General dosage of insulins: The starting dose should be 10-16 units of soluble insulin SC 15-30 minutes (depending on the type of insulin) 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.
Mode of action
Brands containing this Ingredient
Solostar Pens inj
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Mode of Action
Insulin: ||| 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 release of free fatty acid from adipose cells. ||| increases active glucose transport through muscle and adipose cellular membranes ||| promotes 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 hormonferre secretion by producing hypoglycemia, which is used to evaluate 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 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 hypoglycaemia 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; hypoglycaemia; insulin resistance; weight gain
PROMINENT FEATURES OF INSULIN GLARGINE||| In insulin glargine, glycine replaces asparagine at A21 and two arginines are added to the car-boxy terminal of B chain allowing insulin glargine to form a precipitate [hexamer] when injected subcutaneously into the patient.
||| It achieves a peakless level for at least 24hrs and has a duration of action of 18-26 hrs
||| Pharmacokinetically, it resembles basal insulin secretion of non-diabetic pancreatic beta cells.. DRUG INTERACTIONS: Corticosteroids antagonize effects of insulin by stimulating release of catecholamines, causing hyperglycemia; thyroid hormone replacement therapy may increase insulin requirement; androgens may increase tissue sensitivity to insulin resulting in hypoglycemia; MAOIs may require possible adjustment in insulin dose; large quantities of alcohol enhance hypoglycaemic 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 sensitivity to it; hyperglycemia-causing agents include the following-calcium channel blocking agents, clonidine, danazol, dextrothyroxine, epinephrine, estrogen, estrogen-progestin-containing oral contraceptives, glucagons, growth hormone, heparin, H2-blockers, nicotine, phenytoin; hypoglycemia-causing agents include the following - angioten-sin-converting enzyme inhibitors, bromocriptine, clofibrate, ketoconazole, lithium, mebendazole, pyridoxine, sulfonamides, theophylline. USE OF INSULIN IN PREGNANCY ||| Insulin does not cross the placenta. Maternal glucose crosses the placenta and together with insulin antibodies can cause fetal hyperinsulinemia. This may results in problems like large-for-gestational-age infant and macrosomia [big baby syndrome]. ||| High glucose levels in the 5-8 wks of gestation are associated with congenital abnormalities and in later stages of gestation it can lead to increased perinatal morbidity and mortality. ||| Poor control of diabetes in pregnancy may cause increased insulin production in the fetus. This can lead to neonatal hypoglycemia that may require medical control. ||| Insulin requirements drop rapidly after child-birth.