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15 Cards in this Set

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  • Back
Glucose enters cells by facilitated diffusion, or in the intestine and kidneys, by secondary active transport with Na+. TRUE/FALSE
In muscle , aft and some other tissues, insulin facilitates glucose entry into cells by increasing the numbers of glucose transporters in the cell membranes. TRUE/FALSE
Have different glucose transporters been identified?
Seven different glucose transporters, called in order of discovery, GLUT 1-7 have been characterized. They have app 500 amino acid residues, and their affinity for glucose varies.
What is the relationship between glucose transporters and phosphorylation?
In the tissues in which insulin increases the number of glucose transporters in the cell membranes, the rate of phosphorylation of the glucose, once it has entered the cell is regulated by other hormones. Infact, GH and cortisol both inhibit phosphorylation in certain tissues.
When insulin causes the entry of glucose into the liver, how does it acheive this process?
It is not acheived via GLUT 4 transporters. Instead, it induces glucokinase, and this increases the phosphorylation of glucose, so that the intracellular free glucose concentration stays low, facilitating the entry of glucose into the cell.
The maximum decline in plasma glucose occurs 30 min after I/V injection of crystalline insulin. After SQ administration the decline occurs in app. 2-3 hours. TRUE/FALSE
Does insulin cause K+ to enter cells?
Yes. With a resultant lowering of the extracellular K+ concentration. Infusions of insulin and glucose significantly lower the plasma K+ level in normal individuals and are very effective for the temporary relief of hyperkalemia in patients with renal failure.
can insulin deficiency be induced?
Yes. It can be induced by pancreatectomy; by administration of of alloxan, streptozocin or other toxins that in appropriate doses cause selective destruction of the B cells of the islets. Anti-insulin antibodies have produced insulin deficiency as well.
What is HbA1c?
When plasma glucose is episodically elevated over time, small amounts of hemoglobin A are non-enzymatically glycated to form HbA1c. Careful control of the diabetes with insulin reduces the amount formed and consequently HbA1c concentration is measured clinically as an integrated index of diabetic control for the 4-6 week period before the measurement.
What is Kussmaul breathing?
Hydrogen ions from the acids acetoacetic acid and B-hydroxybutyric acids are buffered, but the buffering capacity is soon exceeded if production is increased. The resulting acidosis stimulates respiration, producing rapid deep respiration described by Kussmaul as air hunger. The urine is acidic as well.
What is the pathogenesis of ketosis?
When excess acetyl-CoA is present in the body, some of it is converted to acetoacetyl-CoA and then in the liver, to acetoacetate. Acetoacetate and its derivatives. acetone and B-hydroxybutyrate, enter the circulation in large quantities.
What causes diabetic coma?
It is due to acidosis and dehydration. The hyperosmolarity of the plasma pH, the hyperosmolarity of the plasma causes unconsciousness(hyperosmolar coma). lactic acidosis may complicate diabetic ketoacidosis if tissues become hypoxic.
Does diabetes affect cholesterol metabolism/
Yes. The rise in plasma cholesterol level is due to an increase in the plasma concentration of VLDL and LDL. These in turn, may be due to increased hepatic production of VLDL or decreased removal of VLDL and LDL from the circulation.
What is the relationship between Cyclic AMP and insulin secretion?
Stimuli that increase cAMP levels in B cells increase insulin secretion, probably by increasing intracellular Ca+. These include B adrenergic agonists, glucagon, and phosphodiesterase inhibitors such as theophylline.
Catecholamines have a dual effect on insulin secretion; they inhibit insulin secretion via alpha 2 adrenergic receptors and stimulate insulin secretion via B-adrenergic receptors. TRUE/FALSE
TRUE. The net effect of epinephrine and norepi is usally inhibition.