Semaglutide

Mechanism of Action
Semaglutide is a GLP-1 analogue with 94% sequence homology to human GLP-1. Semaglutide acts as a GLP-1 receptor agonist that selectively binds to and activates the GLP-1 receptor, GLP-1 is a physiological hormone that has multiple actions on glucose, mediated by the GLP-1 receptors. The principal mechanism of protraction resulting in the long half-life of semaglutide is albumin binding, which results in decreased renal clearance and protection from metabolic degradation. Furthermore, semaglutide is stabilized against degradation by the DPP-4 enzyme.
Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers glucagon secretion, both in a glucose-dependent manner. Thus, when blood glucose is high, insulin secretion is stimulated and glucagon secretion is inhibited. The mechanism of blood glucose lowering also involves a minor delay in gastric emptying in the early postprandial phase
Pharmacodynamics:
Semaglutide lowers fasting and postprandial blood glucose and reduces body weight.
In patients with type 2 diabetes, treatment with semaglutide 1 mg resulted in reductions in glucose.
Insulin Secretion
Both first-and second-phase insulin secretion are increased in patients with type 2 diabetes treated with semaglutide compared with placebo.
Glucagon Secretion
Semaglutide lowers the fasting and postprandial glucagon concentrations.
Glucose dependent insulin and glucagon secretion
Semaglutide lowers high blood glucose concentrations by stimulating insulin secretion and lowering glucagon secretion in a glucose-dependent manner. With semaglutide, the insulin secretion rate in patients with type 2 diabetes was similar to that of healthy subjects
During induced hypoglycemia, semaglutide did not alter the counter regulatory responses of increased glucagon compared to placebo, and did not impair the decrease of C-peptide in patients with type 2 diabetes.
Gastric emptying
Semaglutide causes a delay of early postprandial gastric emptying, thereby reducing the rate at which glucose appears in the circulation postprandially.
Drug Interaction Studies
In vitro studies have shown very low potential for semaglutide to inhibit or induce CYP enzymes, and to inhibit drug transporters.
The delay of gastric emptying with semaglutide may influence the absorption of concomitantly administered oral medicinal products.
No clinically relevant drug-drug interaction with semaglutide was observed based on the evaluated medications; therefore, no dose adjustment is required when co-administered with semaglutide.
Semaglutide (OZEMPIC®) may cause serious side effects, including:-
• Inflammation of pancreas (pancreatitis).
• Changes in vision.
• Low blood sugar (hypoglycemia). risk for low blood sugar may be higher if use OZEMPIC® with another medicine that can cause low blood sugar, such as a sulfonylurea or insulin.
• Kidney problems (kidney failure)..
• serious allergic reactions..The most common side effects of OZEMPIC® may include nausea, vomiting, diarrhea, stomach (abdominal) pain and constipation.

By:

Dr.Ban