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The New Paradigm of Weight Loss: Wegovy & Ozempic

Obesity is defined as excessive fat accumulation that presents a health risk. A body mass index (BMI) over 25 is considered overweight and over 30 is considered as obese. These days, obesity has emerged as one of the most significant social and global health problems. According to the World Health Organization (WHO), about 43% of adults were overweight and 16% were classified as obese in 2022¹. Obesity is not just about body size; it is a major risk factor for a wide range of diseases such as diabetes, heart attack, stroke, asthma, and pneumonia². One emerging solution to obesity is the use of semaglutide, a medication that has recently gained global attention. Semaglutide mimics a natural hormone called glucagon-like peptide-1 (GLP-1), which reduces appetite, slows gastric emptying and helps regulate blood glucose levels³. Many pharmaceutical companies have entered this appetite-regulating field. Wegovy and Ozempic, two different semaglutamide-based medications, are widely used to treat obesity and type 2 diabetes. Wegovy was specifically approved for chronic weight management in people with obesity or overweight, whereas Ozempic is approved for type 2 diabetes management, with weight loss as a secondary benefit⁴. In 2023, 10 per 1,000 adults started using Ozempic annually⁵, and more than 100,000 people in Denmark started using Wegovy within roughly one year of its approval, indicating rapid uptake⁶. Glucagon-like peptide-1 (GLP-1) is an incretin hormone released from enteroendocrine L-cells located primarily in the distal ileum and colon. It is secreted in response to nutrient ingestion, particularly carbohydrates and fats, and plays a central role in regulating post-prandial glucose levels⁷. After food enters the gastrointestinal tract, GLP-1 levels rise rapidly, enhancing glucose-dependent insulin secretion, suppressing glucagon release, slowing gastric emptying, and promoting satiety⁷. These coordinated actions help maintain stable blood glucose levels while naturally limiting caloric intake by reducing the motivation to continue eating. Although GLP-1 performs several essential metabolic functions, it is quickly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4), giving it a short half-life of only one to two minutes⁸. Because of this rapid breakdown, GLP-1’s physiological effects are brief, which led to the development of long-acting pharmacological GLP-1 receptor agonists designed to extend and strengthen its natural actions. GLP-1 carries out its functions by binding to the GLP-1 receptor (GLP-1R), a G-protein-coupled receptor expressed in pancreatic β-cells, α-cells, the gastrointestinal tract, vagal afferent neurons, and several regions of the brain involved in appetite regulation⁸. When GLP-1 binds to its receptor on β-cells, it activates adenylate cyclase, raises intracellular cyclic AMP (cAMP) levels, and triggers insulin granule exocytosis in a glucose-dependent manner⁹. This mechanism is important because it prevents insulin release during low blood glucose and reduces the risk of hypoglycemia. At the same time, GLP-1 suppresses glucagon secretion from α-cells, leading to reduced hepatic glucose output after meals³. In the gastrointestinal system, GLP-1 slows gastric emptying by decreasing gastric motility and prolonging the time food remains in the stomach⁹. These actions promote smoother post-prandial glucose control and reduce overall caloric intake by producing an earlier and longer-lasting sense of fullness, a feature that contributes meaningfully to appetite regulation. GLP-1 receptors in peripheral tissues such as the liver and adipose tissue also participate in broader metabolic adjustments that support energy balance, although these effects are less pronounced than their pancreatic and neural actions. Beyond metabolic regulation, GLP-1 strongly influences central appetite pathways. GLP-1R activation stimulates anorexigenic POMC/CART neurons and inhibits orexigenic NPY/AgRP neurons within the hypothalamus, producing significant satiety signals and reducing hunger¹⁰. GLP-1 also communicates with the brain through vagal afferent signaling, reinforcing gut-to-brain feedback that suppresses appetite¹⁰. Semaglutide, the active ingredient in Wegovy and Ozempic, is a long-acting synthetic GLP-1 receptor agonist created to mimic and amplify these natural physiological mechanisms. Structural modifications protect semaglutide from DPP-4 degradation and increase its binding to albumin, giving it an extended half-life of about one week¹¹. With continuous GLP-1R activation, semaglutide produces stronger appetite suppression, more pronounced delays in gastric emptying, improved insulin secretion, and reduced glucagon levels¹¹. In clinical studies, semaglutide has also been associated with improved control over meal size, reduced frequency of eating occasions, and a more consistent pattern of satiety, reinforcing its role as an effective therapy for long-term weight management beyond what endogenous GLP-1 alone can achieve. Wegovy has demonstrated substantial weight loss in adults with overweight or obesity, leading to improvements in quality of life and obesity-related symptoms in clinical trials¹². In addition, its once-weekly injection schedule offers greater convenience and may improve adherence compared to daily medications. Ozempic also provides strong glucose-lowering efficacy, improving symptoms in adults with type 2 diabetes. Although weight reduction is a secondary indication, Ozempic still supports clinically meaningful weight loss¹³. Despite its promising therapeutic effects, several potential consequences have yet to be fully examined. For example, both Wegovy and Ozempic are associated with high rates of side effects, including nausea, vomiting, diarrhea, constipation, and abdominal pain¹⁴. Moreover, Wegovy and Ozempic appear safe within 1–3 years of use, but long-term safety data beyond 3 years remains uncertain, particularly regarding rare or cumulative effects¹⁵. Finally, the availability of such an accessible pharmaceutical solution may introduce new social challenges. While treating individuals at high health risk is essential, it is equally important to address the factors that contribute to obesity for long-term prevention. An easy access treatment may reduce motivation for society to implement meaningful, systemic changes. This reliance is especially concerning given the uncertainties surrounding the long-term safety of semaglutide, reinforcing the need for a sustainable and balanced approach to obesity care. 1. Obesity and overweight. [accessed 2025 Nov 30]. 2. Schmickl CN, Raphelson J, Malhotra A. Forty Percent and Rising — Why Every Specialist Must Care about Obesity. NEJM evidence. 2025;4(4):EVIDe2500054. 3. Bergmann NC, Davies MJ, Lingvay I, Knop FK. Semaglutide for the treatment of overweight and obesity: A review. Diabetes, Obesity & Metabolism. 2023;25(1):18–35. 4. Singh G, Krauthamer M, Bjalme-Evans M. Wegovy (semaglutide): a new weight loss drug for chronic weight management. Journal of Investigative Medicine. 2022;70(1):5–13. 5. Mailhac A et al. Semaglutide (Ozempic®) Use in Denmark 2018 Through 2023 ‒ User Trends and off-Label Prescribing for Weight Loss. Clinical Epidemiology. 2024;16:307–318. 6. Ladebo L et al. Real-World Use of Semaglutide for Weight Management: Patient Characteristics and Dose Titration-A Danish Cohort Study. Diabetes Care. 2024;47(10):1834–1837. 7. Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007;87(4):1409–1439. 8. Müller TD, Finan B, Bloom SR, D’Alessio D, Drucker DJ, Flatt PR, et al. Glucagon-like peptide-1 (GLP-1). Mol Metab. 2019;30:72–130. 9. Nauck MA, Meier JJ. Incretin hormones: Their role in health and disease. Diabetes Obes Metab. 2018;20(S1):5–21. 10. Mohr K, et al. Glucagon-Like Peptide-1 Receptor Agonists for Weight Loss. Journal of Clinical Medicine Research. 2024. 11. Papakonstantinou E, Tsimihodimos V. Spotlight on the mechanism of action of semaglutide. Ther Adv Chronic Dis. 2024;15:1–15. 12. Chao AM, Tronieri JS, Amaro A, Wadden TA. Clinical Insight on Semaglutide for Chronic Weight Management in Adults: Patient Selection and Special Considerations. Drug Design, Development and Therapy. 2022;16:4449–4461. 13. Smits MM, Van Raalte DH. Safety of Semaglutide. Frontiers in Endocrinology. 2021;12:645563. 14. Shu Y et al. Gastrointestinal adverse events associated with semaglutide: A pharmacovigilance study based on FDA adverse event reporting system. Frontiers in Public Health. 2022;10:996179. 15. Shah MY et al. Weight Loss That Lasts: Reviewing the Long-Term Impact of GLP-1 Receptor Agonists. Cureus. 17(7):e88334.

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