Hormone Regulation

Question 1

Allosteric regulation

Answer 1

Binding a negative and/or a positive effectors to allosteric site(s).

Causes enzyme production to speed up or slow down

Question 2

Allosteric regulation of PFK1

Answer 2

ATP = negative effector

F2,6 BP = positive effector

ADP and AMP = positive effectors

ATP + F2,6BP = faster enzyme production

Question 3

Insulin in allosteric regulation

Answer 3

Stimulates F2,6BP production, which in turn speeds up glycolysis by speeding up PFK1 activity.

Question 4

Covalent modification

Answer 4

Adds/removes a functional group to a enzyme covalently.

• most common version is reversible phosphorylation via serine, tyrosine and threonine amino acids

Question 5

Insulin in covalent modification

Answer 5

Activates phosphatase and removes phosphate groups from GS enzyme and phosphorylase when glucose levels are low.

• speeds up GS enzyme, slows down phosphorylase
• increases glycogen synthesis

When glucose levels are high, insulin inhibits phosphorylase by binding a phosphate to it.

Question 6

Glucagon

Answer 6

Activates kinase which phosphorylate both GS enzyme and phosphorylase enzyme.

(Slows down GS enzyme, speeds up phosphorylase)

-inhibits glycogen production

Question 7

Genetic regulation

Answer 7

Induction or repression of genes that increases/decreases amounts of enzymes

Question 8

Insulin in genetic regulation

Answer 8

Increases glucokinase enzyme totals

Represses G6P enzyme totals

(Lowers free glucose totals)

Question 9

Glucagon

Answer 9

Increases G6P levels

Represses glucokinase enzyme levels

(Increases free levels of glucose)

Question 10

In well fed conditions what is happening in liver cells

Answer 10

-high glucose level increase insulin levels

Causes increases in:
Glycolysis
Glycogenesis
PPP
FA synthesis 
Cholesterol synthesis 
Lipogenesis (triglyceride synthesis)

Question 11

In well fed conditions, what is happening in adipose cells?

Answer 11

Insulin prescience causes increase in

Glycolysis
PPP
FA synthesis

(Also increase in FA synthesis and lipogenesis but is much less active compared to liver cells)

adipose cells don’t have glycogen

Question 12

In well fed conditions, what is occurring in muscle cells?

Answer 12

Insulin causes increase in

• glycogenesis only
• in muscle only, insulin DOESNOT increase PFK1 activity*

Question 13

Under fasting conditions, what happens in adipose tissue?

Answer 13

Glucagon present causes

Lipolysis

FA-oxidation

-breakdown of storage molecules to get energy/glucose

Question 14

Under fasting-conditions, what is going on in liver cells (hepatocytes)?

Answer 14

Glucagon present causes

Glycogenolysis

Gluconeogenesis

FA-oxidation (if no glucose building possible)

Ketogenesis (if no glucose building possible)

glycogen stores run out in usually 2 days, causes Keto body production and FA oxidation

Question 15

What amino acids can be converted directly to pyruvate and OAA respectively?

Answer 15

Ala and Asp

Imported to liver from myocytes in fasting conditions

Question 16

Under fasting conditions, what is going on in muscle cells?

Answer 16

Glucagon present causes

FA-oxidation

Ketolysis

epinephrine increase causes glycogenolysis

Question 17

Difference between early and late stage fasting states?

Answer 17

Early state is when the liver has glycogen reserves

Late state begins when liver runs out or extremely low in glycogen and begins gluconeogeneosis and FA oxidation.

Question 18

Why does the brain have to start using ketone bodies during extended fasting, but RBCs don’t have to?

Answer 18

RBCs undergo anaerobic glycolysis all the time, regenerating pyruvate all the time.

Brain uses aerobic which does not allow regeneration of glucose