Mfm - Energy Metabolism

Front 1

Why does lactose without lactase cause gas and diarrhea?

Back 1

It gets converted to to lactic acid, and byproducts are methane.

Lactic acid is osmotically active, pulling water into intestines.

Front 2

How many ATP are produced from glycolysis? NADH?

Back 2

2 ATP

2 NADH

Front 3

Why does most of muscle energy during a sprint come from glycolysis?

Back 3

Not enough O2 for TCA

Fewer mitochondria to have more room for muscle fibers

Front 4

How does insulin affect glucose uptake longterm?

Back 4

Increases GLUT4 receptors.

Front 5

What is the first enzyme in glycolysis? Its effects? Its regulators?

Back 5

Hexokinase

It phosphorylates glucose, preventing it from escaping back into the blood

It is regulated by high G6P

Front 6

What is the rate determining step in glycolysis?

Back 6

PFK.

Front 7

Aldolase

Back 7

Fructose bisphosphate into GAP and dihydroxyacetone phosphate

Front 8

How is ATP formed from glycolysis?

Back 8

Phosphoglycerate kinase and pyruvate kinase convert ADP to ATP.

Front 9

What are regulators of PFK?

Back 9

ATP - inhibits.

AMP - activates.

Protons - inhibit (prevent lactate build up)

Front 10

Inhibitors of PFK

Back 10

Citrate

H+ (representing lactate)

ATP

Front 11

Activators of PFK

Back 11

AMP

F26BP

Front 12

F26BP Cycle

Back 12

Created by PFK2

Broken down by FBPase2

Activates PFK

Front 13

FBPase2 (function, inhibitors, activators)

Back 13

Inhibits glucose breakdown

Inhibited by phosphorylation

Phosphorylated by glucagon via cAMP

Insulin reverses effects

Front 14

Downsides of Cori Cycle

Back 14

Too much H+ leaves cell

Causes pain in muscles

Lactic acidosis

Front 15

Pain in muscles from acid build up (name)

Back 15

Angina pectoris

Front 16

Irreversible steps of glycolysis

Back 16

PFK

Hexokinase

Pyruvate kinase

Front 17

Workaround for PFK

Back 17

Fructose 1,6 bisphosphatase

Front 18

Workaround for hexokinase

Back 18

Glucose 6 phosphatase

Front 19

Workaround for pyruvate kinase

Back 19

Pyruvate carboxylase

Phosphenolpyruvate carboxykinase

Front 20

Number of ATP used in gluconeogenesis

Back 20

6 (number of ATP used in ?)

Front 21

Alcohol's effects on glucose metabolism (3)

Back 21

Cause hypoglycemia

Too much NADH produced (Inhibit gluconeogenesis b/c no pyruvate)

Cause lactic acidosis

Front 22

Purpose of PPP

Back 22

Make NADPH (for biosynthesis)

Make ribose (for biosynthesis)

Front 23

First stage of PPP

Back 23

Make 2 NADPH

Make 1 ribose

Front 24

Starting substrate of PPP

Back 24

G6P

Front 25

G6P Dehydrogenase

Back 25

G6P to lactone

Produces NADPH

Front 26

Lactase (in PPP)

Back 26

Lactone to gluconate

Front 27

6-phosphogluconate dehydrogenase

Back 27

Gluconate to ribulose 5 phosphate

Produces NADPH

Front 28

Isomerase (in PPP)

Back 28

Ribulose 5 phosphate to ribose

Front 29

Second stage of PPP

Back 29

Convert ribose to glycolysis intermediates

2 Fructose 6 phosphate
1 GAP

Front 30

Inhibitors of PPP

Back 30

Low NADP+

High NADPH

Front 31

Need ribose (not NADPH)

Back 31

F6P and GAP (from glycolysis) are diverted to 2nd stage PPP

Front 32

Need NADPH

Back 32

Ribose converted to F6P and GAP

F6P and GAP go through gluconeogenesis

Front 33

Need ATP and NADPH (re: PPP)

Back 33

1st and 2nd stage of PPP

Glycolysis

Front 34

GSH (name, function)

Back 34

Glutathione

Relieves oxidative stress

Gets oxidized to prevent peroxides

Front 35

Low GSH effects (2)

Back 35

Hemolysis, b/c of higher peroxide levels

Hemoglobin forms cross-links after oxidizing

Front 36

Heinz Bodies

Back 36

Cross linked hemoglobin

Caused by low GSH

Front 37

Antibiotics and hemolytic anemia (cause and treatment)

Back 37

Antibiotics cause oxidative stress (if person has defective G6P dehydrogenase)

More glucose (drive PPP to the right)

Front 38

Location of glycogen enzymes

Back 38

On glycogen molecule

Front 39

Degraded product of glycogen (and enzyme of conversion)

Back 39

G1P

Phosphoglucomutase

Front 40

Glucose phosphorylase

Back 40

Breaks the 1,4 glucose linkages

Adds phosphate to glucose

Front 41

Lysosomes (re glycogen)

Back 41

Degrades some glycogen

Digestive organelles

Front 42

Phosphorylase Equilibrium States

Back 42

T (inactive)

R (active)

Front 43

Activators of R state

Back 43

AMP

Front 44

Activators of T state

Back 44

ATP

G6P

Front 45

Phosphorylase a regulation

Back 45

No allosteric effectors

Front 46

Phosphorylase Kinase (role and regulation)

Back 46

Phosphorylates phosphorylase b

Activated by glucagon

Activated by Ca (one subunit is calmodulin)

Insulin activates phosphatase (dephosphorylates phosphorylase)

Front 47

Glycogen synthesis

Back 47

Primer started by glycogenin

Every 7 residues new branch is started

Front 48

Glycogen synthesis regulation

Back 48

cAMP inhibits (caused by glucagon)

G6P activates

Front 49

Von Gierke's Disease (Type I) (cause and treatment)

Back 49

Absence of G6P phosphatase (can't release glucose into blood stream)

Give a lot of glucose (liver won't need to release it)

Front 50

Pompe's Disease (Type II)

Back 50

Lysosomes can't break down glycogen; it accumulates in heart and causes enlargement

Front 51

McArdle's Syndrome

Back 51

Lack of muscle phosphorylase

No breakdown of glycogen during exercise

Front 52

Neonatal glycogen

Back 52

During last 10 weeks, have only insulin to build up glycogen

Front 53

Insulin origin

Back 53

Pancreatic B cells

Front 54

Pancreatic glucose transporter (properties)

Back 54

GLUT2

High Km

Front 55

Glucokinase (location and properties)

Back 55

Liver and pancreas

High Km (for phosphorylating glucose)

Front 56

ATP and Insulin

Back 56

More ATP from more glucose

ATP closes K channels

Depolarized cell lets Ca in

Ca releases insulin

Front 57

cAMP and Insulin

Back 57

Glucagon stimulates cAMP

cAMP stimulates insulin

Front 58

MODY

Back 58

Defect in glucokinase

Can't release insulin, because can't sense glucose

Front 59

Output of TCA

Back 59

3 NADH

1 FADH2

1 GTP

Front 60

Pyruvate Dehydrogenase Complex (purpose)

Back 60

Pyruvate to acetyl CoA

Front 61

Pyruvate Dehydrogenase Complex (subunits and cofactors)

Back 61

E1 decarboxylates pyruvate (uses thiamine)

E2 attaches CoA (uses lipoamide)

E3 oxidizes E2 (produces NADH)

Front 62

PDH Complex Inhibitor (1)

Back 62

Phosphorylation

Front 63

Beriberi (cause and symptoms)

Back 63

Lack of thiamine; affects E1 decarboxylating pyruvate

Neuromuscular deficits (brain depends on glucose for TCA)

Front 64

Arsenic and mercury (cause and symptoms)

Back 64

Attaches to E2; prevents CoA addition

Neuromuscular deficits

Front 65

Arsenic and mercury (treatment)

Back 65

Give sulfurs (compete with E2 for the mercury)

Front 66

Genetic diseases of PDH (symptom)

Back 66

Lead to lactic acidosis (too much pyruvate)

Front 67

PDH diseases acidosis (location)

Back 67

CSF more than RBC

Front 68

TCA intermediates

Back 68

Citrate

Isocitrate

A-ketoglutarate

Succinyl CoA

Succinate

Fumarate

Malate

Oxaloacetate