Biochem 2-8 Metabolism Integration

Front 1

What effect does insulin have on glucose uptake into adipose and muscle tissue?

Back 1

Insulin increases glucose uptake into these tissues

Front 2

Through which protein is glucose uptake into adipose and muscle tissue mediated?

Back 2

GLUT 4

Front 3

How would the process of glucose uptake into adipose and muscle tissue be affected by a lack of insulin?

Back 3

Less glucose would be taken into these cells resulting in elevated blood glucose levels

Front 4

How does insulin/glucagon ratio affect the activity glycogen synthase and glycogen phosphorylase?

Back 4

Increasing insulin/glucagon ratio increases glycogen synthase activity and inhibits glycogen phosphorylase activity

Front 5

Is glycogen phosphrylase a branching or debranching enzyme?

Back 5

debranching; glycogen synthase is a branching enzyme.

Front 6

How would the overall processes of glycogen storage and degradation be affected by a lack of insulin?

Back 6

Without insulin, less glycogen would be stored

Front 7

What effect does insulin/glucagon ratio have on Glukokinase?

Back 7

activity increases with increasing insulin/glucagon ratio; Glucokinase synthesis is induced by insulin

Front 8

What effect does insulin/glucagon ratio have on PFK1?

Back 8

activity increases with increasing insulin/glucagon ratio due to increased PFK2 activity

Front 9

What effect does insulin/glucagon ratio have on PFK2?

Back 9

activity increases with increasing insulin/glucagon ratio

Front 10

What effect does insulin/glucagon ratio have on Pyruvate Kinase?

Back 10

activity increases with increasing insulin/glucagon ratio

Front 11

What effect does insulin/glucagon ratio have on Glucose-6-Phosphatase?

Back 11

activity decreases with increasing insulin/glucagon ratio

Front 12

What effect does insulin/glucagon ratio have on Fructose-1,6-bisphosphatase?

Back 12

activity decreases with increasing insulin/glucagon ratio

Front 13

What effect does insulin/glucagon ratio have on PEP carboxykinase?

Back 13

activity decreases with increasing insulin/glucagon ratio

Front 14

How would lack of insulin affect glucose production by the liver and blood glucose levels?

Back 14

Lack of insulin would lead to increased production of glucose by the liver and increased blood glucose levels

Front 15

What effect does insulin have on Glucose-6-phosphate dehydrogenase?

Back 15

activity increases with increasing insulin/glucagon
ratio; hepatic glucose-6 phosphate dehydrogenase synthesis is induced by insulin

Front 16

What effect does insulin have on Acetyl CoA carboxylase?

Back 16

activity increases with increasing insulin/glucagon ratio; acetyl
Co A carboxylase synthesis is induced by insulin

Front 17

What effect does insulin have on Citrate lyase?

Back 17

activity increases with increasing insulin/glucagon ratio; citrate lyase synthesis is induced by insulin

Front 18

What effect does insulin have on Lipoprotein lipase?

Back 18

activity increases with increasing insulin/glucagon ratio

Front 19

What effect does insulin have on Adipose lipase?

Back 19

activity decreases with increasing insulin/glucagon ratio

Front 20

How would the lack of insulin affect fatty acid synthesis, storage and lipolysis?

Back 20

Lack of insulin would result in reduced storage of fatty acids in adipose tissue and increased lipolysis

Front 21

How would the lack of insulin lead to excess production of ketones?

Back 21

Fatty acids will be mobilized (since adipose lipase will be activated); some of these fatty acids will be in excess of need for beta -oxidation, leading to hepatic ketone body production.

Front 22

The relative risk of coronary heart disease is related to LDL, HDL and triglyceride levels. How
does diabetes affect this risk?

Back 22

The risk is great enough to be statistically equal to existing
coronary heart disease.

Front 23

Insulin resistance occurs when
normal amounts of insulin are inadequate to produce a normal insulin response; what affect will this have on insulin resistant patients?

Back 23

Insulin resistance would lead to decreased usage of glucose and could therefore explain his slightly elevated blood glucose levels. Insulin resistance would also result in decreased removal of fatty acids from TGs by lipoprotein lipase

Front 24

Insulin resistant patients are at a
higher risk of developing type __ diabetes and cardiovascular disease.

Back 24

II

Front 25

How do elevated triglyceride levels affect LDL production?

Back 25

Increased triglycerides (on VLDL)
increase LDL production.

Front 26

Relate genetic deficiencies in LDL receptors to the development of atherosclerosis.

Back 26

individuals with LDL receptor defects exhibit very high serum LDL levels while they are
still children.

Front 27

Why might abnormally low HDL contribute to increased triglyceride levels?

Back 27

HDL are needed to transfer ApoCII to chylomicrons and VLDL. ApoCII is needed for activation of lipoprotein lipase, to breakdown chylomicron and VLDL triglycerides.

Front 28

Epidemiological studies show that smoking is associated with
low ____ levels.

Back 28

HDL

Front 29

A patient has sepsis and muscle wasting due to MRSA infection; how are the amino acids from muscle protein breakdown used by the liver and by cells of the immune system?

Back 29

The liver will use these amino acids for GNG and for
synthesis of necessary proteins. Those that are not gluconeogenic may also be used for energy. Immune cells will also use amino acids for synthesis of proteins and for energy needed to mount an immune response

Front 30

What role does the ubiquitin/proteasome system have in the process of muscle protein breakdown to amino acids for use by the liver and immune system?

Back 30

*Cortisol* will stimulate ubiquitination of proteins which is the signal for proteasomal degradation. This process will
stimulate release of amino acids from muscle protein.

Front 31

Why is it important that fatty acids be mobilized in a hypercatabolic state?

Back 31

FAs are needed to provide energy for processes such as GNG in the liver.

Front 32

Why do hypercatbolic patients have elevated BUN?

Back 32

Increased amino acid catabolism will lead to increased urea production

Front 33

What effect would increased catabolism of muscle protein have on glutamine levels and why?

Back 33

As more ammonia is generated through catabolism of amino acids in muscle cells, they will export the extra ammonia by synthesizing glutamine, which can then be used by other cells as an energy source or can carry the ammonia to the liver where it will be eliminated through the urea cycle.