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biochem > Chapter 12 > Flashcards

Chapter 12 Flashcards

1
Q

What cells carry out glycolysis?

A

All cells

red blood cells rely on glycolysis for energy

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2
Q

What is the first step of glycolysis?

A

transport of glucose (galactose, fructose) across the membrane and phosphorylation by kinase enzyme to prevent it from leaving via the transporter

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3
Q

How are carbohydrates digested?

A

Mouth: salivary amylase hydrolyzes starch polymers to dextrims

somach acid pH destroys salivary amylase

intestine: dextrins are hydrolyzed to disacccharides maltose and isomaltose

intestinal brush border:

*maltase cleaves maltose to 2 glucoses

*isomaltase cleaves isomaltose to 2 glucoses

*lactase cleaves lactose to glucose and galactose

*sucrase cleaves sucrose to glucose and fructose

uptake of glucose into mucosal cells via sodium/glucose transporter–active tranpsort system

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4
Q

Describe GLUT1 and GLUT3 transporters.

A

mediate basal glucose uptake in most tissues, including brain, nerves, and RBC

–high affinity for glucose ensure glucose entry even during periods of relative hypoglycemia

normal glucose concnetration: GLUT1 and 3 are at Vmax

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5
Q

Describe GLUT2 transporter.

A

low affinity transporter in hepatocytes

captures excess glucose for storage

when glucose concentration drops below Km for transporter, remainder leaves liver and enter peripheral circulation

GLUT2 and glucokinase: glucose sensor for insulin release

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6
Q

Describe GLUT4 transporter.

A

adipose tissue, muscle

rate of glucose transport is increased by insulin

–stimulates movment of additional GLUT4 transporters to membrane via exocytosis

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7
Q

How is GLUT4 stimulated in muscle cells?

A

translocation to cell membrane in skeletal muscle is stimulated by exercise

–insulin independent

–involves 5’AMP activated kinase

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8
Q

How is insulin secreted from pancreatic beta cells?

A

biphasic

  1. glucose stimulates first phase (within 15 minutes) with release of preformed insulin
  2. insulin synthesis at gene level (several hours)
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9
Q

How does insulin affect glucose uptake in muscle and adipocytes?

A

basal transport occurs in all cells independent of insulin

–transport rate increases in adipose tissue and muscle when insulin levels rise

–muscle cells stores excess glucose as glycogen

–adipose tissue requires glucose to form DHAP, which is converted to glycerol phosphate used to store incoming fatty acids as triglyceride

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10
Q

Summarize major glucose transporters in human cells.

A
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11
Q

Describe glycosis.

A

cytoplasmic pathway

converts glucose into 2 pyruvates–releasing small amount of energy capture in two substrate level phosphorylation and one oxidation reaction

–cell has mitochondria and oxygen, glycolysis is aerobic

–mitochodnria or oxygen lacking, glycolysis may occur anaerobically (erythrocytes, exercising skeletal muscle)

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12
Q

What is the glycolysis pathway?

A
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13
Q

What are the intermediates for other pathways that glycolysis provides?

A

liver: glycolysis part of process by which excess glucose converted to fatty acids for storage

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14
Q

What is the function of hexokinase/glucokinase?

A

glucose entering the cell is trapped by phosphoylation using ATP

hexokinase: widely distributed in tissues; low Km; inhibited by glucose 6-phosphate
glucokinase: found only in hepatocytes and pancreatic beta islet cells; high Km; induced by insulin in hepatocytes

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15
Q

What does arsenate inhibit in glycolysis?

A

inhibits conversion of glyceraldehyde 3 phosphate to 1,3 bisphosphoglycerate by mimicking phosphate in reaction

–product is water labile, enabling glycolysis to proceed but resulting in no ATP production

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16
Q

What happens in ischemic episodes (ex. MI)?

A

lack of oxygen forces cells to rely on anaerobic glycolysis, which increase production of lactic acid

–intracelular acidosis can cause proteins to denature and precipitate, leading to coagulation necrosis

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17
Q

What is the function of phosphofructokinases (PFK1 and PFK2)?

A

PFK1: rate limiting enzyme

–fructose 6 phosphate is phosphorylated to fructose 1,6 bisphosphate using ATP

–inhibited by ATP and citrate; activated by AMP

–insulin stimulates and glucagon inhibits in hepatocytes by indirect mechanism involving PRK2 and fructose 2,6 bisphosphate

PFK2: insulin activates via tyrosine kinase receptor and activation of protein phosphatases

–converts fructose 6 phosphate to fructose 2,6 bisphosphate

–F26-BP activates PFK1

–glucagon inhibits PFK2 (via cAMP dependent protein kinase A) lowering F2,6-BP and inhibiting PFK-1

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18
Q

What is the function of beta iselt cells of the pancreas?

A

have GLUT2 on the plasma membrane to transport glucose into the cells

have glucokinase to trap incoming glucose as G6P

GLUT2 and glucokinase have high Km so glucose is transported and phosphorylated via first order kinetics (directly proportional to glucose concentration in the blood)

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19
Q

What occurs with deficiency of glucokinase activity?

A

assocaited with permanent neonatal type 1 diabetes

some mutations in glucokinase gene alter Km for glucose

–mutations that decrease Km (increasing the affinity for glucose) result in hyperinsulinemia and hypoglycemia

–mutations that increase Km (decreasing the affinity for glucose) are associated with some cases of maturity-onset diabetes of the young (MODY)

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20
Q

What is the function of glyceraldehyde 3-phosphate dehydrogenase?

A

catalyzes oxidation and additoin of inorganic phosphate to substrate

–produciton of high energy intermediate 1,3 bisphosphoglycerate and reduction of NAD to NADH

–aerobic: NADH can be reoxidized (indirectly) by mitochondrial ETC providing energy for ATP synthesis by oxidative phosphorylation

21
Q

What is the function of 3-phosphoglycerate kinase?

A

transfers high energy phosphate from 1,3-bisphosphoglycerate to ADP forming ATP and 3-phosphoglycerate

–substrate level phosphorylation: not dependent on oxygen; only means of ATP generation in anaerobic tissue

22
Q

What is the function of pyruvate kinase?

A

catalyzes substrate level phosphorylation of ADP using the high energy substrate phosphoenolpyruvate (PEP)

-activated by fructose 1,6-bisphosphate from PFK-1 reaction (feed-forward activation)

23
Q

What is the function of lactate dehydrogenase?

A

only in anaerobic glycolysis

–reoxidizes NADH to NAD, replenishing the oxidized coenzyme for glyceraldehyde 3 phosphate dehydrogenase

reduces pyruvate to lactate and oxidizing NADH to NAD,

in aerobic tissues, lactate doesn’t normally form in significant amounts

–only when oxygenation is poor (skeletal muscle during strenuous exercise, myocardial infarction), most cellular ATP is generated by anaerobic glycolysis and lactate production increases

24
Q

What are the important intermediates of glycolysis?

A

dihydroxyacetone phosphate (DHAP) is used in liverand adipose tissue for triglyceride synthesis

1,3 bisphosphoglycerate and phosphoenolpyruvate (PEP) are high energy intermediates used to generate ATP by substrate level phosphorylation

25
Q

What enzymes of glycosis are irreversible? What is the consequence?

A

glucokinase/hexokinase

PFK-1

pyruvate kinase

–when liver produces glucose, different reactions and enzymes must be used

26
Q

How much energy is generate from anaerobic glycolysis?

A

2 ATP/glucose by substrate level phosphorylation

27
Q

How much energy is generated from aerobic glycolysis?

A

2 ATP/glucose and 2 NADH/glucose that can be utilized for ATP production in mitochondria

–inner membrane is impermeable to NADH

–cytoplasmic NADH is reoxidized to NAD and delivers electrons to electron shuttles in inner membrane

28
Q

What are the two electron shuttles?

A
  1. malate shuttle: cytoplasmic NADH oxidized using malate shuttle to produce mitochondrial NADH and then to the ETC

–3 ATP by oxidative phosphorylation

  1. glycerol phosphate shuttle: cytoplasmic NADH oxidized by shuttle to produce mitochondrial FADH2

–2 ATP by oxidative phosphorylation

29
Q

How much energy is generated in erythrocyte from glycolysis?

A

in red blood cell, anaerobic glycolysis represents only pathway for ATP production

–2 ATP/glucose

30
Q

How do you adapt to high alitudes (low PO2)?

A

increased respiration

respiratory alkalosis

lower P50 for hemoglobin (initial)

increased rate of glycolysis

increased [2,3 BPG] in RBC (12-24 hours)

normal P50 for hemoglobin restored by increased level of 2,3 BPG

increased hemoglobin and hematocrit (days-weeks)

31
Q

What is the function of bisphosphoglycerate mutase in erythrocytes?

A

produces 2,3 bisphosphoglycerate (BPG) from 1,3 BPG in glycolysis

2,3 BPG binds to beta chains of hemoglobin A and decreases it affinity for oxygen

–right shift of curve: allow unloading of oxygen in tissues and allows 100% saturation in lungs

32
Q

What occurs with an abnormal increase in erythrocyte 2,3 BPG?

A

shift curve far enough to right so HbA is not fully saturated in the lungs

33
Q

How does HbF function?

A

2,3 BPG binds to HbA (alpha and beta) but doesn’t bind to HbF well (alpha and gamma)

–HbF has a higher affinity for oxygen than maternal HbA

–transplacental passage of oxygen from mother to fetus

34
Q

What occurs in pyruvate kinase deficiency?

A

second most common genetic deficiency that causes hemolytic anemia

–chronic hemolysis

–increased 2,3 BPG and lower than normal oxygen affinity of HbA

–absense of Heinz bodies (present with G6PDH)

–decrease in ATP causes erythrocyte to lose its characteristic biconcave shape; signals destruction in spleen

–decreased ion pumping by Na/K ATPase results in loss of ion balance and causes osmotic fragility, leading to swelling and lysis

35
Q

What are the steps of galactose metabolism?

A
36
Q

What is the source of galactose in the diet?

A

disaccharide lactose in milk

–lactose is hydrolyzed to galactose and glucose by lactase (brush border membrane of small intestine)

–galactose reaches liver through portal blood

–phosphorylated (galactokinase) to be trapped in cell

–converted to G1P by galactose 1P uridyltransferase and epimerase

37
Q

What causes galactosemia?

A

deficiency to galactokinase and galactose 1-phosphate uridyltransferase

–cataracts results from conversion of excess galactose in peripheral blood to galactitol via aldose reductase in the lens of the eye

–accumulation of galactitol in lens causes osmotic damage and cataracts

–deficiency of galactose 1 phosphate uridyltransferase produces more severe disease becuase galactose 1-P also accumulates in liver, brain and other tissues

38
Q

Why do diabetics get cataracts?

A

aldose reducts converts glucose to sorbitol –> osmotic damage

39
Q

What are the biochemical and physical symptoms of galactosemia?

A

galactose in elevated amount in the blood and urine–> decreased glucose synthesis and hypoglycemia

–cataracts

–jaundice and hyperbilirubinemia (liver is the site of bilirubin conjugation; develops cirrhosis)

–vomiting and diarrhea after milk ingestio: lactose00< glucose + galactose by lactase in intestine but galactose not properly metabolized

–bacterial infection common (E coli sepsis)

–failure to thrive, lethargy, hypotonia, mental retardation

TREATMENT: galactose free carbohydrate diet

40
Q

What is lactose intolerance?

A

hereditary deficiency of lactase

–common in Asian and African decent

–secondary intolerance: precipitated at any age by GI disturbances (celiac sprue, colitis, viral induced damage to intesinal mucosa)

SYMPTOMS: vomiting, bloating, explosive and watery diarrhea, cramps and dehydration (because bacterial fermentation of lactose)

–acids are osmotically active and result in movement of water to intestinal lumen

DIAGNOSIS: positive hydrogen breath test

TREAMENT: dietary restriction of milk, milk products or lactase pills

41
Q

What are the steps of fructose metabolism?

A
42
Q

What is the source of fructose?

A

sucros is hydrolyzed by intestinal brush border sucrase into glucose and fructose

–absorbed into portal blood

–liver phosphorylates fructose and cleaves it into glyceraldehyde and DHAP

43
Q

What are the effects of fructokinase and Fructose 1-P aldolase (aldolase B) deficiency?

A

fructokinase: benign

fructose 1 phosphate aldolase: severe

–accumulation of fructose 1 phsphate in liver and renal proximal tubules

–symptoms reversed when fructose and sucrose removed from diets

–cataracts not feature of disease because not an aldose sugar (not substrate for aldose reductase)

44
Q

What occurs after you drink a high fructose drink?

A

quick source of energy for anaerobic and aerobic cells becuase DHAP and glyceraldehyde (products of fructose metabolism) are downstream from key regulatory and rate limiting enzyme of glycolysis (PFK1)

45
Q

What occurs with hereditary fructose intolerance?

A

autosomal recessive

defect in gene that encodes aldolase B in fructose metabolism

–accumulation of fructose 1 pohsphate in hepatocytes

drop in phosphate levels prevent its use in other pathways (glycogen breakdown and gluconeogenesis)

–liver becomes dmaage becuase of accumulation of trapped fructose 1P

–proximal renal disorder if don’t exclude sugars from diet

46
Q

What is function of pyruvate dehydrogenase?

A

pyruvate from aerobic glycolysis enters mitchondria–converted to acetyl CoA for entry into TCA if ATP needed or for fatty acid syntehsis if sufficient ATP is present

–irreversible

–enzyme activated by insulin in the liver

–enzyme in brain and nerves not responsive to hormones

47
Q

What are the cofactors and coenzymes required for pyruvate dehydrogenase?

A
  1. thiamine pyrophosphate (TPP) from vitamin thiamine
  2. lipoic acid (body makes it)
  3. coenzyme A (CoA) from pantothenate
  4. FAD(H2) from riboflavin
  5. NAD(H) from niacin (some may be synthesized from tryptophan)

–inhibited by its product acetyl CoA

48
Q

What is Wernicke-Korsakoff Syndrome?

A

thiamine deficiency

common in alcoholics

Wernicke peripheral neuropathy and Korsakoff psychosis

alohcol interferes with thiamine absorption from the intestine

SYMPTOMS: ataxia, ophthalmoplegia, nystagmus, memory loss and confabulation, cerebral hemorrhage

wet beri beri: congestive heart failure (inadequate ATP and accumulation of ketoacids in cardiac muscle)

49
Q

What enzymes need thimaine?

A

alpha ketoglutarate dehydrogenase (TCA)

–impairs glucose oxidation, causing highly aerobic tissues, like brain and cardiac muscle, to fail first

branched chain ketoacid dehydrogenase (metabolism of branched chain amino acids)

–sources of energy in brain and muscle

biochem (18 decks)

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