Exam1 Flashcards

(42 cards)

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
Ribosomes
Protein Synthesis
26
Lysosomes
Lipid degradation breakdown
27
HEXOKINASE
* Expressed by most tissues * Not induced by insulin * Lower Km (high glucose affinity) * Lower Vmax (low glucose capacity) * Inhibited by glucose 6-phosphate
28
GLUCOKINASE
* 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
Phosphofructokinase Deficiency
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
Pyruvate kinase Deficiency
*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
IRREVERSIBLE STEPS IN GLYCOLYSIS
Phosphofructokinase (-25 KJ/ mol) * Glucokinase (-27 KJ/mol) * Pyruvate kinase (-14 KJ/mol) * All have DG too large and negative to simply reverse
32
Recall Hexokinase catalyzes:
Glucose + ATP -> G6P + ADP G6P + ADP -> Glucose + ATP
33
Gluconeogenesis: Energy Requirement
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
FADH2 from Riboflavin(Vit B2)
Oxidized- FAD Reduced- FADH2 Sources= milk and dairy Co-Factor = Succinate dehydrogenase
35
NADH from Niacin(Vit B3)
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
Coenzyme A
H2O soluble vitamin essential life
37
Thiamine Pyrophosphate TPP
carbon on thiamine ring aldehyde transfer alcoholism uncooked silkworm/fish = deficiency
38
-Lipoic acid (Lipoamide in proteins)
provide a reactive disulfide or sulfhydryly group that can participate in redox reactions
39
E1 pyruvate dehydrogenase subunit
TPP
40
E2 dihydrolipoyl transacetylase
lipoamide
41
E3 dihydrolipoyl dehydrogenase
FAD
42
The pyruvate dehydrogenase reaction can be broken down into five distinct catalytic steps:
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