Metabolism 4

Question 1

Glucagon and epinephrine’s effect on glycolysis

Answer 1

Shut down glycolysis and promote gluconeogenesis, increasing transcription of the enzymes needed for gluconeogenesis

Question 2

Glucagon and epinephrine’s effect on glycogen

Answer 2

Promotes glycogenolysis

Question 3

Gluconeogenesis

Answer 3

Formation of glucose from non-carbohydrate sources

Question 4

What are precursors for gluconeogenesis?

Answer 4

Pyruvate
Lactate
Glycerol
Glucogenic amino acids

Question 5

How many ATPs are required for gluconeogenesis?

Answer 5

6

Question 6

What enzyme is required to “release” the glucose from both glycogenolysis and gluconeogenesis?

Answer 6

Glucose-6-phosphatase

Question 7

What two cofactors are needed to “activate” pyruvate in gluconeogenesis?

Answer 7

Biotin and bicarbonate

Question 8

How does pyruvate get converted into PEP?

Answer 8

Through an oxaloacetate intermediate, utilizing pyruvate kinase and PEP carboxylase

Question 9

Phase I

Answer 9

Exogenous glucose being used in all parts of the body.

Question 10

Phase II

Answer 10

Glycogenolysis and hepatic gluconeogenesis keep glucose levels above 60 mg/dL. Liver is no longer using glucose. Adipose and muscle decrease glucose use rates.

Question 11

Phase III

Answer 11

Glycogenolysis and hepatic gluconeogenesis are used for glucose balance. Muscle and adipose tissue using glucose at slightly lower rates.

Question 12

Phase IV

Answer 12

Gluconeogenesis from both kidney and liver. Only blood cells, brain, and heart are using glucose, with some muscle use still remaining. Brain begins using ketone bodies.

Question 13

Phase V

Answer 13

Gluconeogenesis from both kidney and liver. Only brain (at diminished rate), blood cells, and renal medulla are using glucose. Brain continues using ketone bodies.

Question 14

What body parts have an absolute requirement for glucose?

Answer 14

The brain, blood cells, and lens of the eye

Question 15

How are odd-numbered fatty acids put through GNG?

Answer 15

They are converted to propionyl coA, then to succinyl coA, then to pyruvate.

Question 16

How is glycerol introduced into GNG?

Answer 16

It is converted into DHAP

Question 17

How is aspartate put into GNG?

Answer 17

It is converted to oxaloacetate

Question 18

How are lactate and alanine introduced into GNG?

Answer 18

They are converted into pyruvate

Question 19

Why are neonates at risk for hypoglycemia?

Answer 19

PEP carboxykinase is needed for the first steps in gluconeogenesis, which takes a few hours after birth to activate

Question 20

Describe the Cori cycle.

Answer 20

RBC’s break down glucose by glycolysis, then shuttles it through LDH and makes lactate. This lactate is transported back to the liver, where it undergoes gluconeogenesis and the glucose is transported back to the red blood cell.

Question 21

How is the Cori cycle different in muscle?

Answer 21

Pyruvate is not made into lactate, but into alanine, which is then transported back to the liver, which uses the carbon backbone for GNG and creates urea as a byproduct

Question 22

What is the major source for GNG during an overnight fast?

Answer 22

Fatty acids

Question 23

Precursors to propionyl coA

Answer 23

Valine
Isoleucine
Cholesterol
Odd chain fatty acids
Phtanic acid

Question 24

Special considerations of oxaloacetate transport

Answer 24

OA is formed in the mitochondria, but cannot be transported out. It must first be converted into malate, then converted back to OA when in the cytosol. Requires biotin.

Question 25

Allosteric activator of pyruvate carboxylase

Answer 25

Acetyl CoA

Question 26

What does biotin do in the pyruvate carboxykinase reaction?

Answer 26

Carries the activated CO2 group

Question 27

Pyruvate carboxylase genetic deficiency: symptoms

Answer 27

Found in patients that have failure to thrive, recurrent seizures, and metabolic acidosis.

Question 28

Pyruvate carboxylase genetic deficiency: clinical signs

Answer 28

High levels of lactic acid and alanine in the blood.

Question 29

Location in the cell of glucose 6-phosphatase

Answer 29

In the cisterna of the endoplasmic reticulum

Question 30

Transporters for G6P

Answer 30

Three of them: if there is a deficiency, then there’s accumulation of glycogen in the liver

Question 31

What happens to GNG after ETOH ingestion?

Answer 31

Decreased because of increased NADH/NAD+ ratio

Question 32

What glucogenic precursors are reduced by the increased NADH in the cell?

Answer 32

Pyruvate and oxaloacetate -> lactate and malate