Semaglutide Changed Obesity Medicine. Here’s What It Actually Does

Semaglutide is a modified peptide designed to activate the glucagon-like peptide-1 receptor.

It is known as a GLP-1 receptor agonist.

GLP-1 is a hormone released by the intestine after food is consumed. It participates in several processes related to appetite, digestion and glucose control.

Natural GLP-1 is broken down rapidly. Semaglutide was engineered to remain active much longer.

The molecule binds strongly to albumin, a protein circulating in the blood, and is protected against rapid enzymatic breakdown. Its elimination half-life is approximately one week, which allows injectable formulations to be administered once weekly.

Semaglutide can remain in circulation for several weeks after the final dose.

This long duration is clinically useful.

It also means that benefits, adverse effects and overdose symptoms may not disappear immediately when treatment is stopped.

The terms semaglutide, Ozempic and Wegovy are frequently used as though they mean the same thing.

They do not.

Semaglutide is the active molecule.

Wegovy, Ozempic and Rybelsus are product names associated with particular formulations, doses and approved uses. The prescribing information depends on the exact product being used.

Wegovy products are approved for long-term weight reduction in specified adults. The injection is also approved for adolescents aged 12 years and older with obesity.

Wegovy injection and tablets are approved to reduce major cardiovascular events in adults who have established cardiovascular disease and either obesity or overweight.

Wegovy injection also has an accelerated-approval indication for certain adults with noncirrhotic metabolic dysfunction-associated steatohepatitis, or MASH, and moderate-to-advanced liver fibrosis.

Ozempic products are primarily associated with type 2 diabetes. Ozempic injection is also approved for cardiovascular-risk reduction in adults with type 2 diabetes and established cardiovascular disease, and for reducing certain kidney and cardiovascular outcomes in adults with type 2 diabetes and chronic kidney disease.

These distinctions matter.

A clinical trial involving Wegovy 2.4 mg cannot automatically be used to describe the expected result from a lower diabetes dose, a different formulation or an unidentified compounded product.

The molecule may be the same.

The clinical product is not necessarily equivalent.

GLP-1 is part of the body’s response to eating.

After nutrients reach the digestive system, GLP-1 signaling helps coordinate several processes.

It can:

- increase insulin secretion when blood glucose is elevated,

- reduce glucagon secretion when glucose is elevated,

- influence appetite-regulating areas of the brain,

- reduce calorie intake,

- and delay early gastric emptying.

These actions help the body manage incoming nutrients.

Semaglutide activates the same receptor but produces a much longer-lasting signal than naturally occurring GLP-1.

This prolonged receptor activity is responsible for both the therapeutic effects and many of the adverse effects.

The central weight-loss effect of semaglutide appears to come from reduced calorie intake.

GLP-1 receptors are present in brain regions involved in hunger, fullness and food intake. By activating those receptors, semaglutide can make a smaller amount of food feel more satisfying.

Many patients report:

- becoming full sooner,

- remaining full for longer,

- feeling hungry less frequently,

- experiencing fewer cravings,

- thinking about food less often,

- and finding highly caloric food less rewarding.

The phrase “food noise” is often used to describe repetitive or intrusive thoughts about eating.

It is not a formal medical diagnosis or a precisely defined clinical endpoint. But it can describe a real subjective change reported by some patients receiving GLP-1 therapies.

Controlled studies support the broader biological effect.

Participants receiving semaglutide have consumed fewer calories during measured meals and reported improvements in hunger, cravings and control of eating.

A 2026 randomized trial found that participants continued to consume fewer calories than those receiving placebo at 20, 40 and 60 weeks, even though some of the early subjective appetite differences became less pronounced over time.

The medication does not make eating physically impossible.

It changes the biological pressure influencing how much and how often a person wants to eat.

Semaglutide is sometimes described as a fat burner or a medication that dramatically raises metabolic rate.

That is not an accurate description of its main action.

Human studies suggest that weight reduction occurs predominantly because people consume less energy.

Semaglutide is not known to create a large increase in resting energy expenditure that independently burns away substantial body fat.

This distinction matters because appetite and calorie intake can change without the patient consciously following a highly restrictive diet.

Someone may naturally leave food unfinished, skip a snack or choose a smaller portion because the expected reward from eating has changed.

That is different from the drug directly dissolving fat.

Body tissue is lost because sustained energy intake becomes lower than energy expenditure.

Semaglutide helps create that condition by changing appetite-related biology.

Semaglutide can delay the early movement of food from the stomach into the small intestine.

This may contribute to:

- earlier fullness,

- reduced post-meal glucose spikes,

- nausea,

- bloating,

- reflux,

- and a prolonged sensation of food remaining in the stomach.

But “it works by paralyzing the stomach” is an inaccurate general explanation.

The effect on gastric emptying is only one part of the medication’s action. Appetite signaling in the brain and reduced calorie intake are central to the weight-loss effect.

The gastric-emptying effect may also change with continued treatment.

Clinical pharmacology studies have not always found a large ongoing delay at steady-state obesity doses, even though the prescribing information continues to warn that the medication may delay gastric emptying and affect certain oral medicines.

The clinically relevant question is not whether every patient’s stomach empties at exactly the same speed.

It is whether the patient develops significant gastrointestinal symptoms or has a condition—such as severe gastroparesis—that changes the treatment’s risk.

Semaglutide was developed first as a diabetes medication.

When blood glucose is elevated, it increases insulin secretion and decreases glucagon secretion.

Insulin helps move glucose from the bloodstream into tissues.

Glucagon generally signals the liver to release glucose.

By influencing both hormones in a glucose-dependent manner, semaglutide can reduce fasting and post-meal blood glucose.

The phrase glucose-dependent is important.

Semaglutide’s insulin-stimulating effect becomes stronger when glucose is high and diminishes as glucose falls. That means semaglutide used alone generally presents a lower risk of severe hypoglycemia than medications that stimulate insulin regardless of the glucose level.

The risk changes when semaglutide is combined with insulin or an insulin-releasing medication such as a sulfonylurea.

In those situations, medication doses may need adjustment and glucose should be monitored appropriately.

Semaglutide does not require diabetes to affect appetite.

The GLP-1 receptor participates in appetite and calorie regulation in people with or without elevated blood glucose.

That is why obesity trials have enrolled participants who did not have diabetes.

The STEP 1 trial included 1,961 adults with obesity—or overweight with at least one weight-related health condition—who did not have diabetes.

Participants received lifestyle intervention plus either weekly semaglutide 2.4 mg or placebo.

After 68 weeks, average body-weight change was:

- a 14.9% reduction with semaglutide,

- and a 2.4% reduction with placebo.

About 86% of semaglutide-treated participants lost at least 5% of their starting weight.

Approximately 69% lost at least 10%.

About half lost at least 15%.

Those results were much larger than the average effects historically associated with many earlier obesity medications.

A trial average combines people with very different responses.

Some participants lose considerably more than the reported mean.

Some lose less.

Some stop because of adverse effects.

Some cannot reach or remain on the target dose.

Some experience little clinically useful weight reduction.

The 14.9% STEP 1 result should therefore not be presented as a promise that every patient will lose 15% of their weight.

It describes the average result in a specific trial population receiving a particular formulation, dose escalation, lifestyle program and follow-up schedule.

Real-world results can be affected by:

- the tolerated dose,

- treatment duration,

- missed doses,

- medication availability,

- cost and insurance coverage,

- other health conditions,

- concurrent medications,

- nutrition,

- physical activity,

- sleep,

- and individual biological response.

The response should be judged over time using more than the number on the scale.

The original obesity dose of weekly injectable Wegovy was 2.4 mg.

In March 2026, the FDA approved a higher-dose 7.2 mg injection called Wegovy HD for weight reduction and long-term maintenance in selected adults.

Under the current prescribing information, an adult who tolerates 2.4 mg for at least four weeks may be increased to 7.2 mg when additional weight reduction is clinically indicated.

The STEP UP trial compared weekly doses of:

- 7.2 mg semaglutide,

- 2.4 mg semaglutide,

- and placebo.

When estimating the effect among participants who remained adherent to treatment, average weight loss at 72 weeks was approximately:

- 20.7% with 7.2 mg,

- 17.5% with 2.4 mg,

- and 2.4% with placebo.

An analysis that included treatment discontinuation and other real-world trial events produced smaller average reductions:

- approximately 18.7% with 7.2 mg,

- 15.6% with 2.4 mg,

- and 3.9% with placebo.

Both analyses are useful.

One estimates what the medication may accomplish when treatment is followed as intended.

The other better incorporates the reality that not everyone remains on treatment.

More medication did not produce only more weight loss. It also produced more adverse effects, including a substantially higher rate of unusual skin sensations known collectively as dysesthesia.

The highest effective dose is not automatically the best dose for every patient.

Wegovy is no longer limited to a weekly injection.

The FDA approved a once-daily oral formulation for adult weight management and cardiovascular-risk reduction in December 2025.

The maintenance dose is 25 mg taken once daily.

The number is much higher than the weekly injectable dose because only a small proportion of oral semaglutide reaches the bloodstream. The tablet includes an absorption-enhancing ingredient and must be taken under specific conditions.

It is taken:

- in the morning,

- on an empty stomach,

- with no more than four ounces of water,

- and at least 30 minutes before food, other drinks or oral medication.

In the OASIS 4 trial, adults without diabetes receiving oral semaglutide 25 mg lost an estimated average of 13.6% of their body weight over 64 weeks, compared with 2.2% with placebo.

The oral and injectable products should not be assumed to produce identical exposure in every person. Oral absorption is low and more variable.

The tablet offers another approved option.

It does not make administration instructions optional.

Weight loss is important, but a medication becomes more consequential when it improves major health outcomes.

The SELECT trial enrolled 17,604 adults who:

- had established cardiovascular disease,

- had obesity or overweight,

- and did not have diabetes.

Participants received weekly semaglutide 2.4 mg or placebo in addition to standard cardiovascular care.

The primary outcome combined:

- cardiovascular death,

- nonfatal heart attack,

- and nonfatal stroke.

A primary event occurred in 8.0% of participants receiving placebo and 6.5% receiving semaglutide.

That represents a 20% relative risk reduction.

The absolute difference was 1.5 percentage points over a mean follow-up of approximately 40 months.

Relative and absolute risk describe different aspects of the same result.

The relative reduction shows the proportional difference between the groups.

The absolute reduction helps show how many events occurred in the populations that were actually studied.

The result does not mean semaglutide reduces cardiovascular risk by the same amount in every person with excess weight.

The trial involved adults who already had established cardiovascular disease. Its findings should not automatically be applied to younger, lower-risk people without cardiovascular disease.

The exact mechanism responsible for cardiovascular-risk reduction has not been established.

Weight loss probably contributes.

Semaglutide can also improve several cardiovascular risk factors, including:

- blood glucose,

- waist circumference,

- blood pressure,

- triglycerides,

- inflammation-related measures,

- and other metabolic markers.

But it is difficult to separate the contribution of each change.

The cardiovascular result should therefore be described as an observed treatment outcome—not reduced to a claim that weight loss alone prevented every event.

Semaglutide appears to alter several interconnected metabolic pathways.

The relative importance of those pathways remains under investigation.

Semaglutide is also associated with kidney benefits in defined clinical populations.

The FLOW trial enrolled adults with type 2 diabetes and chronic kidney disease.

Weekly semaglutide 1 mg reduced the risk of a composite outcome involving kidney failure, a major sustained decline in kidney function, or death from kidney-related or cardiovascular causes.

The relative risk of the primary outcome was 24% lower with semaglutide than with placebo.

These results supported an additional Ozempic indication for adults with type 2 diabetes and chronic kidney disease.

That does not mean semaglutide is a general kidney-repair peptide.

The evidence applies to patients resembling those enrolled in the trial and to the product and dose that were studied.

Semaglutide can also contribute to acute kidney injury when persistent vomiting, diarrhea or reduced fluid intake causes dehydration.

A medication can improve long-term kidney outcomes in one clinical setting while creating short-term kidney risk through volume depletion in another.

Both statements can be true.

In 2025, the FDA granted accelerated approval to Wegovy injection for adults with noncirrhotic MASH and moderate-to-advanced liver fibrosis consistent with stages F2 to F3.

MASH is a progressive form of metabolic liver disease involving fat accumulation, inflammation and fibrosis.

In the ongoing ESSENCE trial, semaglutide improved liver-histology outcomes at 72 weeks.

More participants receiving semaglutide experienced resolution of steatohepatitis without worsening fibrosis, and more experienced fibrosis improvement without worsening steatohepatitis, compared with placebo.

The approval is described as accelerated because it is based on improvement in liver histology rather than completed evidence showing fewer cases of liver failure, transplantation or death.

The trial is continuing to determine whether the histological improvements translate into those longer-term clinical benefits.

The precise mechanism in MASH is not fully understood.

Weight reduction likely contributes, along with changes in glucose control, inflammation and other metabolic pathways.

This is a real approval.

It is also an approval with an important evidentiary condition still being studied.

Weight loss includes changes in several body compartments.

Semaglutide produces greater loss of fat mass than lean mass, but lean tissue can still be lost.

That is not unique to semaglutide.

Lean mass commonly decreases during significant weight reduction, whether the loss occurs through diet, medication or metabolic surgery.

The clinical goal should not be to prevent every measurable change in lean mass. Some lean tissue supports a larger body and may naturally decrease as total weight falls.

But excessive loss of muscle can be important, particularly in:

- older adults,

- frail patients,

- people eating very little,

- patients with chronic disease,

- and people losing weight rapidly without resistance exercise.

A responsible treatment plan should consider:

- adequate protein and overall nutrition,

- resistance training,

- physical function,

- strength,

- rate of weight loss,

- and symptoms suggesting undernutrition.

The scale cannot distinguish fat loss from muscle loss.

A smaller number is not automatically a better health outcome if strength, function or nutrition deteriorates.

Nausea is common during semaglutide treatment, particularly while the dose is being increased.

Some people assume the medication works because it makes patients too sick to eat.

That is not the intended mechanism.

Effective treatment should reduce appetite and calorie intake without requiring persistent vomiting, severe pain or an inability to maintain hydration and nutrition.

Dose escalation is deliberately gradual to improve tolerability.

For standard weekly Wegovy injection, treatment generally begins at 0.25 mg and increases in stages over several months.

If a dose is not tolerated, escalation may be delayed or the maintenance dose may need reconsideration.

Severe or persistent symptoms should not be treated as evidence that the medication is working especially well.

They may represent excessive exposure, an adverse reaction or another medical condition requiring evaluation.

The most common adverse effects are gastrointestinal.

They include:

- nausea,

- diarrhea,

- vomiting,

- constipation,

- abdominal pain,

- indigestion,

- bloating,

- reflux,

- belching,

- and gas.

Other reported effects include:

- headache,

- fatigue,

- dizziness,

- increased heart rate,

- hair loss,

- and unusual skin sensations.

Symptoms are often most noticeable during dose escalation.

Many are mild or moderate and improve with time. Others lead to dose reduction, treatment interruption or permanent discontinuation.

At the 7.2 mg dose, dysesthesia was reported much more frequently than with 2.4 mg or placebo.

Dysesthesia can include:

- tingling,

- burning,

- heightened skin sensitivity,

- pain from normally nonpainful touch,

- or an electrical or altered skin sensation.

Higher-dose treatment should therefore not be viewed as a simple upgrade without trade-offs.

The prescribing information identifies several clinically important warnings.

These include:

- acute pancreatitis,

- gallstones and gallbladder inflammation,

- acute kidney injury related to dehydration,

- severe gastrointestinal reactions,

- allergic reactions,

- diabetic retinopathy complications in patients with type 2 diabetes,

- hypoglycemia when combined with insulin or insulin secretagogues,

- increased heart rate,

- and possible pulmonary aspiration during anesthesia or deep sedation.

The medication delays gastric emptying in some patients.

Rare postmarketing aspiration reports have involved patients who still had stomach contents despite following preoperative fasting instructions.

Patients should inform surgical, procedural and anesthesia teams that they are taking semaglutide.

A clinician can then assess the procedure, symptoms, dose timing and individual aspiration risk.

Patients should not independently apply a universal social-media rule about when to stop the medication before every procedure.

Semaglutide products carry a boxed warning concerning thyroid C-cell tumors.

Semaglutide caused thyroid C-cell tumors in rodents.

It is unknown whether it causes medullary thyroid carcinoma in humans.

The drug is contraindicated in people with:

- a personal history of medullary thyroid carcinoma,

- a family history of medullary thyroid carcinoma,

- or Multiple Endocrine Neoplasia syndrome type 2.

The warning should not be translated into the claim that semaglutide has been shown to cause thyroid cancer in humans.

It should also not be dismissed simply because the original finding came from animals.

The accurate statement is that the human relevance of the rodent finding remains unknown, and the product should not be used in the identified high-risk groups.

Weight loss provides no benefit during pregnancy and may present fetal risk.

For weight reduction or cardiovascular-risk reduction, Wegovy should be discontinued when pregnancy is recognized.

Because semaglutide remains in the body for a prolonged period, the prescribing information recommends stopping it at least two months before a planned pregnancy.

The MASH indication involves a separate benefit-risk consideration because untreated serious liver disease can also affect health. Decisions in that setting require individualized medical assessment.

Semaglutide should not be treated as a cosmetic medication that can be stopped and restarted casually around conception.

Pregnancy planning should be discussed before treatment begins.

Appetite regulation generally does not remain permanently changed after the medication leaves the body.

In the STEP 1 extension, a subgroup of participants was followed for one year after semaglutide and the trial’s lifestyle intervention were discontinued.

Participants regained approximately two-thirds of the weight they had previously lost, on average.

Several cardiometabolic improvements also moved back toward baseline.

That result does not mean every person regains the same amount.

It demonstrates that obesity biology commonly reasserts itself when an effective treatment is removed.

In STEP 4, participants first received semaglutide for 20 weeks.

Those who continued treatment lost additional weight.

Those switched to placebo regained weight despite continuing lifestyle intervention.

This supports viewing obesity as a chronic condition rather than a short challenge solved by a temporary course of medication.

The need for continuing treatment is not evidence of addiction.

Blood-pressure medication often works only while it is taken.

Cholesterol medication often works only while it is taken.

The same principle can apply to obesity pharmacotherapy.

Chronic treatment should not be confused with rigidly remaining on the highest dose forever.

The appropriate maintenance strategy can change with:

- treatment response,

- tolerability,

- health goals,

- weight trajectory,

- aging,

- pregnancy plans,

- changes in other medications,

- and newly diagnosed medical conditions.

Some patients may remain on a stable dose.

Some may require a lower dose.

Some may switch medications.

Some may stop under medical supervision and use another strategy.

Some may undergo metabolic surgery.

Evidence for the best individualized maintenance and discontinuation strategies continues to develop.

The important point is that stopping treatment should be planned with an understanding that hunger, calorie intake and weight can change again.

A patient can consume fewer calories without consuming better nutrition.

When appetite becomes markedly lower, each meal carries more nutritional importance.

A diet made smaller but not more nutrient-dense can result in inadequate:

- protein,

- fiber,

- vitamins,

- minerals,

- and total energy.

Persistent nausea can make this worse.

The goal is not to eat as little as physically possible.

The goal is to create sustainable weight reduction while protecting:

- muscle,

- bone health,

- digestive function,

- energy,

- and quality of life.

Semaglutide can make behavioral change easier by reducing biological hunger.

It does not automatically select nutritious food, create an exercise program or prevent under-eating.

The phrase “diet and exercise” is sometimes used dismissively, as though obesity results only from poor personal choices.

That framing ignores genetics, appetite biology, medications, sleep, environment, socioeconomic conditions and the body’s defense of stored energy.

But rejecting simplistic lifestyle advice does not make nutrition and physical activity unimportant.

Semaglutide and lifestyle measures serve different purposes.

The medication can reduce appetite-related pressure.

Nutrition influences nutrient adequacy and food quality.

Resistance exercise helps preserve strength and muscle.

Aerobic activity supports cardiovascular fitness.

Sleep and stress affect appetite, energy and adherence.

Effective treatment does not require choosing between biology and behavior.

It uses both.

FDA-approved semaglutide products undergo premarket review of:

- the active ingredient,

- formulation,

- dose accuracy,

- delivery system,

- manufacturing,

- stability,

- safety,

- and clinical effectiveness.

Compounded drugs do not undergo the same FDA premarket review.

Compounding can serve a legitimate purpose when an FDA-approved product cannot meet a particular patient’s medical need.

But “compounded semaglutide” should not automatically be presented as generic Ozempic or generic Wegovy.

The FDA has received reports of dosing errors involving compounded injectable semaglutide.

Some patients were instructed to measure small volumes from multidose vials using insulin syringes. Confusion among milligrams, milliliters and syringe “units” resulted in patients administering several times the intended dose.

Reported consequences have included:

- severe nausea,

- vomiting,

- abdominal pain,

- dehydration,

- fainting,

- pancreatitis,

- gallstones,

- and hospitalization.

The FDA has also raised concerns about products using semaglutide salt forms rather than the base form used in approved drugs.

A certificate reporting chemical purity does not establish clinical equivalence to an approved product.

A product sold online as Ozempic, Wegovy or semaglutide may be:

- an authentic approved product,

- a lawfully compounded preparation,

- a counterfeit,

- a diverted product stored improperly,

- or an unapproved research chemical.

Those categories should not be collapsed into one.

An unofficial product could contain:

- too little semaglutide,

- too much semaglutide,

- a different active ingredient,

- no active ingredient,

- contaminants,

- or a formulation with unknown stability.

Injectable products also require reliable sterility and bacterial-endotoxin controls.

A visually convincing pen or professionally designed website does not establish authenticity.

The evidence from STEP, SELECT, FLOW and ESSENCE applies to the controlled products and regimens used in those trials.

It does not validate every vial carrying the semaglutide name.

Semaglutide changed obesity medicine in several ways.

It demonstrated that appetite biology can be treated pharmacologically with substantial average weight reduction.

It helped shift obesity away from being viewed solely as a failure of willpower.

It produced evidence that an obesity medication can reduce major cardiovascular events in high-risk adults without diabetes.

It expanded into kidney and liver indications supported by outcome and histology trials.

It also created new challenges involving:

- long-term access,

- cost,

- muscle preservation,

- nutritional monitoring,

- compounded products,

- counterfeit supply,

- unrealistic expectations,

- and treatment after weight loss.

The medicine is neither a miracle nor a fraud.

It is a powerful clinical tool whose benefits depend on the right product, patient, dose and monitoring.

Semaglutide is a long-acting GLP-1 receptor agonist.

Its primary weight-loss effect comes from changing appetite regulation and reducing calorie intake.

It also improves glucose control by increasing insulin and reducing glucagon when blood glucose is elevated.

It can delay early gastric emptying, but slowed digestion is not the complete explanation for its effects.

In defined populations, specific semaglutide products have also reduced cardiovascular and kidney events and improved liver histology.

The medication does not guarantee a particular amount of weight loss.

It does not remove only fat.

It does not make nutrition and physical activity irrelevant.

And an unapproved or compounded product is not automatically equivalent to the medication studied in clinical trials.

Semaglutide changed obesity medicine because it demonstrated that substantial, sustained weight reduction can result from treating appetite biology directly.

What it actually does is less sensational than much of the marketing—and more medically important.

1. U.S. Food and Drug Administration. Wegovy Prescribing Information. Revised March 2026.

2. U.S. Food and Drug Administration. Ozempic Prescribing Information. Revised October 2025.

3. Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults With Overweight or Obesity. New England Journal of Medicine. 2021.

4. Rubino D, Abrahamsson N, Davies M, et al. Effect of Continued Weekly Subcutaneous Semaglutide Versus Placebo on Weight-Loss Maintenance in Adults With Overweight or Obesity: The STEP 4 Randomized Clinical Trial. JAMA. 2021.

5. Wilding JPH, Batterham RL, Davies M, et al. Weight Regain and Cardiometabolic Effects After Withdrawal of Semaglutide: The STEP 1 Trial Extension. Diabetes, Obesity and Metabolism. 2022.

6. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity Without Diabetes. New England Journal of Medicine. 2023.

7. Perkovic V, Tuttle KR, Rossing P, et al. Effects of Semaglutide on Chronic Kidney Disease in Patients With Type 2 Diabetes. New England Journal of Medicine. 2024.

8. Sanyal AJ, Newsome PN, Kliers I, et al. Phase 3 Trial of Semaglutide in Metabolic Dysfunction-Associated Steatohepatitis. New England Journal of Medicine. 2025.

9. Wharton S, Lingvay I, Bogdanski P, et al. Oral Semaglutide at a Dose of 25 mg in Adults With Overweight or Obesity. New England Journal of Medicine. 2025.

10. Wharton S, Freitas P, Hjelmesæth J, et al. Once-Weekly Semaglutide 7.2 mg in Adults With Obesity: The STEP UP Randomized Trial. The Lancet Diabetes & Endocrinology. 2025.

11. Wadden TA, Tronieri JS, Sugimoto D, et al. Short- and Long-Term Effects of Semaglutide 2.4 mg on Energy Intake, Appetite and Food Reward. American Journal of Clinical Nutrition. 2026.

12. U.S. Food and Drug Administration. FDA’s Concerns With Unapproved GLP-1 Drugs Used for Weight Loss.

13. U.S. Food and Drug Administration. Dosing Errors Associated With Compounded Injectable Semaglutide Products.