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.
What are the inhibitory factors of insulin?
Decreased blood glucose.
Fasting.
Exercise.
Somatostatin.
α-adrenergic agonists.
Norepinephrine.
Diazoxide.
What is the effect of intracellular and extracellular potassium in type I diabetes?
What causes this symptom?
Intracellular levels of potassium will be low, and extracellular levels of potassium will be high.
Insulin stimulates the Na/K ATPase, so its absence diminishes the ability of the Na/K ATPase to push potassium into the cells.
What causes polyuria in type I diabetes?
Once blood glucose rises above about 180, it begins to appear in the urine. This results in an osmotic diuresis by pulling water into the renal tubules.
What is the effect of the phosphorylation of PI3K/AKT/mTOR and MAPK’s as discussed in this lecture?
They are responsible for cell growth, differentiation, and insertion of GLUT4 transporters on the cell membrane. GLUT4 is responsible for insulin mediated glucose uptake.
What important step in glycolysis regulation is inhibited by glucagon?
Creation of Fructose 2,6-bisphosphate. (PFK2)
(Fructose 2,6-bisphosphate activates phosphofructokinase, and promotes glycolysis.
What is secreted by the β-cells?
Insulin.
C-peptide.
What four things, discussed in class, inhibit glucagon?
Insulin.
Somatostatin.
Fatty acids.
Ketoacids.
Why do type I diabetics appear emaciated – specifically with atrophy of muscle tissue?
Insulin is necessary for the anabolic reactions which build muscle.
What is the function of sulfonylurea drugs?
Sulfonylurea drugs close the ATP -dependent K+ channel in the same way that ATP would from glucose. This helps the beta cells of the pancreas produce more insulin.
What is the overall effect of incretin hormones?
Stimulate insulin secretion.
Inhibit glucagon secretion.
Delay gastric emptying.
What would we expect to see in blood insulin levels in a type II prediabetic vs. a normal individual?
Because of the developing insulin resistance, a type II prediabetic will produce much more insulin than a normal person to respond to the same amount of glucose.
How do δ-cells communicate with α and β-cells?
Through “dendrite -like” processes.
What is the effect of insulin on glycolysis and carbohydrate oxidation in the liver?
Increases carbohydrate oxidation and glycolysis.
