Regulation Of Blood Glucose Flashcards

1
Q

Normal fasting glucose is……., after one hour of meal it is….., post-prandial is…..

A

70-100 mg%
150 mg%
140 mg%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

With respect glucose transporters (GLUTs), intestinal is….., hepatic is….., B cells of islets is….., heart/skm/adipose tissue is……& are regulated by………, other tissues is……

A

4 & SGLT1
2
2
4, insulin
1&3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Compare kinetics of Hexokinase & glucokinase

A
  1. H. has high affinity & low Km for glucose, it is saturated in the liver acting at constant rate in all normal conditions. To ensure adequate rate of glycolysis & meet liver needs.
  2. G. has low affinity & high Km for glucose. Allows uptake of large amounts of glucose after meal , for glycogen & fatty acid synthesis. Prevents large amounts of glucose from entering systemic circulation & minimizing absorptive hyperglycemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe structure & biosynthesis of insulin

A

Composed of 51AA consisting of 2 chains A(21) & B linked together by 2 disulphide bridges. Synthesis involves 2 inactive precursors preproinwulin & proinsulin that are seuentially cleaved to form active hormone & C-peptide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

…….is a good indicator of insulin production & secretion

A

C-peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe secretion of insulin

A

B cells are freely permeable to glucose via GLUT2 & is phosphorylated by glucokinase & there is inc glycolysis & TCA activity producing ATP which causes opening ATP-sensitive K+-channels causing depolarization & Ca++ influx causing exocytosis of insulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe intracellular metabolic effects of insulin

A
  1. Inc glycolysis by inducing glucokinase, PK1, PK
  2. Inc glycogenesis by stimulating glycogen synthase & inhibit glycogenolysis by inhibiting glycogen phosphorylase
  3. Inhibit gluconeogenesis by repression of pyruvate carboxylase, PEPCK, G6P&F1-6 bisphosphatase
  4. Inc HMP by induction of G6PD & 6Pgluconic dehydrogenase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List triggers for glucagon release

A
  1. Dec glucose
  2. Inc AAs & CAs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe intracellular metabolic effects of glucagon (epinepherine)

A
  1. Inc glycogenolysis in liver by stimulation of glycogen phosphorylase & inhibition of glycogen synthase
  2. Inc gluconeogenesis by induction of pyruvate carboxykase, PEPCK, G6P, F1-6 bisphosphatase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

GR: Obese people have insulin resistance

A

Bec adipose tissue occasionally secretes glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe intracellular metabolic effects of GH

A

Dec glucose uptake by muscle , may be by indirect effect as it stimulates mobilization of free fatty acids that exert the previous effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypoglycemia is usually considered below……

A

40mg%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List causes of hypoglycemia

A
  1. Neonatal
  2. Insulin-dependent hypoglycemia
  3. Postprandial hypoglycemia
  4. Fasting hypoglycemia
  5. Alcohol-related hypoglycemia
  6. Inborn errors of metabolsim
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of fasting hypoglycemia

A

A. Reduction in the rate of glucose production by hepatic glycogenolysis/gluconeogenesis:
-hepatocellular damage
-renal failure
-adrenal insufficiency
B. Inc rate of glucose used by peripheral tissues due to overproduction of insulin by rare pancreatic tumors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

GR: Occurrence of alcohol-related hypoglycemia

A

Alcohol is metabolized by 2 steps of oxidation, in which NAD+ accepts electrons and becomes NADH. The abundance of NADH leads to shift of pyruvate to lactate, OAA to malate. This causes intermediates of gluconeogenesis to divert to other pathways producing hypoglycemia & behavioural side effects of alcohol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List inborn errors of metabolism causing hypoglycemia

A
  1. Glycogen storage disease type I, Von Geirke, glucose 6-phosphatase def
  2. Hereditary Fructose intolerance
  3. Galactose 1-P uridyl transferase def
  4. Inborn errors of gluconeogenesis
  5. Fatty acid oxidation defects (carnitine, CPT-1, medium chain acyl-CoA dehydrogenase deficiency)