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FHB 3 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Oxidation

A

Loss of electrons from an atom. occurs during the addition of an O2 molecule or when H+ is removed

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2
Q

Reduction

A

addition of electrons to an atom. occurs during the addition of hydrogen or the removal of oxygen

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3
Q

Where does the conversion of pyruvate to acetyl coa take place?

A

Matrix of the mitochondria

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4
Q

What are the 4 fates of Acetyl CoA

A

1) primary fate is the CAC. Produces ATP, H2O, CO2.
2) Lipogenesis. formation of fatty acids which go through esterification to form triacylglycerol
3) Ketogenesis- formation of ketone bodies
4) cholesterologenesis- formation of cholesterol and then steroids. involves the transfer of acetyl units in the cytosol. So Acetylo CoA is the precursor of steroids

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5
Q

Fuel preferences of liver

A

fatty acids

glucose

amino acids

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6
Q

Fuel preferences of skeletal muscle

A

At rest: fatty acids

exertion: glucose

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7
Q

Fuel preference for the brain

A

Fed state: glucose

Starvation: ketone bodies/glucose

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8
Q

Fuel preferences for adipose tissue

A

fatty acids

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9
Q

fuel preferences for heart muscle

A

prefers fatty acids, but it can use anything

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10
Q

Amylopectin

A

found in potatoes, rice, corn, bread

enzyme: isomaltase

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11
Q

amylose

A

potatoes, rice, corn, bread

enzyme: maltase

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12
Q

Starch

A

mixture of amylose and amylopectin

polymer composed entirely of glucose

potatoes, rice, corn, bread

enzyme: maltase and isomaltase and amylase

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13
Q

Sucrose

A

table sugar, desserts

enzyme: sucrase

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14
Q

Lactose

A

milk, milk products

enzyme: lactase

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15
Q

Fructose

A

Fruit, honey

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16
Q

Glucose

A

Fruit, honey, grapes

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17
Q

Maltose

A

Barley

Enzyme: maltase

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18
Q

Trehalose

A

Young mushroom

enzyme: trahalase

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19
Q

Cellulose

A

fiber in plants. not digestable by humans

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20
Q

Calories of Carbs

A

% Caloric Store: 1

% body weight: .6

kcal/g dry: 4

kcal/g wet: 1-1.5

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21
Q

calories of protein

A

% Caloric Store: 23

% body weight: 14

kcal/g dry: 4

kcal/g wet: 1-1.5

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22
Q

Calories of fat

A

% Caloric Store: 76

% body weight: 20

kcal/g dry: 9

kcal/g wet: 9

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23
Q

% body weight of H2O and minerals

A

65%

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24
Q

how much glucose does brain use every day

A

120g

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25
Q

how much glucose does muscle tissue use every day

A

40g

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26
Q

what level must blood glucose be maintained above to avoid hypoglycemia

A

60mg/100mL

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27
Q

affinose

A

carb found in leguminous seeds

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28
Q

Phase I of Starvation

A

Blood glucose is supplied exogenously.

All tissues are using glucose

Brain is also using glucose

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29
Q

Phase II of Starvation

A

Blood glucose originates from glycogen and hepatic gluconeogenesis.

All tissues except the liver are using glucose, muscle and adipose tissue are using them at diminished rated.

Brain is using glucose

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30
Q

Phase III of Starvation

A

Blood glucose oriniated from hepatic gluconeogensis and glycogen

All tissues except the liver are using glucose. Muscle and adipose tissue glucose use is between phase II and IV

Brain is using glucose

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31
Q

Phase IV of Starvation

A

blood glucose from hepatic and renal gluconeogenesis.

Only brain, RBCs, renal medulla, and small maounts of muscle still using glucose

Brain is using glucose and ketone bodies

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32
Q

Phase V of starvation

A

Blood glucose is from hepatic and renal gluconeogenesis

Renal medulla and RBCs using glucose. Brain using glucose at a diminished rate.

Brain using glucose and ketone bodies

33
Q

Insulin

A

peptide hormone secreted by beta cells of the pancreas

regulates glucose metabolism. maintains low blood glucose levels. Counters he function of hyperglycemia generating hormones.

promotes glycolysis on a long term basis, as well as glycogen synthesis

34
Q

glycogenolysis

A

the breakdown of glycogen to glucose-1-phosphate and glucose in the liver and muscles by the enzyme glycogen phosphorylase

activated by hypoglycemia and increased glucagon

35
Q

Glycolysis

A

single glucose molecule converts into:

2 pyruvic acid

2 ATP

2 NADH

2 H2O

activated by hyperglycemia and increased insulin

36
Q

gluconeogenesis

A

generation of glucose from non-carb carbon substrates such as pyruvate, lactate, glycerol, and glucogenic amino acids amino acids

stimulated by hypoglycemia and increased glucagon

37
Q

glucogenesis

A

formation of glycogen from glucose.

stimulated by hyperglycemia and increased insulin

38
Q

Carb metabolism in RBCs

A

lack mitochondria, cannot metabolize fatty acids or amino acids. Entirely dependent on glycolysis

39
Q

Carb metabolism in the brain

A

has an absolute requirement for glucose.

120 grams daily. very smally reserve of glycogen in brain tissue

40
Q

Carb metabolism in muscle and heart cells

A

major glycogen stores. cannot mobilize glycogen or glucose in to the blood.

41
Q

carb metabolism in Adipose tissue

A

convert excess glucose to fat

42
Q

SGLT1

A

sodium glucose transporter 1. Hexose transporter against concentration gradient. Co-transports one molecule of glucose or galactose along with 2 Na ions. Does not tranport fructose

expressed in intestinal mucosa and kidney tubules

43
Q

GLUT 2

A

Hexose transporter with concentration gradient.

Insulin independent and low affinity for glucose, high capacity transport in liver. allows GLUT2 to change transport rate in proportion to increasing glucose concentrations.

found in liver, intestine, and kidneys. bidirectional transport.

serves as a glucose sensor to pancreatic beta cells. transports glucose out of the intestines into the blood stream, and into the liver.

44
Q

GLUT 4

A

Hexose transporters down the concentration gradient

high affinity for glucose

gets glucose after we have eaten it. not active during the fasting state.

functions at max rate when glucose conc is 5mM

skeletal muscle, heart, adipocytes

45
Q

Which transporters have a high affinit for glucose

A

GLUT 1,3,4

46
Q

Which transporters are fructose transporters

A

Class II: 5,7,9,11

47
Q

Which transporters are glucose transporters

A

GLUT 1-4

48
Q

Three key enzymes that regulate glycolysis

A

1) Hexokinase/Glucokinase- priming stage ATP investment
2) PFK-1/phosphofructo kinase-1 -Splitting stage
3) Pyruvate kinase -oxidoreduction phosphorylation stage (these steps occur twice for every glucose molecule)

49
Q

Deficiencies in which enzymes cause hemolytic anemia

A

hexokinase

glucose phosphate isomerase

aldolase

triosephosphate isomerase

phsophoglycerate isomerase

enolase

pyruvate kinase

50
Q

Comapre Hexokinase to Glucokinase

A

Hexokinase: present in all cell types, allosterically inhibited by G6P, constituitive enzyme (present at all times whether activated or not), low Km for glucose (saturated at low glucose concentrations), can’t handle high levels of glucose

Glucokinase: Present in liver and pancreas, inactive in nucleus and active in cytosol, inhibited by F6P, enzyme activity induced by insulin because it increases expression of the gene, high Km for glucose, not saturated at normal physiological glucose concentration, can handle large concentration of glucose in the liver.

51
Q

What are the allosteric regulators of PFK-1

A

positive: F2,6BP, AMP, ADP

Negative: More ATP, More citrate

52
Q

What are the regulators of glucokinase

A

activators promote translocation from nucleus to the cytosol: high levels of glucose. insulin

inhibitors promote translocation to the nucleus: fructose 6 phosphate (a downstream product)

53
Q

PFK2

A

The kinase domain catalyzes formation of fructose 2,6 bisphosphate.

The phosphatase domain catalyzes the reverse reaction to fructose-6-phosphate.

PKA phosphorylates and inhibits PFK2

54
Q

Compare PFK2 in the liver and muscle

A

liver PFK2 is phosphorylated in the kinase domain by PKA in response to glucagon or epi. This inhibits glycolysis. It has both kinase and phosphatase activity.

In the heart epi increases PFK activity because PKA will phosphorylate the phosphatase domain, inhibiting the phosphatase activity. continued production of F26BP and glycolysis

55
Q

Regulation of PFK-1

A

inhibited by: high ATP and citrate. (associated with high energy).

activated by: AMP and ADP and fructose 2,6 bisphosphate. (associated with low energy).

56
Q

Regulation of pyruvate kinase

A

activating: High BGL. F1,6BP. **hepatic kinase inactivated by phosphorylation. Glucagon and epi act via cAMP, PKA, to P PK. **
inhibiting: Low BGL. ATP, alanine (increased infasting mode, precursor to gluconeogenesis)

57
Q

Describe the action of glucagon and epi in the liver.

A

inhibit PFK2, which decreases F26BP; this decreases the activity of PFK1

inhibits PK

represses synthesis of glucokinase, PFK1, PK

58
Q

How does glucagon and epi inhibit glycolysis

A

Inhibit PFK through phosphorylation. This leads to decreased production of F2,6BP which is an allosteric inhibitor of PFK1.

Also directly inhibits PK through cAMP and P by PKA

decreased production of 3 irreversible enzymes of glycolysis.

59
Q

Increased insulin, decreased cAMP, low glucagon, low epi cause

A

increased synthesis of glucokinase, PFK1, and PK

60
Q

How does epi inhibit hepatic glycolysis but activates cardiac glycolysis.

A

Inhibits hepatic glycolysis through P of the kinase domain in PFK2, preventing formation of F2,6BP

Promotes glycolysis in cardiac muscle because it P and inactivates the PFK2 phosphatase domain, which leads to increased PFK2 activity and increased F26BP.

61
Q

How is NAD+ regenerated

A

Through oxidation of NADH when pyruvate is converted to lactate via LDH enzyme. production of lactate or alcohol in an anaerobic environment.

also can use mitochondria linked shuttles: glycerolphosphate, malate aspartate. forms FADH2 and NADH. can be reoxidized in ETC, generates more ATP than LDH pathway. aerobic.

must be regenerated for glycolysis to continue

62
Q

M4

A

Isoenzyme of LDH. Found in muscles. Prefers to catalyze conversion of pyruvate to lactate. allows for high bursts of energy.

63
Q

H4

A

LDH isoenzyme found in heart muscle. prefers to catalyze the conversion of lactate to pyruvate. this allows for sustained production of energy. Pyruvate is then decarboxylated to acetyl-CoA and enters into the CAC

64
Q

what are the different LDH and where are they found?

A

LDH-1 (4H) heart

LDH-2 (3H1M) circulatory system

LDH-3 (2H2M) lungs

LDH-4 (1H3M) kidney placenta pancreas

LDH-5 (4M) liver and striated muscle

65
Q

What does the ratio of LDH-1 to LDH-2 in the blood tell you

A

LDH-1 > LDH-2 = MI

66
Q

Normal ratio of lactate to pyruvate in blood

A

10/1

67
Q

What are the allosteric inhibitors of PDH

A

The end products are the inhibitors: acetyl CoA, NADH

a kinase can be activated that will P and inhibit the enzyme. Factors that inhibit the kinase activate the PDH.

68
Q

Identify the factors that cause PDH to be phosphorylated or dephosphorylated

A

Phophorylation inhibits PDH

NADH, Acetyl CoA - activate the kinase, promote phosphoryltion.

Coenzyme A, NAD+, ADP, Pyruvate: inhibit the kinase, inhibit phosphorylation

MG2+, Ca2+: promote dephosphorylation by activating the phosphatase.

69
Q

What is the reaction PDH catalyzes?

A

Pyruvate + CoASH -> Acetyl-CoA + CO2 + NADH+ + H+.

leads to ATP production.

70
Q

Identify the vitamin cofactors that participate in reaciton catalyzed by PDH

A

E1 - Thiamine (B1)

E2 - Pantothenate (B5)

E3 - FAD, NAD : Riboflavin (B2). Niacin (B3)

71
Q

Predict the effect of a thiamine deficiency, an abnormality of PDH, or arsenic poisoning on circulating levels of lactate and pyruvate

A

A thiamine deficiency (B1) would cause PDH to be less active. Anything that impairs PDH won’t allow it produce acetyl-CoA. Brain and heart tissue most affected.

Aresenic poisoning- inhibits the shuttling of lipoic acid in the oxidized and reduced form. symptoms would be the same as a PDH deficiency.

**pyruvate and lactate accumulate in the blood and cause lactic acidosis. **

72
Q

Lactate dehydrogenase deficiency

A

Cannot regenerate NAD+. glyceraldehyde-3P-dehydrogenase reaction is inhibited. NAD+ levels are inhibited during excercise.

people cannot maintain moderate levels of excercise due to not being able to use glycolysis to produce ATP needed for muscle contraction.

73
Q

Predict the physiological conseqences of a genetic deficiency of fructose aldolase, and identify the foods the affected individual should avoid.

A

recessive genetic deficienct of aldolase B. aldolase B cleaves fructose-1-P. Deficiency results in accumulation of F1P, depletion of Pi and ATP.

Cells are damaged because they cannot maintain normal ion gradients through ATP-dependent pumps. Phosphorylted sugars are toxic to the cell.

hypoglycemia, vomiting, jaundice, hepatic failure/ cirrhosis

have low glucose level, fructose accumulation, high uric acid, high lactic acid, fructose toxicity

avoid foods with fructose.

74
Q

What are the processes that require O2

A

reoxidation of mitochondrial NADH formed by enzyme PDH

reoxidation of cystolic NADH by mitochondrial linked shuttles: glycerol phosphate shuttle, malate spaartate shuttle.

Citric acid cycle

75
Q

Decreased NADH mean

A

lower levels of lactate formation

76
Q

Predict the physiological consequences of a genetic deficiency of either galactokinase or galactose-1-P uridyl transferase, and identify the foods the individual should avoid

A

accumulation of galactose activates a pathway rarely used and results in the formation of galacitol.

causes cataracts, brain damage, jaundice, enlarged liver, kidney damage, galactose uria (from build up of sugars)

remove galactose (lactose) from the diet.

77
Q

pyruvate carboxylase deficiency

A

won’t produce oxaloacetate

leads to increased alanine, lactate, and pyruvate

developmental delay, recurrent seizures metabolic acidosis

78
Q

Inputs and outputs of glycolysis

A

Input: glucose, 2 NAD+, 2 ATP, 4 ADP + 4 P

outputs: 2 pyruvate, 2 NADH, 2 ADP, 4 ATP

Net gain: 2 ATP

FHB 3 (10 decks)

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