While weight loss medications have been around for decades, many are modestly effective at best. Semaglutide is the first of its kind, heading up a new generation of safe and highly effective hormone-based weight loss medications.
In a clinical trial, Semaglutide helped most people with obesity lose at least 10 percent of their body weight, and more than half of them reduced their weight by at least 15 percent, according to results published in February 2021 in the New England Journal of Medicine. Losing 15% of your body weight is an amount that most healthcare professionals say can help reduce the risk for future chronic illnesses.
People taking semaglutide have also experienced greater improvements in cardiovascular risk factors like BMI, waist circumference, blood pressure, and blood sugar levels than participants given a placebo.
Let’s review the health benefits semaglutide provides to overweight and obese patients:
- Weight loss
- Suppressed appetite
- Promotes a sensation of fullness in the brain
- Slows gastric emptying in the intestines to help feel fuller, longer
- Reduces HbA1c
- Enhanced β-cell proliferation with anti-apoptotic effects on these cells, which induces insulin synthesis
- Reduced body weight, lipids, blood pressure, inflammatory markers, oxidative stress, endothelial dysfunction, and subclinical atherosclerosis
- Promotes insulin secretion from b cells, while decreasing glucagon secretion in the pancreas
- Enhanced glucose-dependent insulin secretion
- Deescalates out of control glucagon levels, both in fasting and after eating
- Blood sugar-lowering effects without any increase in hypoglycemia
What is Semaglutide?
Semaglutide an incretin mimetic; specifically, semaglutide is a GLP-1 receptor agonist with 94% sequence homology to human GLP-1. Semaglutide binds and activates the GLP-1 receptor. GLP-1 is an important, gut-derived, glucose homeostasis regulator that is released after the oral ingestion of carbohydrates or fats. In patients with Type 2 diabetes, GLP-1 concentrations are decreased in response to an oral glucose load. GLP-1 enhances insulin secretion; it increases glucose-dependent insulin synthesis and in vivo secretion of insulin from pancreatic beta cells in the presence of elevated glucose. In addition to increases in insulin secretion and synthesis, GLP-1 suppresses Glc secretion, slows gastric emptying, reduces food intake, and promotes beta-cell proliferation. 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; semaglutide is stabilized against degradation by the DPP-4 enzyme. Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers Glc secretion, both in a glucose-dependent manner. Therefore, when blood glucose is high, insulin secretion is stimulated and Glc secretion is inhibited. The mechanism of blood glucose lowering also involves a minor delay in gastric emptying in the early postprandial phase.
