Biochemistry of Diabetic Ketoacidosis

Question 1

What glucose receptor is used by RBCs?

Answer 1

GLUT-1

Question 2

HMG CoA synthase is an enzyme responsible for converting acetyl-CoA to ketones. What is the effect of glucagon on this enzyme?

Answer 2

Glucagon increases the activity of the HGM CoA synthase.

Question 3

How do blood glucose levels between non-diabetic and diabetic patients compare?

Answer 3

Compared to non-diabetic patients, diabetic patients have higher basal glucose levels, greater glucose increase after a meal, and take longer to return to basal levels

Question 4

This receptor is glucose-dependent and is moved to the cell membrane when stimulated by insulin. Where is this receptor found?

Answer 4

GLUT-4 found in skeletal muscle and adipose

Question 5

True/False. Type 1 diabetes has a gradual onset of symptoms.

Answer 5

False. The development of type 1 diabetes is a gradual process; however, symptom onset is sudden.

Type 2 diabetes has a slow and gradual onset of symptoms.

Question 6

SGLT-1 is a receptor in the intestines that absorbs glucose against its concentration gradient. How is this possible?

Answer 6

SGLT-1 is coupled with the Na/K ATPase. This receptor enables 100% absorption of glucose

Question 7

What does blood pH decrease during periods of high ketone body production?

Answer 7

Ketone bodies are acidic and are deprotonated in the blood. They can be buffered by bicarbonate, but if levels continue to rise they can exceed the buffering capacity of bicarbonate and lead to acidosis

Question 8

GLUT-2 is a glucose (dependent/independent) receptor.

Answer 8

Glucose independent. GLUT-2 is specific to the liver and pancreas and senses glucose levels to promote absorption.

Question 9

What ketones are produced through ketogenesis from acetyl-CoA?

Answer 9

Beta-hydroxybutyrate and acetone

Question 10

Increased acetyl-CoA and NADH from beta-oxidation of fatthy acids leads to increased production of OAA. OAA then enters gluconeogenesis. How does this process occur?

Answer 10

Increased acetyl-CoA inhibits the pyruvate dehydrogenase, which is the entry point into TCA.

The increased acetyl-CoA stimulates the pyruvate carboxylase, which produces OAA from pyruvate that was generated in glycolysis.

OAA then enters gluconeogenesis due to high levels of NADH.

Excess acetyl-CoA can also enter into ketogenesis.

Question 11

Muscle metabolism is (increased/decreased) in diabetic patients.

Answer 11

Glucose uptake is decreased and muscle metabolism increased to provide amino acid precursors for gluconeogenesis

Question 12

Fat is metabolized to glycerol and fatty acids in diabetic patients. How are these molecules used to generate energy?

Answer 12

Glycerol is utilized in gluconeogenesis to produce glucose.

Fatty acids undergo beta-oxidation to produce NADH and acetyl-CoA.

Question 13

Insulin is released by what pancreatic cells?

Answer 13

Beta cells

Question 14

True/False. Insulin is always low and glucagon is always high in diabetic patients, regardless of fasting or fed state.

Answer 14

True

Question 15

This receptor functions to move glucose along a concentration gradient in the intestines.

Answer 15

GLUT-1

Question 16

Most amino acids are gluconeogenic. These amino acids are ketogenic only.

Answer 16

Lysine and leucine

Question 17

These amino acids are both gluconeogenic and ketogenic.

Answer 17

Tryptophan, tyrosine, phenylalanine, isoleucine

Question 18

Glucagon is released by what pancreatic cells?

Answer 18

Alpha cells