Indications to the use of insulin
Diabetes mellitus; diabetes keto-acidosis; gestational diabetes mellitus; malnutrition-related diabetes mellitus; diagnosis of growth hormone deficiency.
The starting dose should be 10-16 units of soluble insulin SC 30 minutes before meal TID. The dose is adjusted gradually in 5 unit aliquots to achieve plasma glucose range of 8.3-13.4 mmol/L in hospital and target the range of 4-10mmol/L at home. Once the blood glucose stabilizes at 8-11.0 mmol/L the patient is switched to the intermediate insulin whose dose is 2/3 of the total dose of soluble insulin. Normally 2/3 of the intermediate insulin is administered in the morning and 1/3 before supper.
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Mode of Action
controls the storage and metabolism of carbohydrates, proteins, and fats. This occurs primarily in the liver, in muscle, and in adipose tissues after it binding to receptor sites on cellular plasma membranes.
is known to affect cell membrane transport characteristics, cellular growth, enzyme activation and inhibition, and changes in protein and fat metabolism.
promotes uptake of carbohydrates, proteins, and fats in most tissues.
stimulates protein and free fatty acid synthesis. It inhibits the release of free fatty acid from adipose cells.
increases active glucose transport through muscle and adipose cellular membranes
promotes the conversion of intracellular glucose to glycogen and free fatty acid to triglyceride [storage forms]
increases hepatic glucose conversion to glycogen and suppresses hepatic glucose output.
stimulates growth hormone re secretion by producing hypoglycemia, which is used to evaluate the pituitary growth hormone reserve.
increases the intracellular shift of potassium and magnesium and decreases renal excretion of sodium.
decreases the synthesis of high-density lipoprotein [HDL] cholesterol and increases the synthesis of very-low-density lipoprotein [VLDL] cholesterol in the liver.
increases lipoprotein uptake and utilization in the lactating mammary gland.
stimulates the activity of and tissue response to the sympathetic nervous system.
Recognition of early hypoglycaemic signs; reduce dose in renal failure; some patients have reported a loss of warning of hypoglycemia after transfer from human insulin; beta-blockers; conversion from one type of insulin to another; tolerance to insulin [more common with bovine insulin than with porcine insulin]; close control of blood sugar in pregnancy.
Fat hypertrophy at the injection site; allergic reactions; hypoglycemia; insulin resistance; weight gain
///// It differs from human insulin in that the amino acid asparagine at position B3 is replaced by lysine and the lysine in position B29 is replaced by glutamic acid.
Due to increased charge repulsion there is less likelihood of formation of hexamers hence create faster-acting insulin.
///Corticosteroids antagonize effects of insulin by stimulating release of catecholamines, causing hyperglycemia; thyroid hormone replacement therapy may increase insulin requirement; an-drogens may increase tissue sensitivity to insu-lin resulting in hypoglycemia; MAOIs may require possible adjustment in insulin dose; large quantities of alcohol enhance hypoglycae-mic effect of insulin; NSAIDs increases basal insulin secretion; quinine decreases degradation of insulin, resulting in hypoglycaemic effects; potassium-depleting diuretics may inhibit secretion of insulin and decrease tissue sensitiv-ity to it; hyperglycemia-causing agents include the following-calcium channel blocking agents, clonidine, danazol, dextrothyroxine, epineph-rine, estrogen, estrogen-progestin-containing oral contraceptives, glucagons, growth hormone, heparin, H2-blockers, nicotine, phenytoin; hypoglycemia-causing agents include the following - angiotensin-converting enzyme inhibitors, bromocriptine, clofibrate, ketoconazole, lithium, mebendazole, pyridoxine, sulfonamides, theophylline.