Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SFM > Carb metabolism > Flashcards

Carb metabolism Flashcards

Zaise 7/31

1
Q

Glut1

A

High affinity, is ubiquitous but found in RBC and brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Glut3

A

High affinity, neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Glut 4

A

Insulin dependent!! SK and heart and adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glycolysis location and net yield

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Rate limiting step for glycolysis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PFK-1 regulation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tarui disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

G6P is junction point

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

disorders of glycolysis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Carb. metabolism orchestrated by…

A

relative amounts of insulin and glucagon in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

diabetes

A

group of diseases caused by hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type 1 diabetes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Type 2 diabetes

A

insulin resistance that progress to loss of beta cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fasting blood glucose levels:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hemolytic anemia clinical markers

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

gluconeogenesis location in body

A

only occurs in cells of liver, kidney and small intestine

26
Q

Gluconeo bypasses IR steps of glycolysis by:

A

PK: PEP carboxykinase and pyruvate carboxylase
PFK-1: F1,6-BPase
Hexokinase/glucokinase: G6Pase

27
Q

positive regulators for glycolysis

A

glucose, insulin, AMP, Fri2,6-BP,F1,6-BP

28
Q

Positive reg for gluconeogenesis

A

glucagon, citrate, cortisol, thyroxine, acetyl CoA

29
Q

Neg Reg of glycolysis

A

glucagon, ATP,citrate, G6P, F6P, alanine

30
Q

Neg Reg for gluconeogenesis

A

ADP, AMP, F2,6-BP

31
Q

Pyruvate Carboxylase

A

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
Q

Fate of OAA after PC

A

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
Q

PEPCK

A
  • OAA from mitochondria (via malate intermediate) decarboxylated and phosphorylated to PEP using GTP
  • transcription activated by: cortisol, glucagon, thyroxine
34
Q

F 1,6-Bisphosphotase

A

RL step in gluconeo
(+): cortisol, citrate
(-): AMP and F26BP

35
Q

G6-phosphotase

A

in ER lumen, only in liver, kidneys, SI and pancreas

36
Q

cori cycle

A

links lactate produced from anaerobic glycolysis in RBC and exercising muscle to gluconeo in liver

  • prevents lactate accumulation
  • regenerates glucose
37
Q

precursors of gluconeogenesis

A

Carbs, lipids and proteins

38
Q

F1,6BP deficiency

A

similar to tarui, presents in infancy and early childhood, hypoglycemic, lacic acidosis

39
Q

Von Gierke Disease

A

deficiency in glucose-6-phosphotase
-1 in 100k births
marked fasting hypoglycemia, large liver bc buildup of glycogen

40
Q

Glut 5

A

Fructose uptake from apical and BL

41
Q

SGLT1

A

takes up glucose, galactose, Na+ from apical side (since Glut2 is only on BL side

42
Q

Polyyol Pathway

A

Glucose–> sorbitol—>fructose

-used by sperm

43
Q

Fructose

A
  • metabolizes faster than glucose bc bypasses Rl step (PFK1), ends up being stored as triacylglycerols
  • too much results in fatty liver
44
Q

galactose metabolism

A

galactose—(galactokinase)–> G1P–(GALT)–> glucose1P (via a UDP intermediate)—G6P——>glycolysis

45
Q

Galactosemia classic

A

GALT defective, accumulation of galactitol

46
Q

Galactosemia non classical

A

accumulation of galactitol and galactose in blood and urine, accumulation of galactitol in eye = cataracts

47
Q

PPP

A

occurs in cytosol, produces ribose and NADPH in 2 diff phases an irreversible oxidative step and reversible non -oxidative

48
Q

PPP Rl enzyme

A

G6P DH- creates NADPH and ends with Ribulose-5-p

49
Q

G6PD deficiency

A

mostly AA population, hemolytic anemia, since NADPH regenerates glutathione

50
Q

PPP non oxidative phase

A

series of reversible steps whose products go to glycolysis, gluconeogenesis, nucleotide syn

51
Q

glycogen

A

stored in liver and muscle as granules, these granules store glycogen and the req. enzymes

52
Q

liver glycogen

A

regulates blood glucose levels

53
Q

muscle glycogen

A

provides reservoir of fuel for physical activity

54
Q

Phosphoglucomutase

A

converts G6P to G1P

55
Q

UDP-glucose-pyrophosphorylase

A

converts G1P to UTP which generates UDP-glucose

56
Q

Glycogen Synthase

A

RL Step!!!!!!!!!!!!!!!

-transfer of glucose from UDP-glucose to non-reducing end of glycogen chain

57
Q

branching of glycogen chain

A

glucosyl(4:6) transferase aka ‘branching enzyme’

58
Q

glycogenolysis

A

2 steps: chain shortening (GP) & Branch transfer and release of glucose (debranching enzyme)

59
Q

debranching enzyme

A

uses its transferase (4:4) activity to transfer a block of 3 of the remaining 4 glucose to NR end

60
Q

A-1,6 glucosidase

A

removes remaining 1 singular branched glucose

61
Q

fate of liver vs muscle G1P

A

liver: converted to G6P then glucose=released n blood
muscle: dont have G6Pase so uses G6P to form energy via glycolysis and TCA

62
Q

pathways of glycogen synthesis and degradation regulated by phosphorylation

A

GS: Active when dephosphorylated- active when phosphorylated

GP: opposite

SFM (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions