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SFM Exam 1 > Carb Metabolism > Flashcards

Carb Metabolism Flashcards

1
Q

Anaerobic glycolysis

A

Occurs in cells that lack mitochondria (RBCs)
Critical source of ATP for RBCs
Important in overworked muscles that lack O2
Glucose is converted to pyruvate then metabolized to lactate

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2
Q

True or false: All cells carry out glycolysis

A

True

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3
Q

Why is glucose important in mammals?

A

It is the only fuel that RBCs can use and the only fuel that the brain can use under non-starvation conditions

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4
Q

GLUT 1

A

Ubiquitous but high expression in RBCs and the brain

High affinity

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5
Q

GLUT 2

A

Main transporter in the liver

Low affinity

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6
Q

GLUT 3

A

Main transporter in neurons

High affinity

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7
Q

GLUT 4

A

Present in skeletal muscle, heart and adipose tissue
Insulin dependent
Sequestered in vesicles in cells
Insulin signaling causes fusion of vesicles with plasma membrane and placement/insertion of GLUT 4 in the membrane
-increases GLUT 4 induced glucose uptake
-initiated when exercising

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8
Q

Which of the 4 GLUTs are regulated?

A

Only GLUT 4 is regulated (by insulin) and the rest are unregulated (depend on a concentration gradient)

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9
Q

What is the net yield of glycolysis?

A

2 ATP, 2 NADH and 2 pyruvate

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10
Q

What is the RLS of glycolysis?

A

Phosphorylation of F6P to F16BP catalyzed by PFK-1

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11
Q

List the substrates of glycolysis in order

A 
Glucose 
G6P 
F6P 
F16BP —> DHAP and G3P 
13BPG 
3PG 
2PG 
PEP 
Pyruvate
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12
Q

List the enzymes of glycolysis in order

A 
Hexokinase/glucokinase 
Phosphoglucose isomerase 
PFK-1 
Triose phosphate isomerase/aldolase 
G3P dehydrogenase 
Phosphoglycerate kinase 
Phosphoglycerate mutase 
Enolase
Pyruvate kinase
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13
Q

Which enzymes of glycolysis use ATP?

A

Hexokinase/glucokinase and PFK-1

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14
Q

What inhibits hexokinase?

A

G6P (its product)

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15
Q

What is PFK-1 activated by?

A

AMP and F26BP

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16
Q

What inhibits PFK-1?

A

ATP and citrate

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17
Q

How does high insulin/low glucagon affect PFK-1?

A

It activates protein phosphatases, dephosphorylates PFK-2/FBPase-2 (triggers kinase activity) producing F26BP which activates PFK-1

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18
Q

How does high glucagon/low insulin affect PFK-1?

A

It induces high cAMP concentration, activates PKA, phosphorylates PFK-2/FBPase-2 (triggering phosphorylation activity) and reducing PFK-1 activity

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19
Q

Tarui disease

A

Deficiency in PFK-1
Exercise induced muscle cramps and weakness
Hemolytic anemia
High bilirubin and jaundice

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20
Q

What activates pyruvate kinase?

A

F16BP and insulin

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21
Q

What is pyruvate kinase inhibited by?

A

ATP, alanine and glucagon

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22
Q

How does a high insulin concentration influence pyruvate kinase?

A

Stimulates phosphorylase, dephosphorylation of PK (active form)

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23
Q

How does high glucagon concentration influence pyruvate kinase?

A

cAMP activates PKA, phosphorylates PK (inhibited form)

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24
Q

What is G6P a precursor for?

A

PPP

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25
G6P is converted to glucose 1 phosphate which is used in what?
Galactose metabolism, glycogen synthesis, uronic acid synthesis
26
Fancon-Bickel syndrome is caused by what?
Mutation in GLUT 2 transporter | Pts are unable to take up glucose, fructose and galactose
27
Why is maintaining levels of glucose important?
Because the brain depends on glucose as its primary fuel and RBCs use glucose as their only fuel
28
How many grams of glucose is needed by the whole body?
160g per day
29
Daily glucose requirement of the brain?
120g
30
Glucose present in body fluids?
20g
31
Glucose readily available from glycogen?
190g
32
Direct glucose reserves are sufficient to meet glucose needs for how long?
About a day
33
When does gluconeogenesis occur?
When glucose and glycogen stores are depleted (ex. Starvation, exercise and ketogenic diet (low carb))
34
Gluconeogenesis bypasses the 3 irreversible steps of glycolysis catalyzed by hexokinase/glucokinase, PFK-1 and PK, and replaces them with what?
Pyruvate carboxylase, PEP carboxykinase, F16BPase and G6Pase
35
List the precursors for gluconeogenesis
Fructose, galactose, glycogen, glycerol, propionate, lactate, alanine and amino acids (except leucine and lysine)
36
What is the RLE of gluconeogenesis?
F16BPase which breaks down F16BP to F6P
37
What is pyruvate carboxylase (gluconeogenesis) activated by?
Acetyl CoA and cortisol
38
What is PEP carboxykinase (gluconeogenesis) activated by?
Cortisol, glucagon and thyroxine
39
What is F16BPase (gluconeogenesis) activated by?
Cortisol and citrate
40
What inhibits F16BPase (gluconeogenesis)?
AMP and F16BP
41
What is glucose 6 phosphatase (gluconeogenesis) activated by?
Cortisol
42
Explain the Cori cycle
Links lactate produced from anaerobic glycolysis in RBCs and exercising muscle to gluconeogenesis in the liver then the glucose produced in the liver is transported back to RBCs and muscle
43
What is the purpose of the Cori cycle?
Prevents lactate accumulation and re-generates glucose
44
F16BP deficiency
Similar to Tarui disease in glycolysis Presents in infancy or early childhood Hypoglycemia, lactic acidosis and ketosis
45
Von Gierke disease (GSD 1a)
Deficiency in G6Pase | Inefficient release of free glucose into the blood stream by the liver in gluconeogenesis and glycogenolysis
46
When sucrose is cleaved by sucrase what are the products?
Glucose and fructose
47
When lactose is cleaved by lactase what are the products?
Galactose and glucose
48
What is the RLE in the PPP?
G6P dehydrogenase which reduces NADP to NADPH and oxidizes G6P to G-phosphoglucono-delta-lactose
49
Which phase of PPP is favored if cells (like rapidly dividing cells) have a high demand for ribulose 5 P?
Oxidative phase is favored to produce ribulose 5P
50
Which phase of the PPP is favored if cells have a high demand for NADPH?
Non oxidative products are channeled into gluconeogenesis for re-entry into the PPP to produce NADPH
51
Glucose molecules within a glycogen chain are linked together via what?
Alpha 1,4 glycosidic bonds
52
Branch points within a glycogen molecule are formed via what?
Alpha 1,6 glycosidic bonds
53
Non-reducing ends of glycogen contain a
Terminal glucose with a free OH group at C4
54
Reducing ends of glycogen consist of
Glucose monomer connected to a protein called glycogenin
55
Glycogenin creates a
Short glycogen polymer on itself and serves as a primer of glycogen synthesis
56
How is glycogen stored?
It is stored as granules that contain glycogen and enzymes that are needed for glycogen metabolism Stored in the liver, muscle and other tissues
57
What is the function of liver glycogen?
Regulate blood glucose levels
58
What is the function of muscle glycogen?
Provides a reservoir of fuel (glucose) for physical activity
59
What is the RLE of glycogenesis?
Glycogen synthase which catalyzes the transfer of glucose from UDP glucose to the NRE of the glycogen chain
60
What is the RLE of glycogenolysis?
Glycogen phosphorylase which catalyzes the cleavage of glucose residue as glucose 1 phosphate from NRE of glycogen
61
What is the fate of glucose 1 phosphate in the liver?
It is converted to glucose 6 phosphate by an epimerase and then glucose by glucose 6 phosphatase. Free glucose is then released into the blood stream
62
What is the fate of glucose 1 phosphate in muscle?
Skeletal and cardiac myocytes lack G6Pase and cannot hydrolyze Glu6P so instead they use it to generate energy via glycolysis and the TCA cycle
63
Why is regulation of glycogen metabolism important?
To maintain blood sugar and to provide energy to muscle
64
What is the active form of glycogen synthase?
Dephosphorylated
65
What is the active form of glycogen phosphorylase?
Phosphorylation
66
Type 2 diabetes
Also called insulin resistance Reduced sensitivity to insulin Mutations in insulin receptor &/or downstream signaling proteins
67
What are some causes for down regulation of insulin receptors seen in type 2 DM?
Triggered by elevated insulin Endocytosis and degradation of the insulin receptor Defective receptors not replaced by translation
68
Normal blood glucose criteria
70-100 fasting | <140 fed
69
Pre-diabetic/at risk blood glucose criteria
100-125 fasting | >140 fed
70
DM blood glucose criteria
>126 fasting | >199 fed
71
Disorders that affect glycogen breakdown lead to what?
Hepatomegaly and hypoglycemia (inability to maintain blood sugar)
72
Pts that suffer from disorders that affect glycogen synthesis depend on what?
Glucose rather than glycogen
73
GSD 0
Deficiency in glycogen synthase Pts cannot synthesize and store glycogen Rely on glucose in the diet Vulnerable to hypoglycemia when fasting (ex during sleep) Have muscle cramps due to lack of glycogen in the muscle and need to eat frequently
74
GSD 1a (Von Gierke disease)
Deficiency in glucose 6 phosphate Inefficient release of free glucose into the blood stream by the liver following gluconeogenesis and glycogenolysis Pts exhibit marked fasting hypoglycemia, lactic acidosis, hepatomegaly due to glycogen buildup and HLD
75
GSD II (Pompe disease)
Deficiency in acid maltase aka acid alpha glucosidase Impairs lysosomal glycogenolysis resulting in accumulation of glycogen in lysosomes Disrupts normal fxn of muscle and and hepatocytes Progressive muscle weakness in body including heart and skeletal
76
GSD III (Cori disease)
Deficiency in alpha 1,6 glucosidase (debranching enzyme) Pts possess glycogen molecules with large numbers of short branches Light hypoglycemia and hepatomegaly
77
GSD IV (Andersen disease)
Deficiency in glucosyl 4:6 transferase (branching enzyme) | Pts have long chain glycogen with few branches
78
GSD V (McArdle disease)
Deficiency in muscle glycogen phosphorylase RLS in glycogen breakdown Pts unable to supply muscles with enough glucose Have weakness, fatigue, muscle cramping and breakdown Exercise intolerance
79
GSD VI (Hers disease)
Deficiency in liver glycogen phosphorylase Prevents glycogen breakdown in liver hence it accumulates in the liver casing hepatomegaly Low blood glucose levels
80
When does PFK-2/FBPase-2 work as a kinase?
When it is dephosphorylated which is favored by insulin
81
When does PFK-2/FBPase-2 works as a phosphatase?
When it is phosphorylated which is favored by glucagon

SFM Exam 1 (8 decks)

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