA transferase is NOT present in the liver… i.e., ketones can be made in the liver, but they cannot be catabolized. Why is this important?

A

This ensures that extra-hepatic tissues (heart and skeletal muscle) have access to ketone bodies as a fuel source during prolonged starvation.

78
Q

What happens in prolonged starvation and diabetic ketoacidosis in terms of oxaloacetate?

A

Oxaloacetate is depleted for gluconeogenesis, causing a buildup of acetyl-CoA, which shunts glucose and FFA toward the production of ketone bodies.

i.e., In untreated diabetes (type 1), glucose uptake is insufficient in various tissues. Thus, gluconeogenesis and ß-oxidation are accelerated in the liver to compensate for the lack of glucose in tissues, raising blood glucose and leading to the production of ketone bodies. Ketone bodies lower the blood pH (acidosis) and may reach critically high levels in the both the blood and urine (ketosis).

79
Q

Be able to define and correctly use the following term:

Free energy

A
  • High energy electrons
  • Catabolic processes, such as glycolysis and the citric acid cycle, transfer free energy to the mitochondrial electron transport chain in the form of high energy electrons
80
Q

Be able to define and correctly use the following term:

Oxidative phosphorylation

A
  • The coupling of electron transport (oxidation by ETC) to the formation of ATP (phosphorylation by ATP synthase)
  • Occurs in mitochondria
  • “The culmination, the end point of the energy-yielding pathways of metabolism”
81
Q

Be able to define and correctly use the following term:

Proton gradient

A

The electron transport chain carries out a series of oxidative
reactions that pump protons out of the mitochondrial matrix, creating a pH/proton gradient across the inner mitochondrial membrane

82
Q

Be able to define and correctly use the following term:

Oxidation and reduction

A

The energy of oxidation drives the synthesis of ATP (creates proton gradient)

Oxidation-reduction drives the ETC

83
Q

What theory is being described?

Oxidative phosphorylation occurs across the inner
mitochondrial membrane and produces transmembrane differences in proton
concentration (a.k.a. pH gradient)–>
Creates driving energy for ATP formation by ATP synthase–>
Discharge of proton gradient–>
ATP

The British scientist Peter Mitchell won Nobel prize

A

Chemiosmotic theory,

“One of the great
unifying principles of twentieth century biology”xf

84
Q

Be able to define and correctly use the following term:

Brown fat mitochondria

A

-Newborns have a type of adipose tissue called brown fat
-ATP formation and electron transport are NOT coupled so that electron transport continues even when there is plenty of ATP–>
Uncoupling!–>
More heat produced keeping the newborn warm!

(newborns have a relatively large surface area from which heat dissipates, necessitating more heat production to maintain body temperature)

85
Q

Be able to define and correctly use the following term:

Thermogenin

A
  • Causes uncoupling in brown fat

- Enables electrons to cross the membrane bypassing/without ATP synthase

86
Q

Be able to define and correctly use the following term:

NADPH

A

Made by the PPP for:

  • biosynthesis of fatty acids, cholesterol, steroid hormones, and bile salts
  • hydroxylation reactions for the detoxification and excretion of many drugs
  • maintains glutathione in the reduced state
87
Q

Be able to define and correctly use the following term:

Glutathione

A

NADPH keeps glutathione (a tripeptide) in a reduced state which is important in protecting the red cell membrane from damage that can be caused by peroxides and superoxide free radicals

88
Q

Describe the general organization and function of the components of oxidative phosphorylation (i.e., the electron transport chain and ATP synthase)

A

ETC: creates proton gradient

ATP synthase: forms ATP by flow/discharge of protons back through inner membrane

89
Q

Explain the effects of ATP and ADP in the regulation of oxidative phosphorylation

A
  • ADP promotes oxidative phosphorylation, ATP slows it (oxidative phosphorylation is generally limited by the amount of ADP present in the cell)
  • The total amount of ATP + ADP is fairly constant in a cell, so when ADP is high ATP is low (and vice versa)
90
Q

TQ

What is the key enzyme in the regulation of the pentose phosphate pathway?

A

Glucose 6-phosphate dehydrogenase (G6PD)

oxidative

91
Q

How does NADPH affect G6PD’s activity?

A

-High NADPH inhibits G6PD

G6PD activity is controlled by the ratio of NADP to NADPH:

  • A high NADP/NADPH ratio increases G6PD activity.
  • A low NADP/NADPH ratio decreases G6PD activity (NADPH allosterically blocks NADP from binding)
92
Q

Explain why G6PD activity in RBCs is severely reduced in the most common form of G6PD deficiency

How this can lead to a hemolytic anemia?

A

X-linked recessive trait and leads to inadequate formation of NADPH

  • NADPH is a required cofactor, w/ glutathione reductase, in maintaining glutathione in a reduced state
  • Reduced glutathione removes H2O2 and superoxide free radicals generated in the metabolism of foods and drugs (e.g., fava beans and primaquine).
  • Oxidized glutathione (a hexapeptide) allows peroxides and superoxide free radicals to accumulate in the red cell.
  • If not removed, the peroxides and superoxide free radicals can cause membrane lipid peroxidation, leading to massive RBC membrane destruction, i.e., severe hemolytic anemia
  • ALSO: mutated G6PD is blocked by low levels of NADPH
93
Q

Explain the effects of NADH & NAD+ in the regulation of oxidative phosphorylation

A

Incr NAD+/NADH–> Incr oxidative phosphorylation

Incr NADH/NAD+–>decr oxidative phosphorylation

94
Q

-This defect affects the CNS, including the optic nerves, causing bilateral loss of vision in early adulthood.
-A single base change in the mitochondrial gene ND4
changes an Arg–>His residue in a polypeptide of complex I of the ETC–>
-Impaired electron transport reduces ATP synthesis below the level needed to support energy requirements of neurons (optic n.)

A

Leber’s hereditary optic neuropathy (LHON)

not enough ATP made to support growth and metabolism of neurons

95
Q

When ADP is high and ATP synthase is inactive, what happens in the cell?

A

-When ATP synthase is inactive, protons do not (cannot) flow back through the inner mitochondrial membrane to discharge the pH gradient.
-When the transmembrane pH (proton) gradient is
“locked in place” the ETC stops ( since ATP formation and electron transport are coupled)
-Stopping electron transport causes NADH levels to
rise (and NAD+ to fall) resulting in decr. activity of energy-generating pathways (glycolysis, fatty acid oxidation, citric acid cycle, etc.).

96
Q

What drives the formation of ATP?

A

Discharge of proton gradient (flow of protons back into the matrix)

97
Q

Which of the following compounds is most important in the regulation of oxidative phosphorylation: ADP, ATP, NAD, NADH?

A

ADP

High ADP–>
Incr ATP synthesis–>
Oxi of NADH and FADH2–>
Incr NAD and FAD (co-substrates in CAC, Gly, FA oxi)

98
Q
  • Produces riboses
  • Produces NADPH for biosynthesis, detoxification, & glutathione reactions
  • Alternate pathway for glucose oxidation
A

Pentose Phosphate Pathway

99
Q

PPP:

  • _____ stage produces riboses and NADH
  • Interconversion stage produces glycolytic intermediates (leftovers)
A

Redox

Endocrine Midterm (8 decks)

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