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biochemistry > Exam1 > Flashcards

Exam1 Flashcards

1
Q

Glucose transporter (SGLT) Sodium dependent glucose transport

A

SLC gene 5
Symporter
Uses Na to go down its gradients while glucose goes against. (secondary active transport)

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2
Q

GLUTX uniporters

A

SLC gene 2
Glucose transported bidirectionally down gradient

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3
Q

GLUT 1 (Tissue Location)

A

Brain, Ethrocytes, colon, placenta kidney

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4
Q

(Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport)
GLUT 1 (Function)

A

Constitutively and widely
expressed, highest glucose
affinity(lowest K m) and basal
glucose uptake

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5
Q

(Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport)
GLUT 1 (Deficency)

A

Epileptic encephalopatny
movement disorder, development delats, immature tight junctions

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6
Q

(Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport)

GLUT 2 (Location)

A

Liver, Pancreatic β cells, Small intestines, kidney
tubular cells

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7
Q

Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport

GLUT 2 (Function)

A

Rapid glucose uptake and
release, Lower V max than GLUT
1/3, High K

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8
Q

Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport

GLUT 2 Deficiency

A

Bickel syndrome, hepatomegaly , Ricketts, hepatomegaly, glucose, galactose, fructose intolerance , hypoglycemia

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9
Q

Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport

GLUT 3 (Location)

A

Brain, Kidney, Placenta

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10
Q

Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport

GLUT 3 (Function)

A

Similar to GLUT 1

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11
Q

Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport

GLUT 5 (Location)

A

Small intestines

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12
Q

Facilitated Bidirectional
Non-Insulin-Dependent
Glucose Transport

GLUT 5 (Function)

A

Fructose uptake

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13
Q

Facilitated
Bidirectional Insulin-
Dependent Glucose
Transport

GLUT 4 (Location)

A

Adipose tissues, Heart and skeletal muscle

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14
Q

Facilitated
Bidirectional Insulin-
Dependent Glucose
Transport

GLUT 4 (Function)

A

Insulin-induced/regulated
glucose uptake

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15
Q

Sodium-Dependent
Unidirectional
Glucose Transport

SGLT-1 (Location)

A

Small intestines and kidney tubules (apical
surfaces)

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16
Q

Sodium-Dependent
Unidirectional
Glucose Transport

SGLT-1 (Function)

A

SGLT1 accepts glucose and
galactose and is a 2 Na+:1
monosaccharide cotransporter.

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17
Q

Sodium-Dependent
Unidirectional
Glucose Transport

SGLT-1 (Deficency)

A

-Glucose Galactose malabsorption
-Newborn diarrhea
- Stool acidic , H+ brain

18
Q

Sodium-Dependent
Unidirectional
Glucose Transport

SGLT-2 (Location)

A

Kidney tubules (apical surface

19
Q

Sodium-Dependent
Unidirectional
Glucose Transport

SGLT-2 (Function)

A

SGLT2 accepts glucose (not
galactose) and is a 1 Na+:1
monosaccharide cotransporter;
it moves the bulk of filtered
glucose.

20
Q

Sodium-Dependent
Unidirectional
Glucose Transport

SGLT-2 (Deficiency)

A

Renal glucosuria
hypovolemia
hyperaminoaciduria
It is a target of a class of oral hypoglycemic
agents including canagliflozin, dapagliflozin, and
empagliflozin
* Possible gout treatment

21
Q

Nucleus

A

(Brain) Control center of cell

22
Q

Mitochondria

A

(Powerhouse) Provides Energy

23
Q

Golgi Apparatus

A

sort, packages transports protein

24
Q

Endoplasmic Reticulum

A

Protein Synthesis

25
Q

Ribosomes

A

Protein Synthesis

26
Q

Lysosomes

A

Lipid degradation breakdown

27
Q

HEXOKINASE

A
  • Expressed by most tissues
  • Not induced by insulin
  • Lower Km (high glucose affinity)
  • Lower Vmax (low glucose
    capacity)
  • Inhibited by glucose 6-phosphate
28
Q

GLUCOKINASE

A
  • Present on liver, small intestines
    and pancreatic β cells
  • Induced by insulin
  • Higher Km (low glucose affinity)
  • Higher Vmax (high glucose
    capacity)
  • Inhibited by Glucokinase
    regulatory protein via fructose
    6-phosphate
29
Q

Phosphofructokinase
Deficiency

A

inability to utilize free or glycogen derived
glucose as a fuel source with the accumulation of
glycogen.
* (Myophosphorylase
deficiency) – muscle cramps, exercise intolerance,
rhabdomyolysis, , hemolytic anemia (not present in
McArdle’s) and hyperuricemia – floppy babies.
*A forearm ischemic exercise test shows a flat lactate
curve and a normal increase in ammonia.
*Management : a high fat, high protein, low
carbohydrate diet and rest (avoiding strenuous activity)

30
Q

Pyruvate kinase Deficiency

A

*Most common glycolytic enzymopathy. Commonly autosomal recessive
disorder that causes both acute and chronic hemolysis
*Increased 2,3-bisphosphoglycerate(BPG or DPG) and lower than
normal O2 affinity of Hb
*Reduced ATP production in RBCs due to its deficiency causes them
to become abnormally shaped and easily destroyed in the spleen.
They form echinocytes – “Burr cells” that look like a hedgehog with
evenly spaced thorny spikes on the surface.
*Also loss Na+/K+ pump activity causes cell swelling, membrane
rigidity, osmotic fragility and lysis
*This condition is characterized by an absence of Heinz bodies
(inclusion bodies)
*May require partial splenectomy to reduce the incidence of hemolysis

31
Q

IRREVERSIBLE STEPS
IN GLYCOLYSIS

A

Phosphofructokinase (-25 KJ/
mol)
* Glucokinase (-27 KJ/mol)
* Pyruvate kinase (-14 KJ/mol)
* All have DG too large and
negative to simply reverse

32
Q

Recall Hexokinase catalyzes:

A

Glucose + ATP -> G6P + ADP
G6P + ADP -> Glucose + ATP

33
Q

Gluconeogenesis: Energy
Requirement

A

The vast amount of energy required to drive
gluconeogenic reactions is derived from fatty acid
oxidation – therefore impaired fatty acid oxidation is
often characterized by failure of gluconeogenesis
leading to hypoglycemia.
* From pyruvate, 3 moles of ATP are consumed by the;
–Pyruvate carboxylase reaction
–PEPCK reaction
–PGK reaction
And since 2 pyruvates are used to produce 1 mole of
glucose, a total of 6 moles of ATP is used.
* From glycerol, 1 mole of ATP is used by glycerol
kinase and since 2 moles of glycerol yield 1 mole of
glucose, the total ATP involved is 2
* Glycerol is more energy efficient!

34
Q

FADH2 from Riboflavin(Vit B2)

A

Oxidized- FAD
Reduced- FADH2
Sources= milk and dairy
Co-Factor = Succinate dehydrogenase

35
Q

NADH from Niacin(Vit B3)

A

Useful for NAD+, NADH,
- anti-hyperlipidemic agent, providing ADP-ribosylation
of proteins for gene regulation, apoptosis and signaling
Hartnup disease
carcinoid syndrome
*Deficiency – Pellagra

36
Q

Coenzyme A

A

H2O soluble vitamin
essential life

37
Q

Thiamine Pyrophosphate TPP

A

carbon on thiamine ring
aldehyde transfer
alcoholism
uncooked silkworm/fish
= deficiency

38
Q

-Lipoic acid (Lipoamide in
proteins)

A

provide a reactive disulfide or sulfhydryly group that
can participate in redox reactions

39
Q

E1 pyruvate
dehydrogenase subunit

A

TPP

40
Q

E2 dihydrolipoyl transacetylase

A

lipoamide

41
Q

E3
dihydrolipoyl dehydrogenase

A

FAD

42
Q

The pyruvate dehydrogenase reaction can be
broken down into five distinct catalytic steps:

A
  1. Decarboxylation
  2. Transfer of the acetyl group to lipoamide
  3. Formation of acetyl-CoA
  4. Redox reaction to form FADH2
  5. Redox reaction to form NADH

biochemistry (7 decks)

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