Wvsom Msk - 9/15/14 - Ds Glycolysis, Tca, Glycogen

Front 1

Name the starting materials, products of Glycolysis & whether it occurs in the fed or fasted state.

Back 1

Glycolysis occurs in the fed state. . .

Starting materials include glucose, NAD+, and ADP. . .

The products include pyruvate, ATP & NADH.

Front 2

Name two ways to regenerate NAD+.

Back 2

NAD+ is regenerated through the lactate dehydrogenase reaction and donation of an NADH electron to the electron transport chain.

Front 3

Name the starting materials, products of the Citric Acid Cycle & whether it occurs in the fed or fasted state.

Back 3

The Citric Acid Cycle occurs in the fed state. . .

The starting materials include Acetyl CoEnzymeA . .

The products include carbon dioxide, NADH, FADH2, and small amounts of GTP.

Front 4

Name the starting materials, products of the Glycogen Synthesis/Degradation & whether it occurs in the fed or fasted state.

Back 4

Glycogen synthesis occurs in fed state while degradation occurs in fasted state. . .

The synthesis begins with glucose & produces glycogen. Degradation process is the reverse.

Front 5

List the three types of irreversible enzymes of glycolysis.

Back 5

Hexokinase. . .

Phosphofructokinase-1. . .

Pyruvate kinase.

Front 6

Describe the Hexokinase enzyme.

Back 6

Hexokinase converts glucose to Glucose-6-phosphate. The brain isoform has a high affinity for glucose & is not regulated by insulin. This is important due to its high dependence on glucose. . . . . .

Muscle & liver isoforms have a low affinity for glucose and both are upregulated by insulin. This property allows these tissues to take in more glucose & make glycogen in a fed state.

Front 7

What is the name for the Hexokinase isoform found in the liver?

Back 7

Glucokinase.

Front 8

Describe the Phosphofructokinase-1 (PFK-1) enzyme.

Back 8

PFK-1 phosphorylates fructose-6-phosphate to form fructose-1,6-bisphosphate. This is the rate limiting enzyme for glycolysis & is highly regulated by the liver.

Front 9

Describe how Phosphofructokinase-1 is rate-limited by the liver.

Back 9

This enzyme is controlled by the levels of AMP and ATP. . . . .

When AMP levels are high then ATP has been used & more is needed so glycolysis should increase. . . .

When ATP levels are high, it signals that enough energy is available & glycolysis slows.

Front 10

Describe the Pyruvate Kinase enzyme.

Back 10

Pyruvate kinase converts phosphoenolpyruvate to pyruvate. . . .

The liver isoform is upregulated by insulin & inhibited by glucagon. . . .

The muscle isoform is not regulated at all.

Front 11

Describe the importance of pyruvate dehydrogenase & how it is regulated.

Back 11

Pyruvate dehydrogenase converts pyruvate to Acetyl CoEnzymeA so that pyruvate can be used for aerobic ATP production. It is activated by its substrates, ADP, & Calcium. It is inhibited by its products & ATP. Well oxygenated muscle tissue will have elevated calcium & ADP levels during exercise will encourage the production of acetyl CoA from pyruvate.

Front 12

Name the rate limited step of the TCA cycle & describe its regulation.

Back 12

The key rate limiting enzyme for the TCA cycle is isocitrate dehydrogenase which converts isocitrate to alpha-ketoglutarate. . . .

It is stimulated by ADP & Calcium but is inhibited by NADH.

Front 13

Explain the effect of oxygen insufficiency on pyruvate dehydrogenase & the TCA cycle.

Back 13

With reduced oxygen availability, Oxidative Phosphorylation will slow down meaning NADH which is produced in the TCA cycle has nowhere to go. . . .

With no oxygen, both TCA & Pyruvate DeHydrogenase are inhibited by NADH, stopping both processes.

Front 14

What are the most common causes of reduced TCA cycle.

Back 14

Ischemia or hypoxia.

No Oxidative Phosphorylation (no oxygen) then no TCA cycle or Pyruvate DeHydrogenase.

Front 15

List the two main enzymes involved in glycogen synthesis & how the synthesis is regulated

Back 15

Glycogen is built by using branching enzyme & glycogen synthase. . . .

It is stimulated by insulin but inhibited by glucagon & epinephrine.

Front 16

List the two main enzymes involved in glycogen degradation & how the synthesis is regulated

Back 16

Glycogen is degraded by debranching enzyme & glycogen phosphorylase. . . .

It is stimulated by glucagon & epinephrine but inhibited by insulin. In Muscle cells it is activated by AMP and Calcium.

Front 17

Explain the importance of the enzyme glucose-6-phosphatase.

Back 17

Glucose-6-phosphatase degrades glucose-6-phosphate to glucose and releases a phosphate group.

Front 18

Explain how skeletal muscle glucose transporters differ from those found in red blood cells, brain, and liver.

Back 18

Red blood cells & brain tissue have high affinity transporters for glucose while the liver has low affinity transporters.

Muscle & adipose tissue have insulin-sensitive transporters with high affinity for glucose. When stimulated by insulin, vesicle-stored glucose transporters are sent to the cell's surface increasing the amount of glucose that enters the muscle & adipose during the fed state.

Front 19

Explain how hexokinase in skeletal muscle cells differ from that found in other tissues.

Back 19

The muscle isoform of hexokinase is upregulated by insulin. . . .

Muscle has a lower affinity for glucose than the brain but a higher affinity than the liver.

Front 20

Compare regulation of PFK-1 in the liver and muscle.

Back 20

PFK-1 in the muscle is activated by AMP but inhibited by ATP. . . . When AMP is high, glycolysis should increase. . . . When ATP is high, glycolysis should slow. . . .

PFK-1 in the liver is inhibited by ATP and citrate but activated by AMP.

Front 21

Describe the influence of PFK-2.

Back 21

PFK-2 converts some of the fructose-6-phosphate to fructose-2,6-bisphosphate which activates PFK-1 activity.

This process is useful when excess glucose needs to be stored. PFK-1 is the rate limiting enzyme in glycolysis which slows down in High ATP levels. Excess glucose + high levels of ATP + PFK-2 causes a bypass of the rate-limiting check and continued breakdown of glucose.

Front 22

Compare regulation of glycogen synthesis & degradation in the muscle & liver including the effects of insulin, glucagon, calcium, & epinephrine.

Back 22

Glycogen synthesis in the liver is stimulated by insulin but inhibited by glucagon & epinephrine. Glycogen degradation is stimulated by glucagon & epinephrine but inhibited by insulin.

Glycogen degradation in the muscles is regulated the need for ATP, Exercise, Epinephrine, AMP, & Calcium.

Front 23

Describe the metabolism of Resting Skeletal Muscle.

Back 23

Resting Skeletal Muscle stores glycogen when in the fed state in order to replenish glycogen used during exercise and to store excess glucose as glycogen. . . .

Skeletal Muscle mobilizes glycogen (a little) when in the fasted state but prefers to use fatty acids for energy while reserving most of its glycogen.

Front 24

Describe the metabolism of Exercising Skeletal Muscle.

Back 24

Exercising Skeletal Muscle will mobilize glycogen stores regardless of the fed or fasted state. . . .

Creatine can be converted to creatine phosphate which is stored in muscle cells is easily reversed to create ATP. Skeletal Muscle cells also express copious myokinase which converts 2 ADP to 1 ATP & 1 AMP. . . .

Anaerobic glycolysis is the primary way in which skeletal muscle cells obtain energy at the onset of exercise.

Lactate produced by exercising muscles can be used as a fuel by other tissues or by the liver to produce glucose,

Front 25

Explain how serum AST may be affected by diseases of Skeletal Muscles.

Back 25

Elevated serum AST may reflect damage to skeletal & cardiac muscles.

Front 26

Explain how serum CK-MM & Myoglobin may be affected by diseases of Skeletal Muscles.

Back 26

Serum CK-MM may be elevated where skeletal muscle has been damaged. Conditions include rhabdomyolysis, myositis.

Myoglobin will also leak out of the cells under these conditions.

Front 27

Explain how serum Creatine may be affected by diseases of Skeletal Muscles.

Back 27

Serum Creatine will show low levels in diseases associated with low muscle mass. . . .

Serum Creatine will show increased levels in rhabdomyolysis and increased muscle mass such as gigantism.

Front 28

Define rhabdomyolysis.

Back 28

a condition in which damaged skeletal muscle tissue breaks down. Symptoms include muscle pain, weakness, & dark urine.

Front 29

Define myositis.

Back 29

general term for inflammation of the muscles.