Metab Insulin/Glucagon

Question 1

What type of cell makes insulin? Where is it stored?

Answer 1

insulin a polypeptide hormone produced by the Beta-cells of the islets of Langerhans-clusters of cells that are embedded in the exocrine portion of the pancreas. Insulin is stored in the cytosol in granules that if given the proper stimulus are released by exocytosis.

Question 2

What kind of effect does insulin has, Anabolic or catabolic?

Answer 2

Insulin has an anabolic effect, favoring the synthesis of glycogen, triacylglecerols, and protein.

Question 3

What is the structure of insulin?

Answer 3

Insulin is composed of 51 amino acids arranged in two polypedtide chains, designated A and B, which are linked together by two disulfide bridges.

Question 4

What enzyme degrades insulin? Where is this enzyme present? What is the half-life of inuslin?

Answer 4

Insulin is degraded by the enzyme insulinase which is present in the liver and, to a lesser extent, in the kidneys. Insulin has a half-life of aprox. 6 minutes. This short duration of action permits rapid changes in circulation levels of the hormone.

Question 5

What kind of GLUT transporters do we find in Beta-cells?

Answer 5

GLUT-2

Question 6

What amino acid will increase in fed state and will serve as a stimulus for insulin synthesis?

Answer 6

Elevated plasma Arginine is a particularly potent stimulus for insulin synthesis and secretion.

Question 7

What are referred to as incretins?

Answer 7

IN - intestine CRE-secretion tIN-insulin. The intestinal peptides Cholecystokinin and gastric-inhibitory polypeptide increase insulin secretion in response to oral glucose.

Question 8

What effect does the rise of ATP has on pancreatic beta islet cells?

Answer 8

The rise in ATP causes ATP-sensitive potassium channels to close. Causing depolarization of the plasma membrane, activation of voltage-gated calcium channels, and influx of calcium into the cell.

Question 9

What kind of receptors does epinephrine binds to and what is the effect on beta cells?

Answer 9

Binding of epinephrine to alpha-adrenergic receptors on beta cells causes cAMP and, thus, a decrease in insulin secretion.

Question 10

When insulin level is high, what happens to lipoprotein lipase activity in adipose tissue? what happens to the activity of Hormone sensitive lipase in the same cell?

Answer 10

HSL (hydrolyzes stored Triacylglycerols into free FA) activity is decreased. While lipoprotein lipase activity is increased , bringing in more F.A. into the cell for esterification. Insulin promotes the conversion of glucose into triacylglycerols.

Question 11

How does insulin causes intake of glucose?

Answer 11

1- Insulin binds to its receptors in the cell membrane 2-Activated receptor promotes recruitment of glucose transporters from intracellular pool to cell membrane 3-Glucose transporters increase insulin-mediated uptake of glucose into cell. 4-When insulin levels decrease, glucose transporters move from cell membrane to intracellular storage pool, where they can be recycled. 5-Vesicles fuse to form an organelle called the endosome.

Question 12

What is the beta subunit of insulin?

Answer 12

The cytosolic domain of the beta subunit is tyrosine kinase, which is activated by insulin.

Question 13

Which tissues are insulin insentive?

Answer 13

Erythrocyte, leukocytes, Lens of eye, Cornea, Liver, Brain.

Question 14

what happens to insulin once it is inside the cell? how about its receptors?

Answer 14

Binding of insulin is followed by internalizaiton of the hormone-receptor complex. Once inside the cell, insulin is degraded in the lysosomes. The receptors may be degraded but most are recycled to the cell surface.

Elevated levels of insulin promote the degradation of receptors, thus decreasing the number of surface receptors. This is one type of “down regulation”.

Question 15

What effect does caffeine has on glucagon?

Answer 15

Caffeine increases glucagon effects by inhibiting the enzyme phosphodiesterase, thus increasing the half life of cAMP, since it won’t be converted to 5’-AMP

Question 16

what happens to plasma level of amino acids in the presence of glucagon?

Answer 16

It decreases, because glucagon increases uptake of A.A. by the liver, resulting in increased availability of carbon skeletons for gluconeogenesis.

Question 17

Where we won’t find any glucagon receptors?

Answer 17

Skeletal muscle

Question 18

What is the difference between Adrenergic and Neuroglycopenia symptoms of hypoglycemia?

Answer 18

Adrenergic: causes axiety, palpitations, sweating, and tremors. These sympoms are the result of epinephrine release, regulated by the hypothalamus in response to hypoglycemia. Usually this occurs when blood glucose levels fall abruptly!

Neuroglycopenia: The impaired delivery of glucose to the brain. This results in impairment of brain function, causing headache, confusion, slurred speech, seizures, coma, and death. The slow Gradual decline in glucose fails to trigger an adequate epinephrine response.

Question 19

As far glycogenolysis and gluconeogenesis goes.. which of these two pathways get activated by cortisol, epinephrine, and glucagon?

Answer 19

Cortisol activates gluconeogenesis. Less important on short term maintenance of glucose, but important on the long term one.

Epinephrine activates glycogenolysis and lipolysis

Glucagon activates both.

Question 20

what are the 3 types of hypoglycemia?

Answer 20

1: Insulin induced
2: Postprandial (reactive hypoglycemia)
3: Fasting hypoglecymia. (alcohol intoxification in fasting individuals, can be associated with hypoglycemia).

Question 21

what is postprandial hypoglycemia?

Answer 21

This is the second most common form of hypoglycemia. It is caused by an exaggerated insulin release following a meal, prompting transient hypoglycemia with mild adrenergic symptoms. The plasma glucose levels returns to normal even if the pt. is not fed. The only treatment usually required is that the patient eat frequent small meals rather than the usual 3 large meals.

Question 22

What is the metabolism of alcohol?

What is the medication that inhibits the accumulation of acetate?

Answer 22

1: Ethanol is converted to acetaldehyde by alcohol dehydrogenase.

2: Acetaldehyde is subsequently oxidized to acetate by Aldehyde dehydrogenase.

The latter enzyme is inhibitted by disulfiram, a drug that causes accumulation of acetaldehyde in blood, which in turns cuases hyperventilation, nausea, and tachycardia.

Question 23

why alcohol intoxification causes hypoglycemia?

Answer 23

Because everytime alcohol is metabolize from ethanol all the way acetate it generates NADH+. This in turns accumulates in the cell, which drives the rx of pyruvate to lactate and OAA to malate.

Pyruvate and OAA are precursors needed for gluconeogenesis, hence when these are not available it decreases teh synthesis of glucose.