3.7-Diabetics

Question 1

Concerning insulin release…Does it oscillate or is it consistently released?

Answer 1

It oscillates: big surge, then after 10min it decreases. Then bumps up again..

Question 2

Does the presence of insulin stimulate or inhibit protein synthesis?

Answer 2

Stimulates! A common theme, Insulin=building stuff!

Question 3

What effect does insulin have on acetyl-CoA carboxylase?

Answer 3

Increases its activity: (also called B7 Biotin. Committed stop to FA syn

Question 4

About how many times increase for the uptake of glucose in the presence of insulin?

Answer 4

15x (GLUT4s!)

Question 5

Type I: Age of Onset

Answer 5

Usually in childhood RAPID development

Question 6

Type I: Nutritional Status

Answer 6

Undernourished

Question 7

Type I: Genetic Disposition

Answer 7

Moderate

Question 8

Which Type?:Beta Cells are destroyed, eliminating the product insulin

Answer 8

Type I

Question 9

Type I: Frequency of Ketosis

Answer 9

Common

Question 10

Type I: Plasma Insulin

Answer 10

Low to Absent

Question 11

Type I: Acute Complications

Answer 11

KetoAcidosis

Question 12

Type I: Treatment

Answer 12

Insulin Always Necessary

Question 13

Type II:Age of Onset

Answer 13

after age 35

Question 14

Type II: Nutritional Status

Answer 14

Obesity usually present

Question 15

Type I: Prevalence

Answer 15

~10% of Diabetes diagnosis

Question 16

Type II: Prevalence

Answer 16

~90% of diagnosis

Question 17

Type II: Genetic predisposition

Answer 17

Very Strong, huge factor, Pima Indian example

Question 18

Which Type? Insulin resistance combined with inability of Beta cells to produce appropriate quantities of insulin…

Answer 18

Type II

Question 19

Type II: Frequency of Ketosis

Answer 19

Rare

Question 20

Type II: Plasma Insulin

Answer 20

High early, then Beta cells get poisoned and make less

Question 21

Type II: Acute Complications

Answer 21

Hyperosmolar coma

Question 22

Type II: Treatment

Answer 22

Diet, exercise, oral hypoglycemic drugs, +/- insulin

Question 23

What is the primary cause of Type I?

Answer 23

Autoimmune destruction of Beta cells

Question 24

What is the direct result of Lipoprotein Lipase activity being diminished?

Answer 24

Build up of chylomicrons

Question 25

How does hyperglycemia relate to body pH?

Answer 25

Water gets pulled into blood, making a higher proton concentration in the cells

Question 26

What is the lipase IN the adipose cell? What is the lipase on the endothelial cell?

Answer 26

Adipose: Hormone-Sensative Lipase, Endothelial: LipoProtien Lipase

Question 27

Why does type II NOT get Ketosis?

Answer 27

Since there is still SOME insulin, the HORMONE-SENSATIVE lipase is inhibited and there is less FA to the liver, ergo less ketones out of the liver

Question 28

What does hemoglobin A become after sugar has bound to it? (Dr.’s read this..) Is it a covalent or non-covalent bond?

Answer 28

Hemoglobin A1C, it is a non-covalent bond of heme to sugar (the more [A1C] the more insulin needed)

Question 29

REVIEW! What enzyme will convert glucose to sorbitol? What enzyme do you need to prevent a build up of sorbitol that is not present in the lens, nerve tissue and kidney…

Answer 29

ALdose Reductase (ALcohol maker)…..Sorbitol Deydrogenase (weird, we use a dehydrogenase to change an OH again!)

Question 30

Which type of diabetic sees the Hyperglycemic Hyperosmolar State (HHS)?

Answer 30

Type II…Much like the reasons for KetoAcidosis, except no acidosis because of some insulin present…

Question 31

What does AGE stand for? How is it related to Hyperglycemia?

Answer 31

Advanced Glycosylation End-product. Sugar binding to proteins, changing their function and stuff.

Question 32

Which type of diabetes is the “Metabolic Syndrome” an indicator of?

Answer 32

Type II