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Managing diabetes mellitus involves a combination of lifestyle adjustments, such as a healthy diet and regular exercise, alongside medication or insulin therapy to regulate blood sugar levels.
Treatment of diabetes mellitus differs from person to person and should be taken only as suggested by doctor.
Along with life style modification, following are the drugs used in the treatment of diabetes mellitus : ( JUST FOR BROAD INFORMATION )
Metformin decreases hepatic glucose production, principally due to reduced gluconeogenesis and also through reduced glycogenolysis. It also increases the insulin-receptor binding and stimulates tissue uptake of glucose.
Thiazolidinediones increase insulin mediated glucose uptake in muscle and increase adipogensis. It increases subcutaneous fat and not visceral, and hence, despite increase in adipogenesis it increase insulin sensitivity. It converts the larger adipocyte into smaller one. These convert small dense LDL into large LDL, increase HDL, decreases TG, decreases plasma free fatty acids.
Sulphonylureas stimulate insulin release by blocking ATP sensitive potassium channels in the Beta cells, reducing potassium permeability. This causes depolarization of the cell and increases calcium entry, increasing insulin secretion.
Meglitinides are similar to that of sulfonylureas in mechanism but they bind to a site on the SUR 1 sub unit of the beta cell ATP dependent potassium channel that is different from binding site for sulphonylureas.
GLP 1 analogues bind to GLP 1 receptors and stimulate glucose dependent insulin release, therefore act as antihyperglycemics. They also suppress appetite and inhibit glucagon secretion. They slow gastric emptying and as a result prevent steep rise in post-prandial blood glucose levels.
Dpp-IV inhibitors slow the inactivation and degradation of GLP-1, a hormone involved in glucose removal from gut. Dpp-IV inhibitors improve blood glucose control and reduce both fasting and postprandial blood glucose levels, without causing weight gain.
Alpha-glucosidase inhibitors are competitive suppressants of small intestine brush border alpha-glucosidases, which are essential to hydrolyse disaccharides, oligosaccharides, and polysaccharides to monosaccharides. Therefore, carbohydrate absorption and digestion is delayed and prolonged resulting in lowering of postprandial hyperglycemia. It also increases the secretion of GLP-1 ad decrease secretion of GIP.
Sodium glucose cotransporter-2 inhibitors, SGLT-2 INHIBITORS, inhibit SGLT-2 proteins located in the renal tubules of the kidneys which are responsible for reabsorbing glucose back into the blood. As a result, more glucose is excreted in the urine.
This type of insulin begins to work within 5 to 15 minutes and are active for 3 to 4 hours.
This type of insulin begins to work within 1 to 3 hours and is active for 16 to 24 hours.
This type of insulin begins to work within 1 to 2 hours and continue to be active, without major peaks or dips, for about 24 hours.
It begins to work within 30-90 minutes and continues to be active for greater than 24 hours.
Rather than receiving multiple daily subcutaneous injections of short and either long or intermediate acting insulin, patients using an insulin pump receive a continuous subcutaneous infusion of short acting insulin.
These devices hold insulin reservoir and supply insulin via a plastic tube into subcutaneous tissue.
Pumps are able to more precisely dose insulin compared to insulin syringes or pens. Pumps are also programmable to provide different doses of basal insulin throughout the day.
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