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Carb metabolism Flashcards

Zaise 7/31

1
Q

Glut1

A

High affinity, is ubiquitous but found in RBC and brain

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2
Q

Glut 2

A

low affinity (so high Km) found in liver, kidneys

  • does all glucose, galactose and fructose
  • only on BL side not apical (lumen)
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3
Q

Glut3

A

High affinity, neurons

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4
Q

Glut 4

A

Insulin dependent!! SK and heart and adipose tissue

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5
Q

Glut4 depndecy

A

Dependent on insulin, is sequestered until insulin binds to membrane insulin receptor, after a kinase mediated insulin cascade th microvesicles fuse w membrane

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6
Q

Glycolysis location and net yield

A

occurs in cytoplasm, yields 2 ATP, 2 NADH, 2 pyruvate

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7
Q

3 phases of glycolysis

A

Investment: req 2 ATP
Splitting: 1 six C molecule to 2 three C molecules
Recoup/payoff: 4 ATP generated

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8
Q

hexokinase

A

traps glucose in cell making G6P. in all cells, low Km and high affinity, substrate is glucose and other sugars, Inhibited by G6P

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9
Q

Glucokinase

A

Only in liver/pancreas, high Km & low affinity, high Vmax, substate is glucose only, not inhibited by G6P, F6P translocates to nucleus, F1P moves it to cytosol, insulin induces and glucagon inhibits

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10
Q

Rate limiting step for glycolysis

A

PFK-1; uses ATP converts F6P to F1,6-BisPhos

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11
Q

PFK-1 regulation

A

Activated by PFK-2/FBPase-2,AMP inhibited by ATP, citrate

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12
Q

PFK-2/FBPase-2

A

dimeric enzyme: is kinase when dephosphorylated and a phosphatase when -P; de-P favored by insulin, -P favored by glucagon

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13
Q

Tarui disease

A

Deficiency in PFK-1; exercise induced muscle cramps & weakness, hemolytic anemia, high blirubin/jaundice

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14
Q

Pyruvate Kinase

A

PEP into pyruvate; (+): F1,6-BP (feed fwd) y insulin, (-): ATP, Alanine, glucagon; high insulin: phosphatase dephospho PK= active; glucagon: cAMP activates PKA, Phosphorylation = PK inhibited

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15
Q

G6P is junction point

A

PPP: ribose, NADPH
Glycogenesis: glycogen
Glycolysis: pyruvate-F6P
Gluconeogenesis: Glucose

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16
Q

disorders of glycolysis

A

most defects cause hemolytic anemias (since RBCs only have glycolysis)
-95% of disorders are defects in PK

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17
Q

Carb. metabolism orchestrated by…

A

relative amounts of insulin and glucagon in blood

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18
Q

diabetes

A

group of diseases caused by hyperglycemia

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19
Q

Type 1 diabetes

A

severe insulin deficiency due to defective pancreatic Beta cells (likely due to immune destruction)

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20
Q

Type 2 diabetes

A

insulin resistance that progress to loss of beta cell function

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21
Q

Fasting blood glucose levels:

A

70-100 mg/dL
prediabetic: 100-125
above 12 is diabetic

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22
Q

Hemolytic anemia clinical markers

A

elevated LDH in plasma (due to cells breaking and releasing), unconjugated bilirubin

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23
Q

Fanconi-Bickel Syndrome

A

AR, mutation in Glut 2, unable to take up glucose, fructose, galactose

  • failure to thrive, hepatomegaly, tubular nephropathy, abdominal bloating, resistant rickets
  • treat w vit. D and phosphate
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24
Q

Body needs of glucose vs reserve

A

whole body: 160g (brain is 120 of that)
present in body fluids: 20
present in glycogen reserves: 190g
so have about a days worth in reserve wo replenish

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25
gluconeogenesis location in body
only occurs in cells of liver, kidney and small intestine
26
Gluconeo bypasses IR steps of glycolysis by:
PK: PEP carboxykinase and pyruvate carboxylase PFK-1: F1,6-BPase Hexokinase/glucokinase: G6Pase
27
positive regulators for glycolysis
glucose, insulin, AMP, Fri2,6-BP,F1,6-BP
28
Positive reg for gluconeogenesis
glucagon, citrate, cortisol, thyroxine, acetyl CoA
29
Neg Reg of glycolysis
glucagon, ATP,citrate, G6P, F6P, alanine
30
Neg Reg for gluconeogenesis
ADP, AMP, F2,6-BP
31
Pyruvate Carboxylase
PC is mitochondrial enzyme, catalyzes first step in gluconeo, pyruvate in mito is carboxylated to form OAA, biotin is cofactor (+): acetyl CoA and cortisol
32
Fate of OAA after PC
since OAA cant get past Mito matrix its reduced to malate by mitochondrial malate DH,' malate shuttle' to cytoplasm, reoxidized to OAA by cytosolic malate DH
33
PEPCK
- OAA from mitochondria (via malate intermediate) decarboxylated and phosphorylated to PEP using GTP - transcription activated by: cortisol, glucagon, thyroxine
34
F 1,6-Bisphosphotase
RL step in gluconeo (+): cortisol, citrate (-): AMP and F26BP
35
G6-phosphotase
in ER lumen, only in liver, kidneys, SI and pancreas
36
cori cycle
links lactate produced from anaerobic glycolysis in RBC and exercising muscle to gluconeo in liver - prevents lactate accumulation - regenerates glucose
37
precursors of gluconeogenesis
Carbs, lipids and proteins
38
F1,6BP deficiency
similar to tarui, presents in infancy and early childhood, hypoglycemic, lacic acidosis
39
Von Gierke Disease
deficiency in glucose-6-phosphotase -1 in 100k births marked fasting hypoglycemia, large liver bc buildup of glycogen
40
Glut 5
Fructose uptake from apical and BL
41
SGLT1
takes up glucose, galactose, Na+ from apical side (since Glut2 is only on BL side
42
Polyyol Pathway
Glucose--> sorbitol--->fructose | -used by sperm
43
Fructose
- metabolizes faster than glucose bc bypasses Rl step (PFK1), ends up being stored as triacylglycerols - too much results in fatty liver
44
galactose metabolism
galactose---(galactokinase)--> G1P--(GALT)--> glucose1P (via a UDP intermediate)---G6P------>glycolysis
45
Galactosemia classic
GALT defective, accumulation of galactitol
46
Galactosemia non classical
accumulation of galactitol and galactose in blood and urine, accumulation of galactitol in eye = cataracts
47
PPP
occurs in cytosol, produces ribose and NADPH in 2 diff phases an irreversible oxidative step and reversible non -oxidative
48
PPP Rl enzyme
G6P DH- creates NADPH and ends with Ribulose-5-p
49
G6PD deficiency
mostly AA population, hemolytic anemia, since NADPH regenerates glutathione
50
PPP non oxidative phase
series of reversible steps whose products go to glycolysis, gluconeogenesis, nucleotide syn
51
glycogen
stored in liver and muscle as granules, these granules store glycogen and the req. enzymes
52
liver glycogen
regulates blood glucose levels
53
muscle glycogen
provides reservoir of fuel for physical activity
54
Phosphoglucomutase
converts G6P to G1P
55
UDP-glucose-pyrophosphorylase
converts G1P to UTP which generates UDP-glucose
56
Glycogen Synthase
RL Step!!!!!!!!!!!!!!! | -transfer of glucose from UDP-glucose to non-reducing end of glycogen chain
57
branching of glycogen chain
glucosyl(4:6) transferase aka 'branching enzyme'
58
glycogenolysis
2 steps: chain shortening (GP) & Branch transfer and release of glucose (debranching enzyme)
59
debranching enzyme
uses its transferase (4:4) activity to transfer a block of 3 of the remaining 4 glucose to NR end
60
A-1,6 glucosidase
removes remaining 1 singular branched glucose
61
fate of liver vs muscle G1P
liver: converted to G6P then glucose=released n blood muscle: dont have G6Pase so uses G6P to form energy via glycolysis and TCA
62
pathways of glycogen synthesis and degradation regulated by phosphorylation
GS: Active when dephosphorylated- active when phosphorylated GP: opposite

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