Carbohydrates 2 Flashcards

1
Q

Glycolysis Stage 1

A

Phosphorylation of glucose to trap it in cell; uses energy to destabilize molecule to make break down easier in stage 2 (2 ATPs used)

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2
Q

Glycolysis Stage 2

A

6C F-1,6-BisP spilts into 2 3C molecules (DHAP and GAP; DHAP CANNOT proceed on in glycolysis pathway, must be converted to GAP or to glycercol for synthesis of storage fat)

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3
Q

Glycolysis Stage 3

A

3C GAP molecule is oxidized in 5 steps to generate pyruvate; energy-yielding phase; 2 molecules of ATP are synthesized by substrate level phosphorylation; 2 ATP’s per 1 GAP so 4 ATP’s per 1 glucose molecule

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4
Q

Degradation of Fructose: Liver and Muscle

A

Liver—Fructose metabolized in liver; converted to F-1-P by fructokinase and then further cleaved into DHAP enters at Stage 2 glycolysis; remember fructose doesn’t trigger insulin release
Muscle—fructose is -P’d by hexokinase, then enters glycolysis

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5
Q

Degradation of Galactose

A

must be converted to glucose; is first -P’d then linked to UDP, UDP-galactose is then transformed into UDP-glucose; in pathway once Galac-1-P is formed it must be degraded–but if accumulated; also the UDP is recycled back in reaction

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6
Q

Essential Fructosuria

A

Deficiency of liver fructokinase, fructose is NOT utilized and excreted in urine; no harmful effects

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7
Q

Hereditary Fructose Intolerance

A

Deficiency in Aldolase B enzyme; fructose-1-P CANNOT be converted to DHAP and then is accumulated in the liver; liver phosphate pools are depleted and then it cannot break down glycogen; enlarged liver, coma, hypoglycemia, jaundice, decrease liver function

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8
Q

Galactosemia

A

failure to utilize galactose in glycolysis; 3 types based on enzyme effected— galactokinase, galactose-1-phosphate uridyltransferase, UDP-galactose epimerase; intellectual disability, vision loss, liver damage, jaundice

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9
Q

Regulatory Signals of Glycolysis

A

Intermediates of energy metabolism (ATP, citrate); Hormones (insulin, glucagon, epinephrine); Fructose-2,6-BisP

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10
Q

3 Regulated Steps of Glycolysis

A

Phosphofructokinase, Hexokinase, pyruvate kinase

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11
Q

Regulation of Phosphofructokinase

A

most important regulated step/rate controlling step; F-6-P –> F-1,6-P
inhibited by ATP, citrate
stimulated by hormones (via F-2,6-BisP), ADP and AMP

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12
Q

Regulation of Hexokinase

A

Glucose –> G-6-P; Stimulated by insulin

Inhibited by end product (G-6-P), acetyl-CoA

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13
Q

Regulation of Pyruvate Kinase

A

PEP –> Pyruvate; stimulated by F-2,6-BisP, insulin

inhibited by ATP

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14
Q

Fructose-2,6-Bisphosphate

A

synthesized from F-6-P; accelerator of glycolysis; regulates PFK1/Fructose bisphosphatase

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15
Q

Common Misconception about Glycolysis

A

glycolysis is NOT performed solely for energy generation; it is also for removal of glucose from circulation and building up long term stores of energy–if glucose is available, glycolysis is very active regardless of cellular energy demands

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16
Q

Regulation of Glycolysis in Starvation State

A

Glucagon activates PKA via cAMP cascade; PKA inhibits PFKII so F-2,6-BisP is no longer made from F-6-P; w/o F-2,6-BisP then gluconeogenesis can proceed uninhibited

17
Q

Regulation of Glycolysis in Well Fed State

A

Insulin inhibits PKA (cAMP cascade not started); inhibition of PKA leads to active PFKII which produces F-2,6,-BisP; F-2,6-BisP upregulates PFKI and glycolysis proceeds while GNG is shutdown

18
Q

PFKII

A

F-6-P –> F-2,6-BisP; upregulated by AMP, F-6-P and downregulated by PKA

19
Q

Glycerol Phosphate Shuttle

A

muscle and brain; gets electrons from NADH in cytosol and puts them on FADH in mito matrix; less efficient than other shuttle; for tissues that utilize a lot of glucose; loss of 1 ATP formation by going from NADH to FADH; glycercol-3-phosphate dehydrogenase

20
Q

Malate-Aspartate Shuttle

A

Liver/heart tissue; NADH reduces OAA to malate, malate transported across inner mito membrane, inside it is converted back to OAA and NADH is produced; more efficient than other shuttle

21
Q

If O2 is not available–Fermentation

A

pyruvate must accept electrons from NADH to regenerate NAD+ for glycolysis; pyruvate–> lactate; occurs in RBC’s since they have no mito; lactate taken up by liver; accumulation = lactic acidosis

22
Q

Pyruvate Kinase Deficiency

A

deprives RBC’s of ATP; leads to lysis of RBC’s b/c membrane potential cannot be maintained; hemolytic anemia;

23
Q

Arsenate Poisoning

A

Aresnate can micmic phosphate; causes glycolysis to not be able to produce ATP (via substrate level -P); BAD for RBC’s = hemolytic anemia

24
Q

Cori Cycle

A

RBC’s/muscles convert pyruvate to lactate; lactate enters circulation and is picked up by liver; liver uses GNG to convert lactate–> pyruvate–> glucose; glucose sent back into circulation for RBS’s to utiltize to create ATP