[BG] Pancrease-Carbohydrate Metabolism Flashcards

1
Q

After ingested glucose is gone, what is the next process that will provide the body with glucose for energy?

A

Glyogenolysis: Glycogen –> Glucose

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2
Q

The GLUT 2 transporter is a high Km transporter. Where is it present and What does the Km tell you?

A

It is present in the Kidney, Liver, Pancreas and GI; The higher the Km, the faster the glucose can enter the cell and leave the blood. Therefore, it allows equilibrium across the membrane and is responsive to the changes in the glucose concentration (say after a meal).

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3
Q

In the liver, pancreas and kidney, _____________________ regulates carbohydrate metabolism by acting as a glucose sensor, and converts Glucose –> G6P.

A. Glucokinase
B. Hexokinase 
C. PFK-1 
D. F-1,6-BP
E. PEPCK
A

A. In these organs, glucokinase works on glucose –> G6P

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4
Q

In the muscle, _____________________ regulates carbohydrate metabolism by acting as a glucose sensor, and converts Glucose –> G6P.

A. Glucokinase
B. Hexokinase 
C. PFK-1 
D. F-1,6-BP
E. PEPCK
A

B. Hexokinase; a low Km enzyme (rate limiting step) Traps glucose in the cell.

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5
Q

After a meal, _______________or _____________ can release glucokinase, which moves into the cytoplasm.

A
  1. Glucose

2. Fructose -1- Phosphate

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6
Q

In the fed state, after glucose or fructose-1-phosphate releases glucokinase, It binds to a bifunctional enzyme _______________:_________________, which keeps it in the active state

A

Phosphofructokinase-2:Fructose-2,6-Bisphosphatase

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7
Q

Metabolism of Fructose: Fructose is converted into Fructose-1-phosphate by ___________________.

A

Fructose Kinase

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8
Q

Does fructose raise Insulin levels?

A

No

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9
Q

Does galactose raise insulin levels?

A

No

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10
Q

Fructose-1-Phosphate is not an intermediate of Glycolysis. Therefore, it requires an additional enzyme, __________________, which converted F1P –> Glyceraldehyde and DHAP

A

Aldolase B

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11
Q

After Aldolase B has converted F1P into glyceraldehyde and DHAP. Glyceraldehyde is converted into DAG via ____________________.

A

Triose Kinase.

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12
Q

Fructose intolerance can be explained by a deficiency in what enzyme?

A

Aldolase B; This is a hereditary fructose intolerance. Autosomal recessive.

Or

Malabsorption of Fructose due to a deficiency in the GLUT5 fructose transporter

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13
Q

The biosynthesis of Fructose occurs via what bioenzymatic pathway?

A

Polyol Pathway

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14
Q

What compound accumulates in some cells during hyperglycemia and can cause osmotic effects on the eye, kidney and Nerves?

A

Sorbitol

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15
Q

Glucose is converted to Sorbitol with the help from what enzyme?

A

Aldose Reductase

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16
Q

Sorbitol is converted into Fructose by what enzyme?

A

Sorbitol Dehydrogenase

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17
Q

In cells that need to produce fructose (i.e. Fructose is found in high concentration in the seminal fluid), what enzyme is present that is not present in other tissues/cells?

A

Sorbitol Dehydrogenase which converted Sorbitol –> Fructose

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18
Q

UDP-Galactose is converted into UDP-Glucose by what enzyme?
A. Galactose-1-Phosphate uridyltransferase
B. Phosphoglucomutase
C. Glucose-6-Phosphatase
D. UDP-Hexose-4-epimerase
E. UDP-Glucose Pyrophosphorylase
F. Galactokinase

A

D. UDP-Hexose-4-Epimerase

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19
Q

Glycogenolysis involves the conversion of Glycogen storage molecules into Glucose-6-phosphate by what enzyme?

A

Glycogen Phosphorylase

20
Q

After glycogen phosphorylase has chewed its way through the glycogen molecule, it will reach a point where it can no longer work. What is this point called?

A

Limit Dextrin

21
Q

At the limit dextrin, _____________________works by removing the limit dextrin, leaving 1 glucose molecule and substrate for the glycogen phosphorylase.

A
  1. Debranching enzyme
22
Q

The debranching enzyme has 2 main functions. The function of removing glucose, ______________________ function and the function removing the limit dextrin, ______________________ function.

A
  1. Glucosidase Function

2. Transferase Function

23
Q

Glucose - 6- phosphate is converted into glucose by what enzyme?

A

Glucose Dismutase

24
Q

What enzyme is not present in skeletal muscle and therefore, glucose can be produced from glycogen stores?

A

Glycogen phosphorylase

25
Q

What is the starting substrate for gluconeogenesis?

A. Acetyl-CoA
B. Pyruvate 
C. Oxaloacetate 
D. PEP 
E. ATP
A

B. Pyruvate

26
Q

Gluconeogenesis: Pyruvate is converted into ______________________ by _________________

A

Oxaloacetate via Pyruvate Carboxylase and B7

27
Q

Gluconeogenesis: Oxaloacetate is converted into PEP via _______________________ and requires transfer via ______________.

A

PEPCK; Malate

28
Q

What is the main source of fuel for the synthesis of glucose during gluconeogenesis?

29
Q

What are the sources of gluconeogenic precursors?

A

Glutamine
Glycerol
Lactate
Alanine

30
Q

Open Ended: Explain how Ethanol consumption effects Gluconeogenesis.

A

NADH is produced in the consumption of alcohol which cause pyruvate to convert into lactate and oxaloacetate to convert into Malate. Recall that Gluconeogenesis must start from either pyruvate or oxaloacetate. Therefore, while drinking, the substrate for gluconeogenesis are being used up and therefore can not be used towards glucose production.

31
Q

__________________ increases the synthesis of PEPCK for gluconeogenesis.

A. Glucagon 
B. Epinephrine 
C. Cortisol 
D. Insulin 
E. ATP
A

C. Cortisol

32
Q

Fill in the blank: Glycogen Synthase Kinase __________________Glycogen Synthase A, this ____________________ Glycogen Synthase A by converting it into ________________________.

Glycogen Synthase Kinase is inactivated by ______________. Thus, Insulin prevents _________________ by Glycogen Synthase Kinase.

A
  1. Phosphorylates
  2. Inactivates
  3. Glycogen Synthase B
  4. Akt (protein Kinase B)
  5. Phosphorylation
33
Q

What stimulates Fructose-6-Phosphate –> Fructose 1,6-Bisphosphate?

A
  1. F-2,6-BP

2. AMP

34
Q

What inhibits Fructose-6-Phosphate –> Fructose 1,6-Bisphosphate?

A
  1. ATP
  2. Citrate
  3. H+
35
Q

What stimulates the Gluconeogenesis mechanism of Fructose-1,6-Bisphosphate –> Fructose-6-Phosphate?

A

A. Citrate

36
Q

What inhibits the Gluconeogenesis mechanism of Fructose-1,6-Bisphosphate –> Fructose-6-Phosphate?

A
  1. AMP

2. Fructose-2,6-BP

37
Q

This syndrome will not allow you to display transferase or glucosidase activities.

A

Cori Syndrome

38
Q

This syndrome is the result of a deficiency in the Glycogen synthase enzyme.

A

McArdle’s Syndrome

39
Q

This disease involves a deficiency in the glycosidases involved in glycogen breakdown inside of lysosomes.

A

Pompe’s Disease.

40
Q

What are the 2 main reasons that the hexose monophosphate shunt is important?

A
  1. NADPH

2. Ribose-5-phosphate

41
Q

Hannibal Lecter Coined the famous phrase, “I ate his liver with some fava beans.” What is the deficiency that Hannibal Lecter may suffer from as a result?

A

G6P Dehydrogenase Deficiency

42
Q

Give at least 2 examples of secondary forms of diabetes. Secondary forms of diabetes are conditions that result in diabetes but do not originate in the insulin system.

A
  1. Cushing Syndrome
  2. Pancreatectomy
  3. Acromegaly
43
Q

Hyperglycemia in diabetics result from increased ___________________________ and a reduced glucose utilization.

A

Gluconeogenesis

44
Q

Why is Glycogenolysis not an important cause of chronic hyperglycemia in diabetes?

A

Because glycogen synthesis and glycogen breakdown cancel out; steady state

45
Q

A 22 yo college student of Asian Ancestry has returned from a visit to his friends in Sardinia on a summer break. He arrives at the airport complaining of Fatigue, Nausea, abdominal Pain and fever. He has a mild hemoglobinuria and Jaundice. He ate a large dinner just prior to departure which included a local bean salad. What is the problem?

A

Fava Bean; G6P Dehydrogenase Deficiency –> hemolytic crisis/membrane damage