Brainscape's Knowledge GenomeTM

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


See full index

Biochemistry FA > Gluconeogenesis, HMP Shunt > Flashcards

Gluconeogenesis, HMP Shunt Flashcards

1
Q

Gluconeogenesis irreversible enzymes

A
  1. Pyruvate carboxylase
  2. Phosphoenoyruvate carboxykinase
  3. Fructose-1,6-bisphosphatase
  4. Glucose-6-phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pyruvate carboxylase reaction and location

A

Pyruvate + CO2+ATP –> oxaloacetate

Mitochondia

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

Pyruvate carboxylase is activated by

A

Acetyl coa

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

Pyruvate carboxylase requirement

A

Biotin

ATP

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

Phosphoenolpyruvate carboxykinase requirements

A

GTP

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

Phosphoenolpyruvate carboxykinase reaction and location

A

Oxaloacetate to phosphoenolpyruvate

cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Fructose -1,6- bisphosphatase reaction and location

A

Fructose -1,6-BP–>fructose-6-P

cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Fructose -1,6- bisphosphatase regulation

A

Citrate+
Fructose 2,6-BP-
AMP -
ATP +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Glucose-6-phosphatase reaction

A

Glucose -6-P–>glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Glucose-6-phosphatase LOCATION / AND ORGAN

A

ENDOPLASMIC RETICULUM

PRIMARILY IN LIVER

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

Gluconeogenesis serves

A

To maintain euglycemia during fasting

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

Gluconeogenesis tissues

A

Liver(primary)
Kidney
Intestinal epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Deficiency of key gluconeogenic enzymes cause

A

Hypoglycemia

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

Muscle - gluconeogenesis

A

no –> lacks glucose -6 phosphatase

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

fatty acids/gouconeogenesis

A

Even chain fatty acids –> cannot produce new, since they yield only acetyl-CoA equivalents
Odd-chain fatty acids –> yield one propionyl-CoA during metabolism, which can enter TCA (as succinyl-CoA), undergo gluconeogenesis

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

Propionyl-CoA can enter TCA cycle as

A

Succinyl - CoA

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

Odd-chain fatty acids/gluconeogenesis

A

They yield one propionyl-CoA during metabolism, which can enter TCA (as succinyl-CoA), undergo gluconeogenesis

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

Source of NADPH

A

HMP shunt

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

HMP

A

Pentose phosphate pathway

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

HMP provides a source of

A

NADPH

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

HMP provides a source of from abundantly available

A

Glucose-6-P

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

HMP yields

A
  1. NADPH
  2. Ribose for nucleotide synthesis
  3. Glycolytic intermediates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How many pathways for HMP shunt

A

2.

Oxidative and nonoxidative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

NADPH function

A
  1. Glutathione reductase
  2. Cytochrome P-450
  3. Respiratory burst
  4. Anabolic process (steroid and farry acids synthesis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Location of of oxidative HMP shunt

A

Cytoplasm

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

Location of nonoxidative HMP shunt

A

Cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ATP/HMP shunt

A

NO ATP IS USED OR PRODUCED IN HMP SHUNT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Is oxidative HMP shunt reversible or irreversible

A

Irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Sites of HMP shunt (organs)

A

Sites of fatty acid or steroid synthesis (lactating mammary glands, liver, adrenal glands), RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Is nonoxidative reaction reversible or irreversible

A

Reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

HMP shunt rate determining enzyme

A

G6PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

G6PD regulators

A

NADP+

NADPH-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Oxidative HMP shunt reaction

A

Glucose-6-P + 2NADP –> CO2 + 2NADPH + Ribulose-5-P (G6PD/irreversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

G6PD deficiency cellular features

A
  1. Heinz bodies

2. Bite cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Most common enzyme deficiency / mode of inheritance / PURPOSE

A

G6PD / XR

increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Bite cells

A

Result from the phagocytic removal of Heinz bodies (RBCs) by splenic macrophages

36
Q

Most common enzyme deficiency / mode of inheritance

A

G6PD / XR

increases

37
Q

Heinz bodies

A

Oxidized/denaturated Hemoglobin precipitated within RBCs

39
Q

G6PD deficiency anemia - mechanism

A

Decreased NADPH in RBCs leads to hemolytic anemia due to poor RBC defense against oxidizing agents

40
Q

Factors that precipitate hemolysis in G6PD deficiency

A
  1. Drugs: sulfonamides, primaquine, antituberculosis
  2. Fava beans
  3. Infections (ROS generated via inflammatory response can diffuse into RBCs and cause oxidative damage
41
Q

Fructose metabolism

A

Fructose + ATP –> Fructose-1-P + ADP (Fructokinase)
Fructose-1-P –> Dihydroxyacetone-P + Glyceraldehyde (Aldolase B):
- Dihydroxyacetone-P –> Glyceraldehyde-3-P –> glycolisis
- Glyceraldehyde + ATP –> Glyceraldehyde-3-P (Trise kinase) –> glycolisis
- Glyceraldehyde + NADH –> Glycerol

41
Q

Fructokinase reaction

A

Fructose + ATP –> F1P+ ADP

42
Q

Is Essential fructosuria a severe disease?

A

No. It is a benign symptomatic condition

43
Q

Essential fructosuria - mechanism and mode of inheritance

A

Defect in fructokinase

AR

44
Q

Essential fructosuria pathophysiology

A

Defect in fructokinase (AR)

Fructose is not trapped in cells –> fructose in blood and urine

45
Q

Essential fructosuria findings

A

Fructose appears in blood and urine

46
Q

Fructose intolerance mode of inheritance

A

AR

48
Q

Disorder of fructose metabolism vs galactose metabolism according symptoms

A

Disorder of fructose metabolism cause milder symptoms

48
Q

aldolase B reaction

A

Fructose-1-P to glyceraldehyde or dihydroxyacetone -P

49
Q

Fructose intolerance - deficiency of

A

Hereditary deficiency of aldolase B

50
Q

Fructose intolerance pathophysiology

A

Hereditary deficiency of aldolase B. Fructose-1-P accumulates causing decreased availability of phosphate –> inhibition of glycogenolysis and glyconeogenesis

51
Q

Fructose intolerance inhibits

A
  1. Glycogenolysis

2. Gluconeogenesis

53
Q

Symptoms of fructose intolerance present following

A

CONSUMPTION of fruit, juice, honey

54
Q

Fructose intolerance/urine

A
  1. Urine dipstick - (test for glucose only)

2. Reducing sugar can be detected in the urine (nonspecific for inborn errors of carbohydrate metabolsim)

55
Q

Fructose intolerance symptoms

A
  1. Hypoglycemia
  2. Jaundice
  3. Cirrhosis
  4. Vomiting
55
Q

Sucrose sequence

A

Glucose and fructose

56
Q

Fructose intolerance treatment

A

Reduce fructose and sucrose (glucose and fructose) intake

57
Q

Glyceraldehyde to glyceraldehyde-3-P - reaction

A

Triose kinase + ATP

58
Q

Galactokinase deficiency

A

Hereditary deficiency of galacktokimase

60
Q

Galactose metabolism

A

Galactose –>

a. Galactiol (Aldose reductase)
b. Galactose-1-P (Galactokinase) –> Glucose-1-P (Uridiltransferalase, 4-epimerse reverse it) –> Glycolysis/glycogenesis

60
Q

Galactokinase deficiency pathophysiology

A

Galactitol (reduction product of galactose) accumulates if galactose present in diet

61
Q

Is Galactokinase deficiency a severe condition / mode of inheritance

A

No. It is a relatively mild condition

AR

63
Q

Galactokinase deficiency sympoms

A
  1. Galactose in urine and blood
  2. Infantile cataracts
  3. May initially present as failure to track objects or to develop a social smile
63
Q

Classic galactosemia mode of inheritance

A

AR

64
Q

Classic galactosemia pathophysiology

A

Damaged is cause by accumulation of toxic substances (including galactitol, which accumulate in the lens of the eye)

65
Q

Classic galactosemia

A

Absence of galactose-1-phosphate uridyltransferase

66
Q

Classic galactosemia treatment

A

Exclude galactose and lactose (galactose and glucose) fro diet

67
Q

Lactose sequence

A

Galactose and glucose

68
Q

Classic galactosemia symptoms

A
  1. Failure to thrive
  2. Jaundice
  3. Hepatomegaly
  4. Infantile cataracts
  5. Intellectual disability
  6. E. Coli sepsis in neonates
  7. Pi depletion (in most serious defect)
69
Q

Galactose/glycolisis/glycogenesis

A

Galactose–>galactose-1-P(galactokinase) –> glucose-1-P (uridyltransferase) –> glycolysis/glyconeogenesis

71
Q

Lactase deficiency? types?

A

Insufficient lactase enzyme–> dietary lactose intolerance

types: 1ry, 2ry, congenital

72
Q

Lactase function

A

It is on the brush border and digests lactose (human and cow milk) into glucose and galactose

72
Q

Secondary lactose deficiency

A

Loss of brush border due to gastroenteritis (rotavirus), autoimmune etc

73
Q

Primary lactose deficiency

A

Age dependent decline after childhood (absence of lactase-persistent allele, common in people of Asia, Africa, native american descent

74
Q

lactose deficiency symptoms

A

Bloating, cramps, flatulence, osmotic diarrhea

75
Q

Congenital lactose deficiency

A

Rare, due to defective gene

76
Q

Lactase deficiency treatment

A

Avoid dairy products
Add lactase pills to diet
Lactose free milk

77
Q

Glucose alcohol counterpart

A

Sorbitol

78
Q

Lactase intolerance lab findings

A

Stool-low ph
Breath- high hydrogen
Intestinal biopsy - normal with hereditary

79
Q

Alternative method of trapping glucose in the cell

A

Convert it to sorbitol (its alcohol counterpart)

80
Q

Glucose to sorbitol reaction

A

Aldose reductase and NADPH

81
Q

Sorbitol to fructose

A

Sorbitol dehydrogenase + NAD

83
Q

Tissues with sorbitol dehydrogenase

A

Liver, ovaries, seminal vesicles

84
Q

Tissues without sorbitol dehydrogenase

A

Scwann cells, retina, kidneys has only aldose reductase

Lens has primarily aldose reductase

84
Q

G6PD deficiency is mom common in black or white

A

Black

85
Q

Insufficient amount of sorbitol reductase consequences

A

Intracellular accumulation –> osmotic damage (cataracts, retinopathy, peripheral neuropathy) seen in chronic hyperglycemia in diabetes

87
Q

G6PD deficiency evolutionary benefits

A

Malarial resistance

88
Q

MCC of hemolyisis in G6PD anemia

A

infection

Biochemistry FA (16 decks)

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