An oral hypoglycemic drug called gliclazide is used to treat type 2 diabetes. It is a member of the sulfonylurea class of drugs, which are used to increase the pancreas' production of insulin. Both immediate-release and modified-release versions of gliclazide are available, and patients often tolerate them well.
How does Gliclazide function ?
Gliclazide functions by directly promoting the pancreatic release of insulin. The beta cells in the pancreas create the hormone insulin, which is in charge of controlling blood glucose levels. The beta cells in the pancreas release insulin in response to an increase in blood glucose levels, telling the body's cells to take up glucose from the bloodstream.
A sulfonylurea drug called gliclazide is used to treat type 2 diabetes. It functions by physically causing the body to secrete insulin. In this article, we'll examine Gliclazide's mode of action and how it affects the body's production of insulin.
The beta cells in the pancreas may not produce enough insulin in persons with type 2 diabetes, or the body's cells may be resistant to insulin's effects. High blood glucose levels may arise from this, which may eventually cause a number of health issues. Gliclazide works by encouraging the pancreatic beta cells to make more insulin, which lowers blood glucose levels.
Gliclazide, sometimes referred to as a sulfonylurea medication, is frequently used to treat Type 2 Diabetes Mellitus (T2DM). It belongs to a group of medications that increase peripheral tissues' ability to absorb glucose by boosting the release of insulin from pancreatic beta cells. In order to exert its effects, gliclazide must first connect to the sulfonylurea receptors on pancreatic beta cells. This conformational shift causes the beta cell membrane to become depolarized and the activation of voltage-gated calcium channels. This increase in calcium ions enhances the exocytosis of insulin-containing vesicles, which in turn stimulates the production of insulin.
A key factor responsible for controlling glucose metabolism is the hormone insulin, which is produced by the pancreatic beta cells. Insulin's main job is to increase peripheral tissues including muscle, the liver, and adipose tissue to absorb and use glucose. By increasing the translocation of glucose transporter proteins (GLUTs) to the plasma membrane, it increases the absorption of glucose. Also, insulin promotes adipose tissue's synthesis of fatty acids and the liver and muscle's conversion of glucose to glycogen.
The interaction of several hormones, neurotransmitters, and nutrients controls the secretion of insulin. When blood glucose levels alter in healthy persons, insulin secretion is closely regulated. Pancreatic beta cells release insulin in response to an increase in the input of glucose when blood glucose levels rise, such as after a meal. In contrast, as blood sugar levels drop, insulin secretion is blocked and the release of the hormone glucagon, a counter-regulatory hormone, is boosted, which aids in the liver's release of glucose.
With T2DM, there is a breakdown in the usual control of insulin secretion, which results in hyperglycemia. This results from a confluence of insulin resistance in peripheral organs and pancreatic beta cell failure. Because they increase insulin secretion by directly attaching to the sulfonylurea receptor on pancreatic beta cells, sulfonylurea medications like gliclazide are effective in treating T2DM regardless of blood glucose levels. Sulfonylureas are advantageous in T2DM patients with mildly reduced pancreatic beta cell function due to their ability to boost insulin production.
Gliclazide is processed by the liver using cytochrome P450 enzymes and has a short half-life of about 10 hours. Gliclazide's principal metabolite is an inactive substance that is eliminated by urine. Depending on the patient's specific requirements, the dosage of gliclazide needed for efficient glycemic management might range from 40 to 320 mg per day.
HbA1c is a measurement of average blood glucose levels over a 3-month period, and gliclazide has been demonstrated to be beneficial in lowering HbA1c levels. Gliclazide and metformin were compared in Hanefeld et al(1991) .'s study on the management of T2DM. According to the research, metformin and gliclazide both effectively lowered HbA1c levels, with gliclazide doing so by an average of 1.9% and 1.7%, respectively. A considerable decrease in fasting plasma glucose levels was noticed after 1 week of treatment, indicating that gliclazide also had a quicker beginning of effect.
Another study was done in 1992 by Yki-Järvinen ., comparing the effectiveness of gliclazide versus insulin in the management of T2DM. It was observed Gliclazide reduced blood pressure, according to the study.