wk 3 - Glycogenesis & Glycogenolysis

Question 1

4?

(fasting)

Answer 1

cAMP

Question 2

3?

(fasting)

Answer 2

protein kinase

Question 3

Downstream Metabolic Effects of Insulin increases glucose uptake by most tissues EXCEPT for the ——-

Answer 3

Liver

Question 4

To synthesise glycogen, glycogen synthase is the active form, whereas, glycogen synthase-P is the inactive form.

a) True
b) False

Answer 4

a) True
- glycogen synthase phosphate must be phosphorylysed (have its phosphate group removed) for it to synthesise glycogen

Question 5

Glycogen phosphorylase-P acts to degrade glycogen, whereas glycogen synthase acts to synthesise glycogen.

a) True
b) False

Answer 5

a) True

Question 6

During feeding state, glycogen phosphorylase (dephosphorylated) is in the ______ form.

Answer 6

During feeding state, glycogen phosphorylase (dephosphorylated) is in the inactive form.

Question 7

In a ________ state, glycogenolytic and lipolytic processes increase.

Answer 7

In a fasting state, glycogenolytic and lipolytic processes increase.

Question 8

Deficiency of alpha-1,4-glucosidase causes glycogen storage disease ___________

a) Type I
b) Type II
c) Type III
d) Type IV

Answer 8

Deficiency of alpha-1,4-glucosidase causes glycogen storage disease Type II

Question 9

In ————- state, glycogenic and lipogenic processes increase.

Answer 9

In a feeding state, glycogenic and lipogenic processes increase.

Question 10

What is the second messenger to be phosphorylated in the insulin’s receptor mechanism of action?

Answer 10

hasnt been identified yet?

Question 11

Glycogen storage disease type 1a/Von GIerkes disease is caused by _____________ deficiency.

a) Glucose-1-Phosphatase
b) Glucose-6-Phosphatase
c) Translocase T1
d) Translocase T2

Answer 11

Glycogen storage disease type Ia/Von GIerkes disease is caused by Glucose-6-Phosphatase deficiency.

Question 12

Glycogen storage disease type 1b resulting from deficiency of a specific _______________

a) Glucose-1-Phosphatase
b) Gucose-6-Phosphatase
c) Translocase T1
d) Translocase T2

Answer 12

Glycogen storage disease type Ib resulting from deficiency of a specific Translocase T1

Question 13

Accumulation of abnormal amounts or types of glycogen in tissues is termed _______________

a) Glycogen abnormality
b) Glycogen storage disease
c) Tissues abnormality
d) Tissues storage disease

Answer 13

b) Glycogen storage disease

Question 14

During fasting state, which of the following is true:

I. cAMP is active

II. Glycogen phosphorylase-P

III. Glycogen synthase-P

IV. Protein kinase is inactive

a) I, II, IV
b) II, IV
c) I – IV
d) I, II, III

Answer 14

d) I, II, III

Question 15

1?

(fasting)

Answer 15

glycogen phosphorylase phosphate

(active form of enzyme)

Question 16

during fasting state, plasma glucose is ______. Thus _________ and ___________ are dominating.

they inactivate ______________ and activate ________________ to breakdown glycogen in order to ________ glucose level in blood

Answer 16

during fasting state, plasma glucose is low. Thus glucagon and epinephrine are dominating.

they inactivate glycogen synthase (to glycogen synthase phosphate) and activate glycogen phosphorylase (to glycogen phosphorylase P) to breakdown glycogen in order to increase glucose level in blood

Question 17

What is the name of the protein that adds phosphate groups to other proteins?

Answer 17

Kinase

Question 18

Glycogenolysis is the breakdown of the ———- & ———– linkages in glycogen.

Answer 18

Glycogenolysis is the breakdown of the alpha-1,6 & alpha-1,4 linkages in glycogen.

Question 19

_________________ & _________________ are the 2 enzymes that makeup the Debranching enzyme complex for glycogenolysis

Answer 19

Glucan transferase & alpha 1-6 glucosidase are the 2 enzymes that makeup the Debranching enzyme complex for glycogenolysis

Question 20

The enzyme that cleaves glycogen is called ——-

Answer 20

Glycogen phosphorylase-P

Question 21

hypocalcemia triggers the parathyroid glands to secrete parathyroid hormone (PTH) to reabsorb calcium from bones and reabsorb calcium from kidney. This is a type of ——– stimuli.

Answer 21

hypocalcemia triggers the parathyroid glands to secrete parathyroid hormone (PTH) to reabsorb calcium from bones and reabsorb calcium from kidney. This is a type of humoral stimuli.

Question 22

name the GLUT protein:

Tissue distribution: Mucosal surface in small intestine, sperm.

Special properties: Primarily fructose carrier in intestine.

Answer 22

GLUT 5

Question 23

3?

(Fed)

Answer 23

cAMP - decreased by insulin

(cyclic adenosine monophosphate)

Question 24

A baby with enlarged liver could be the result of:

Answer 24

Glycogen Storage Disease Type IIIB

Question 25

In the feeding state, insulin stimulates protein ----- to activate glycogen synthase to form glycogen.

Answer 25

In the feeding state, insulin stimulates protein **Phosphatase-1** to activate glycogen synthase to form glycogen.

Question 26

During feeding state, plasma glucose is \_\_\_\_\_\_, thus _________ is dominating. it activates _______________ and inactivates ______________ to form glycogen in order to ________ glucose level in the blood and _________ glycogen production

Answer 26

During feeding state, plasma glucose is **high**, thus **insulin** is dominating. it activates **glycogen synthase** **(dephosphorylates glycogen synthase - P)** and inactivates **glycogen phosphorylase** **P (phosphorylates glycogen phosphorylase)** to form glycogen in order to **decrease** glucose level in the blood and **increase** glycogen production

Question 27

Glycogen storage disease **type 1d** is deficiency of \_\_\_\_\_\_\_\_\_ ## Footnote a) Translocase T1 b) Translocase T2 c) A Transporter that Translocates free glucose molecules d) A Transporter that Translocate free glycogen molecules

Answer 27

Glycogen storage disease **type 1d** is deficiency of a Transporter that Translocates free glucose molecules

Question 28

name the GLUT protein: ## Footnote **Tissue distribution:** Neurons, placenta, testes. **Special properties:** Low Km (1mM) and high capacity.

Answer 28

GLUT 3

Question 29

Glycogen Storage Disease type Ia is caused due to a deficiency in ---------

Answer 29

Glucose-6-Phosphatase (G6P)

Question 30

**GSD type III/Forbes-Cori disease** is also known as or \_\_\_\_\_\_\_\_\_\_\_\_\_, which affects the liver and skeletal muscles. ## Footnote Glycogen deposited in these organs has an _________ \_\_\_\_\_\_\_\_\_. Differentiating patients with GSD type III from those with GSD type I solely on the basis of physical findings is not easy.

Answer 30

**GSD type III/Forbes-Cori disease** is also known as or limit dextrinosis, which affects the liver and skeletal muscles. ## Footnote Glycogen deposited in these organs has an **abnormal structure**. Differentiating patients with GSD type III from those with GSD type I solely on the basis of physical findings is not easy.

Question 31

True or false ## Footnote Glycogen phosphorylase cleaves glucose molecules faster when glycogen is more branched.

Answer 31

True - alpha 1-6 linkages (branches) can be cleaved by **alpha 1-6 glucosidase**

Question 32

In contrast to glycogen storage disease type I, the _____________ are involved in glycogen storage disease **type III**. ## Footnote a) Kidney and heart b) Liver and skeletal muscles c) Liver and kidney d) Pancreas and liver e) Pancreas and skeletal muscles

Answer 32

In contrast to glycogen storage disease type I, the **Liver and skeletal muscles** are involved in glycogen storage disease type III.

Question 33

name the GLUT protein: ## Footnote **Tissue distribution:** Liver, beta cells, hypothalamus, basolateral membrane small intestine. **Special properties:** High capacity but low affinity (high Km, 15-20mM) part of "the glucose sensor" in ß-cells. Carrier for glucose and fructose in liver and intestine!

Answer 33

GLUT 2

Question 34

GSD type IV, also known as \_\_\_\_\_\_\_\_\_\_\_\_\_ It is a rare disease that leads to early death. In 1956, Andersen reported the first patient with progressive hepatosplenomegaly and accumulation of abnormal polysaccharides. The main clinical features are ______ insufficiency and abnormalities of the heart and nervous system.

Answer 34

GSD type IV, also known as **amylopectinosis** It is a rare disease that leads to early death. In 1956, Andersen reported the first patient with progressive hepatosplenomegaly and accumulation of abnormal polysaccharides. The main clinical features are **liver** insufficiency and abnormalities of the heart and nervous system.

Question 35

Glycogenolysis is the break down of _________ in glycogen. ## Footnote a) α1→2 branch b) α1→3 branch c) α1→4 branch d) α1→5 branch e) α1→6 branch

Answer 35

e) α1→6 branch - cleaving a glycogen branch is done by **alpha 1-6 glucosidase** - cleaving individual glucose molecules from this glycogen branch is done by **glycogen phosphorylase P,** converting them to G6P

Question 36

One -------------- can initiate many cascades of reactions at the same time

Answer 36

One hormone can initiate many cascades of reactions at the same time

Question 37

2? | (Fed)

Answer 37

protein phosphatase-1

Question 38

**GSD type 0** is when your body synthesises ______ glycogen

Answer 38

GSD type 0 is when your body synthesises **zero glycogen**

Question 39

What is the name of the hormone that inhibits insulin and glucagon secretion?

Answer 39

Somatostatin

Question 40

During a feeding state, plasma glucose is high, thus insulin is high. Insulin works to lower plasma glucose by **2 mechanisms:** 1. _________ cAMP = _________ glycogen phosphorylase = _________ **glycogenolysis** 2. _________ Protein phosphatase-1 = _________ glycogen synthase = _________ **glycogenesis**

Answer 40

During a feeding state, plasma glucose is high, thus insulin is high. Insulin works to lower plasma glucose by 2 mechanisms: 1. **inhibits** cAMP = **inhibits** glycogen phosphorylase = **inhibits** glycogenolysis 2. **activates** Protein phosphatase-1 = **activates** glycogen synthase = **activates** glycogenesis

Question 41

The more _________ in glycogen, the more glucose molecules are released as an effect of **glycogen phosphorylase.** a) α-1,2- linkage b) α-1,4- linkage c) α-1,5- linkage d) α-1,6- linkage

Answer 41

d) α-1,6- linkage | (branched bonds)

Question 42

In the downstream Metabolic Effects of Insulin, gluconeogenesis is inhibited in ------- & ------- (which organs)

Answer 42

In the downstream Metabolic Effects of Insulin, gluconeogenesis is inhibited in the **Liver & kidneys**

Question 43

For people who have glycogen storage diseases that cause low blood sugar levels, levels are maintained by giving uncooked cornstarch every 4 to 6 hours... ## Footnote a) Because it increases the glucose level suddenly b) Because it decreases the glucose level suddenly c) Because it increases the glucose level gradually d) Because it decreases the glucose level gradually

Answer 43

For people who have glycogen storage diseases that cause low blood sugar levels, levels are maintained by giving uncooked cornstarch every 4 to 6 hours Because **it increases the glucose level gradually**

Question 44

Glycogen storage disease **type 1d** is deficiency of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. ## Footnote a) Translocase T1 b) Translocase T2 c) A transporter that Translocates free glucose molecules d) A Transporter that Translocates free glycogen molecules

Answer 44

c) A transporter that Translocates free glucose molecules

Question 45

For people who have glycogen storage diseases that cause low blood sugar levels, levels are maintained at night by giving them \_\_\_\_\_\_\_\_\_\_\_ ## Footnote a) Oral glucose solution b) Carbohydrate solutions through a stomach tube c) IV glucose solution d) IV carbohydrate solution

Answer 45

For people who have glycogen storage diseases that cause low blood sugar levels, levels are maintained at night by giving them **Carbohydrate solutions through a stomach tube**

Question 46

2? | (fasting)

Answer 46

phosphorylase kinase phosphate

Question 47

Diagnosis of glycogen storage disease is via \_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote a) Biopsy b) Blood samples examination c) Physical examination d) X-ray

Answer 47

Diagnosis of glycogen storage disease is via **Biopsy**

Question 48

name the GLUT protein: ## Footnote **Tissue distribution:** Most cells. **Special properties:** High capacity, relatively low Km (1-2mM).

Answer 48

GLUT 1

Question 49

During fasting state, glucagon and epinephrine ________ cAMP, which ________ protein kinase, which ________ phosphorylase kinase, which ________ the active glycogen phosphorylase phosphate to break down glycogen in order to _______ plasma glucose levels

Answer 49

During fasting state, glucagon and epinephrine **increase cAMP**, which **increases protein kinase**, which **increases phosphorylase kinase**, which **increases** the **active glycogen phosphorylase phosphate** to break down glycogen in order to **increase** plasma glucose levels

Question 50

**Glycogen synthase** is essential to synthesise glycogen during fasting state. ## Footnote a) True b) False

Answer 50

b) False - glycogenesis does not occur during fasting state, glycogen synthase would be **phosphorylated** by protein kinase (inactivated)

Question 51

In **fasting** state, glucagon and epinephrine (via protein kinase A) phosphorylate _____________ to inactive it

Answer 51

In fasting state, glucagon and epinephrine (via protein kinase A) phosphorylate **glycogen synthase** to inactivate it

Question 52

During **fasting** state, glycogen phosphorylase should be in the _______ form(glycogen phosphorylase-P) .

Answer 52

During **fasting** state, glycogen phosphorylase should be in the active form (glycogen phosphorylase-P) .

Question 53

Glycogenesis happens when there is excess of glucose. ## Footnote a) True b) False

Answer 53

a) True

Question 54

during a fasting state, glucagon and epinephrine work by 2 mechanisms: 1. _______ cAMP = _______ protein kinase = ________ phosphorylase kinase = _______ glycogen phosphorylase phosphate = **glycogenesis** **inhibited** 2. _______ protein kinase = ________ glycogen synthase phosphate = **glycogenesis inhibited**

Answer 54

during a fasting state, glucagon and epinephrine work by 2 mechanisms: 1. **increased** cAMP = **increased** protein kinase = **increased** phosphorylase kinase = **increased** glycogen phosphorylase phosphate = glycogenesis inhibited 2. **increased** protein kinase = **increased** glycogen synthase phosphate = glycogenesis inhibited

Question 55

During **fasting** state, glycogen phosphorylase should be in the active form, which is \_\_\_\_\_\_\_\_\_\_\_\_\_\_

Answer 55

During fasting state, glycogen phosphorylase should be in the active form, which is **glycogen phosphorylase phosphate**

Question 56

In contrast to glycogen storage disease **type I**, ____________ are involved in glycogen storage disease **type III.** ## Footnote a) Kidney and heart b) Liver and skeletal muscles c) Liver and kidney d) Pancreas and liver e) Pancreas and skeletal muscles

Answer 56

b) Liver and skeletal muscles

Question 57

During **fasting** state, _________ and ___________ are dominating.

Answer 57

During fasting state, **glucagon** and **epinephrine** are dominating.

Question 58

When glucagon and epinephrine are dominating, they increase, ------- which increases protein kinase.

Answer 58

When glucagon and epinephrine are dominating, they increase, **cAMP** which increases protein kinase.

Question 59

1? | (Fed)

Answer 59

glycogen synthase

Question 60

The most common form of glycogen storage disease (GSD) is \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_, which occurs in one out of every 50,000-100,000 births.

Answer 60

The most common form of glycogen storage disease (GSD) is **Type 1a, or Von Gierke disease**, which occurs in one out of every 50,000-100,000 births.

Question 61

Insulin’s receptor is made of ------------------------------- subunits

Answer 61

Insulin’s receptor is made of **2 alpha and 2 beta subunits**

Question 62

Glycogen storage disease **type Ib** is the result of a deficiency in \_\_\_\_\_\_\_\_\_\_\_ ## Footnote a) G1Pase b) G6Pase c) Translocase T1 d) Translocase T2

Answer 62

Glycogen storage disease type Ib is the result of a deficiency in **Translocase T1**

Question 63

Signal sequence plus c-peptide plus proinsulin is called --------

Answer 63

Preproinsulin

Question 64

In the feeding state, insulin stimulates ______________ to activate glycogen synthase to form glycogen.

Answer 64

In the feeding state, insulin stimulates **protein phosphatase-1** to activate glycogen synthase to form glycogen.

Question 65

Glycogen storage disease **type Ia** is caused by _________ deficiency. ## Footnote a) G1Pase b) G6Pase c) Translocase T1 d) Translocase T2

Answer 65

Glycogen storage disease type Ia is caused by a **G6Pase deficiency.**

Question 66

Glycogen storage disease **type 1c** is deficiency of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote a) G1Pase b) G6Pase c) Translocase T1 d) Translocase T2

Answer 66

Glycogen storage disease type 1c is deficiency of **Translocase T2**

Question 67

During **fasting** state, glucagon and epinephrine stimulates _____ to activate _____________ to **inactivate/phosphorylate** ____________ to glycogen synthase-P so that its action of synthesising glycogen is _________ to ultimately block the ___________ pathway

Answer 67

During fasting state, glucagon and epinephrine stimulates **cAMP** to activate **protein kinase A** to inactivate/phosphorylate **glycogen synthase** to glycogen synthase-P so that its action of synthesising glycogen is **inhibited** to ultimately block the **glycogenesis** pathway

Question 68

Glycogen storage disease **type 1c** is deficiency of \_\_\_\_\_\_\_\_\_\_ ## Footnote a) G1Pase b) G6Pase c) Translocase T1 d) Translocase T2

Answer 68

Glycogen storage disease type 1c is deficiency of **Translocase T2**

Question 69

The glucose transporter in case of muscle is --------------. ## Footnote a) GLUT-2 b) GLUT-3 c) GLUT-4 d) GLUT-5

Answer 69

c) GLUT-4

Question 70

4? | (Fed)

Answer 70

glycogen phosphorylase | (**inactive** form of enzyme)

Question 71

Glucose molecules are bound together to form glycogen. In the same chain, they are linked via α-1,4- linkage, whereas branched chains are linked via: a) α-1,2- linkage b) α-1,3- linkage c) α-1,5- linkage d) α-1,6- linkage

Answer 71

d) α-1,6- linkage

Question 72

During **feeding** state, glycogen synthase should be in the active form, which is: ## Footnote a) Glycogen synthase b) Glycogen synthase-P

Answer 72

a) Glycogen synthase

Question 73

Glucagon and insulin are examples of hormones with a _____________ structural makeup

Answer 73

Glucagon and insulin are examples of hormones with a **polypeptide** structural makeup

Question 74

An essential pathologic finding in Glycogen storage disease ___________________ is the accumulation of normally structured glycogen in most tissues

Answer 74

An essential pathologic finding in Glycogen storage disease **type II/ Pompe disease** is the accumulation of normally structured glycogen in most tissues

Question 75

An essential pathologic finding in Glycogen storage disease type _____________ disease is the accumulation of normally structured glycogen in **most tissues**

Answer 75

An essential pathologic finding in Glycogen storage disease type **Type II/Pompe disease** is the accumulation of normally structured glycogen in most tissues

Question 76

During feeding state, glycogen phosphorylase should be in the inactive form ____________ to avoid glycogen breakdown. a) Glycogen synthase b) Glycogen synthase-P c) Glycogen phosphorylase-P d) Glycogen phosphorylase

Answer 76

d) Glycogen phosphorylase

Question 77

The glucose transporter in case of liver is --------------. ## Footnote a) GLUT-2 b) GLUT-3 c) GLUT-4 d) GLUT-5

Answer 77

a) GLUT-2

Question 78

Deficiency of **alpha-1,4-glucosidase** causes glycogen storage disease of \_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote a) Type I b) Type II c) Type III d) Type IV

Answer 78

Deficiency of alpha-1,4-glucosidase causes glycogen storage disease of **Type II**

Question 79

The most common forms of GSD are types __ to __ & \_\_. The most common form form is type \_\_

Answer 79

The most common forms of GSD are **types 1 to 5 & 9.** The most common form form is **type 1a - Von Gierke disease**

Question 80

During **fasting** state, glycogen synthase should be in the inactive form, which is \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Answer 80

During fasting state, glycogen synthase should be in the inactive form, which is **glycogen synthase phosphate**

Question 81

Glucagon has no action in muscle as they have no -----------------------------------.

Answer 81

Glucagon receptor

Question 82

Removal of a terminal glucose residue from the non reducing end of a glycogen chain is carried out by the enzyme ---------

Answer 82

Removal of a terminal glucose residue from the non reducing end of a glycogen chain is carried out by the enzyme **glycogen phosphorylase-P**

Question 83

What is the role of tyrosine kinase in the insulin’s receptor?

Answer 83

phosphorylation of tyrosine

Question 84

-------- in Greek, means to stir up or to excite.

Answer 84

Hormone

Question 85

All of the following enzymes act during glycogen degradation EXCEPT: ## Footnote a) Alpha-1,6-glucosidase b) Glucan transferase c) Glycogen phosphorylase-P d) Glycogen synthase

Answer 85

d) Glycogen synthase - used in **glycogenesis** the order of enzymes involved in glycogenolysis are: 1. Glycogen phosphorylase-P 2. Glucan transferase 3. Alpha-1,6-glucosidase

Question 86

Diagnosis of glycogen storage disease is caried out prior to birth/prenatal via \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Answer 86

Diagnosis of glycogen storage disease is caried out prior to birth/prenatal via **chorionic villi sampling and amniocentesis** ## Footnote **chorionic -** pertaining to the chorion. chorionic villi numerous branching projections from the external surface of the chorion that provide for exchange between the maternal and fetal circulation. Oxygen and nutrients in the maternal blood diffuse through the walls of the villi and enter the blood of the embryo or fetus. **Amniocentesis -** (also referred to as amniotic fluid test) is a medical procedure used in prenatal diagnosis of chromosomal abnormalities and fetal infections, and also for sex determination, in which a small amount of amniotic fluid, which contains fetal tissues, is sampled from the amniotic sac surrounding a developing fetus, and then the fetal DNA is examined for genetic abnormalities.

Question 87

**Glycogen** is stored in: ## Footnote a) Kidney and muscle b) Liver and muscle c) Muscle and pancreas d) Pancreas and liver

Answer 87

b) Liver and muscle

Question 88

Removal of a terminal glucose residue from the non reducing end of a glycogen chain is done by \_\_\_\_\_\_\_\_\_\_\_\_\_ a) Glycogen hydrolase b) Glycogen phosphorylase-P c) Glycogen synthase d) Glycogen synthase-P

Answer 88

b) Glycogen phosphorylase-P - alpha 1-4 glycosidic bonds only, alpha 1-6 glycosidase cleaves the alpha 1-6 bonds

Question 89

Insulin’s receptor subunits are stabilized by ----------- bonds

Answer 89

Insulin’s receptor subunits are stabilized by **disulfide bonds**

Question 90

Glycogen Storage Disease can lead to enlarged ---------

Answer 90

Liver

Question 91

During **feeding** state, glycogen phosphorylase should be in the ________ state.

Answer 91

During feeding state, glycogen phosphorylase should be in the **inactive** state.

Question 92

5? | (fasting)

Answer 92

glycogen synthase phosphate | (inactive form of enzyme)

Question 93

For people who have glycogen storage diseases that cause low blood sugar levels, levels are maintained by giving them -------- every 4 to 6 hours around the clock

Answer 93

For people who have glycogen storage diseases that cause low blood sugar levels, levels are maintained by giving them **uncooked cornstarch** every 4 to 6 hours around the clock

Question 94

Liver doesn’t contain the insulin sensitive transporter -------- ## Footnote a) GLUT 1 b) GLUT 2 c) GLUT 3 d) GLUT 4 e) GLUT 5

Answer 94

d) GLUT 4

Question 95

During feeding state, plasma glucose is high, thus insulin is dominating. It increases \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_, which activates _____________ to form glycogen in order to _______ plasma glucose levels

Answer 95

During feeding state, plasma glucose is high, thus insulin is dominating. It increases **protein phosphatase-1**, which activates **glycogen synthase** to form glycogen in order to **decrease** plasma glucose levels

Question 96

In contrast to GSD type I, ------------------ are involved in GSD type III.

Answer 96

In contrast to GSD type I, **liver & skeletal muscles** are involved in GSD type III.

Question 97

name the GLUT protein: ## Footnote **Tissue distribution:** Skeletal and cardiac muscle, fat. **Special properties:** Activated by insulin. Km 5mM.

Answer 97

GLUT 4

Question 98

The second messenger for glucagon is -------, whereas that for insulin is --------.

Answer 98

The second messenger for glucagon is **cAMP**, whereas that for insulin is **-not yet identified**

Question 99

Some types of glycogen storage disease can be detected even before __________ occurs, if both parents are tested for the presence of the defective gene.

Answer 99

Some types of glycogen storage disease can be detected even before **conception** occurs, if both parents are tested for the presence of the defective gene.

Question 100

During **feeding** state, glycogen synthase should be in the _______ state.

Answer 100

During feeding state, glycogen synthase should be in the **active** state.

Question 101

During **fasting** state, glycogen synthase should be in the _______ state.

Answer 101

During fasting state, glycogen synthase should be in the **inactive** state.