6. Endocrine Cells of the Pancreas Flashcards
How do α-cells and β-cells communicate in the islets of Langerhans?
Gap junctions and paracrine actions.
What changes in the incretin effect in type II diabetic patients?
The incretin effect loses the ability to increase insulin secretion.
What is the effect of glucosuria on blood electrolyte levels?
The osmotic diuresis of type I diabetes blunts the reabsorption of electrolytes and therefore decreases their serum levels.
What causes insulin independent mobilization of GLUT4?
Muscle contraction stimulates AMPK, which causes GLUT4 translocation to the plasma membrane.
What are the stimulatory factors of insulin? (9 things)
↑ Glucose / amino acid concentration.
↑ Fatty acid / ketoacid concentration.
Glucagon (facilitates).
Cortisol.
GIP.
K+.
Acetylcholine (parasympathetic).
Sulfonylurea drugs.
Obesity (leptin).
Which phase of insulin secretion is lost first in diabetic individuals?
The initial spike – “first phase insulin secretion.”
What is secreted by the F cells of the islets of Langerhans?
Pancreatic polypeptide. (Satiety signal.)
How does glucose stimulate insulin secretion?
Glucose enters via GLUT2 -> is converted to glucose 6-phosphate -> is oxidized into ATP -> ↑ ATP closes ATP -dependent K+ channels -> membrane depolarizes -> voltage gated calcium channels open -> calcium scratch that Ca2+ causes the release via exocytosis of insulin.
Through which cell population in the islets of Langerhans does blood travel first?
The β-cells of the islets of Langerhans.
Both insulin increase or decrease blood ketoacid levels?
Decreases blood ketoacid levels.
Why might blood glucose be normal when some of the patient’s β-cells have been destroyed by autoantibodies?
Because the remaining β-cells will become overactive to compensate.
What are the two incretin hormones discussed in class?
GLP-1
GIP
What is the effect of insulin on the hexose monophosphate shunt?
Favors metabolism towards the hexose monophosphate shunt.
What is a diagnostic relevance of C-peptide in the blood?
C-peptide is released along with insulin in equimolar amounts.
It is a way to determine beta cell function independent of blood insulin levels – which may be masked by the patient taking therapeutic insulin.
Do we see diabetic ketoacidosis more frequently in insulin-dependent or non-insulin-dependent diabetes?
Insulin-dependent (type I) diabetics are more likely to develop diabetic ketoacidosis.