6. Endocrine Cells of the Pancreas Flashcards

1
Q

How do α-cells and β-cells communicate in the islets of Langerhans?

A

Gap junctions and paracrine actions.

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2
Q

What changes in the incretin effect in type II diabetic patients?

A

The incretin effect loses the ability to increase insulin secretion.

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3
Q

What is the effect of glucosuria on blood electrolyte levels?

A

The osmotic diuresis of type I diabetes blunts the reabsorption of electrolytes and therefore decreases their serum levels.

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4
Q

What causes insulin independent mobilization of GLUT4?

A

Muscle contraction stimulates AMPK, which causes GLUT4 translocation to the plasma membrane.

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5
Q

What are the stimulatory factors of insulin? (9 things)

A

↑ Glucose / amino acid concentration.
↑ Fatty acid / ketoacid concentration.
Glucagon (facilitates).
Cortisol.
GIP.
K+.
Acetylcholine (parasympathetic).
Sulfonylurea drugs.
Obesity (leptin).

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6
Q

Which phase of insulin secretion is lost first in diabetic individuals?

A

The initial spike – “first phase insulin secretion.”

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7
Q

What is secreted by the F cells of the islets of Langerhans?

A

Pancreatic polypeptide. (Satiety signal.)

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8
Q

How does glucose stimulate insulin secretion?

A

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.

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9
Q

Through which cell population in the islets of Langerhans does blood travel first?

A

The β-cells of the islets of Langerhans.

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10
Q

Both insulin increase or decrease blood ketoacid levels?

A

Decreases blood ketoacid levels.

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11
Q

Why might blood glucose be normal when some of the patient’s β-cells have been destroyed by autoantibodies?

A

Because the remaining β-cells will become overactive to compensate.

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12
Q

What are the two incretin hormones discussed in class?

A

GLP-1

GIP

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13
Q

What is the effect of insulin on the hexose monophosphate shunt?

A

Favors metabolism towards the hexose monophosphate shunt.

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14
Q

What is a diagnostic relevance of C-peptide in the blood?

A

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.

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15
Q

Do we see diabetic ketoacidosis more frequently in insulin-dependent or non-insulin-dependent diabetes?

A

Insulin-dependent (type I) diabetics are more likely to develop diabetic ketoacidosis.

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16
Q

What are the inhibitory factors of insulin?

A

Decreased blood glucose.
Fasting.
Exercise.
Somatostatin.
α-adrenergic agonists.
Norepinephrine.
Diazoxide.

17
Q

What is the effect of intracellular and extracellular potassium in type I diabetes?

What causes this symptom?

A

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.

18
Q

What causes polyuria in type I diabetes?

A

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.

19
Q

What is the effect of the phosphorylation of PI3K/AKT/mTOR and MAPK’s as discussed in this lecture?

A

They are responsible for cell growth, differentiation, and insertion of GLUT4 transporters on the cell membrane. GLUT4 is responsible for insulin mediated glucose uptake.

20
Q

What important step in glycolysis regulation is inhibited by glucagon?

A

Creation of Fructose 2,6-bisphosphate. (PFK2)

(Fructose 2,6-bisphosphate activates phosphofructokinase, and promotes glycolysis.

21
Q

What is secreted by the β-cells?

A

Insulin.

C-peptide.

22
Q

What four things, discussed in class, inhibit glucagon?

A

Insulin.

Somatostatin.

Fatty acids.

Ketoacids.

23
Q

Why do type I diabetics appear emaciated – specifically with atrophy of muscle tissue?

A

Insulin is necessary for the anabolic reactions which build muscle.

24
Q

What is the function of sulfonylurea drugs?

A

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.

25
Q

What is the overall effect of incretin hormones?

A

Stimulate insulin secretion.

Inhibit glucagon secretion.

Delay gastric emptying.

26
Q

What would we expect to see in blood insulin levels in a type II prediabetic vs. a normal individual?

A

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.

27
Q

How do δ-cells communicate with α and β-cells?

A

Through “dendrite -like” processes.

28
Q

What is the effect of insulin on glycolysis and carbohydrate oxidation in the liver?

A

Increases carbohydrate oxidation and glycolysis.