Purpose

The Semaglutide Injection is a weekly treatment that operates by replicating hormones that focus on parts of the brain responsible for controlling appetite and food consumption. This can aid in reducing your food intake, resulting in weight loss. We have blended our Semaglutide with Vitamin B12 to increase energy, regulate sleep patterns and enhance the overall patient experience.

Advantages

• Weight Reduction
• Potential Improvement in Blood Pressure
• Potential Improvement in Cholesterol
• Improved Blood Sugar Control

Diet and Physical Activity

 It is recommended to adopt a balanced diet and engage in physical activity.

Dosage and Frequency

Weekly Dosing: Consumed once a week, on the same day every week, at any time, with or without food.

IMPORTANT

This product follows a step-by-step dosing process. All patients must begin with the “Month 1” dose. The dose per injection will gradually increase in Months 2, 3, and 4. Finally, the maintenance dose can be continued for up to 8 months, based on your desired outcomes.

Most Prevalent Side Effect (Complete List Below)

Nausea (Advice to Minimize Nausea: Consume bland, low-fat foods such as crackers, toast, and rice. Incorporate foods high in water content, such as soup and gelatin. Refrain from lying down after eating. Eat at a slow pace. Take a walk outside for fresh air.)

What is Semaglutide?

Semaglutide is a type of incretin mimetic and more specifically, a GLP-1 receptor agonist with 94% similarity in sequence to human GLP-1. It binds and activates the GLP-1 receptor, which is a crucial gut-derived regulator of glucose homeostasis that is released after the consumption of carbohydrates or fats. In individuals with Type 2 diabetes, GLP-1 levels are reduced in response to oral glucose intake. GLP-1 stimulates insulin secretion and increases glucose-dependent insulin synthesis and insulin secretion from pancreatic beta cells in the presence of elevated glucose. Besides boosting insulin secretion and synthesis, GLP-1 also suppresses glucose secretion, slows gastric emptying, reduces food intake, and promotes beta-cell growth. The long half-life of semaglutide is due to its binding to albumin, which reduces its renal clearance and protects it from metabolic degradation; semaglutide is stabilized against degradation by the DPP-4 enzyme. Semaglutide lowers blood glucose through a mechanism that stimulates insulin secretion and lowers glucose secretion in a glucose-dependent manner. Thus, when blood glucose is high, insulin secretion is stimulated and glucose secretion is inhibited. The mechanism of blood glucose reduction also includes a slight delay in gastric emptying during the early post-meal period.

Cyanocobalamin

Cyanocobalamin plays a crucial role in cell division and growth, blood cell formation, and the synthesis of nucleoproteins and myelin. This vitamin is also involved in protein synthesis, neural metabolism, the production of DNA and RNA, and the metabolism of fats and carbohydrates. Some cells, such as bone marrow and epithelial cells, have a high demand for cyanocobalamin due to their rapid division.

Cyanocobalamin binds to plasma proteins in the systemic circulation and joins specific cobalamin-binding proteins, known as transcobalamin I and II, to enter into tissues. Within cells, this vitamin functions as a cofactor for two vital enzymatic reactions: (1) methionine synthase, which regenerates methionine from homocysteine and (2) methylmalonyl-CoA mutase, which isomerizes methylmalonyl-CoA to succinyl-CoA. Both of these methylation reactions are essential for growth and cell reproduction.

Methionine, an essential sulfur-containing amino acid, is a precursor of S-adenosylmethionine, a cofactor for one-carbon metabolism and the final methyl donor for the methylation of DNA, RNA, proteins, and phospholipids. Methionine synthase plays a crucial role in the synthesis of nitrogenous bases (purines and pyrimidines) involved in DNA formation. If there is a shortage of cobalamin in the body, the regeneration of tetrahydrofolate is hindered, leading to megaloblastic anemia due to functional folate deficiency. The methylmalonyl-CoA mutase helps to metabolize odd-chain fatty acids and branch-chain amino acids. Cobalamin is also thought to maintain the body’s level of sulfhydryl (SH) groups in the reduced form. SH groups activate many enzyme systems involved in protein synthesis and the metabolism of fats and carbohydrates. If there is a deficiency of cobalamin, methylmalonyl CoA accumulates, which is believed to lead to the neurological symptoms of B12 deficiency.

The replacement of parenteral cyanocobalamin leads to a rapid and complete improvement in megaloblastic anemia and gastrointestinal symptoms caused by B12 deficiency. The parenteral administration also stops the progression of neurological damage associated with B12 deficiency, but complete improvement may depend on the severity and extent of the deficiency.