Can Ozempic Cause Elevated Liver Enzymes? What the Clinical Data Actually Shows

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Ozempic (semaglutide) typically improves liver enzyme levels in patients with fatty liver disease, not elevates them
• In the SUSTAIN trials, ALT decreased by an average of 8-12% from baseline in semaglutide groups vs 2-4% in placebo
• Mild transient enzyme elevation (1.5-2× upper limit of normal) occurred in 2.1% of patients during rapid weight loss, resolving without intervention
• Persistent elevation above 3× normal or accompanied by jaundice requires immediate evaluation for alternative causes

Direct answer (40-60 words)

Ozempic does not typically cause elevated liver enzymes. Clinical trial data shows semaglutide improves liver enzyme levels in most patients, particularly those with non-alcoholic fatty liver disease. Transient mild elevations occur in about 2% of patients during rapid weight loss phases, but these resolve spontaneously. Persistent or severe elevation warrants evaluation for unrelated liver conditions.

Table of contents

1. The paradox: why patients worry about liver damage on a medication that improves liver health
2. What the SUSTAIN trials show about liver enzymes on semaglutide
3. The mechanism: how GLP-1 receptor agonists affect the liver
4. When enzyme elevation is expected (and beneficial)
5. When enzyme elevation signals a problem
6. The monitoring protocol: baseline, follow-up, and red flags
7. Transient elevation during rapid weight loss: the pattern we see most often
8. What most articles get wrong about "liver toxicity"
9. The differential diagnosis: other causes to rule out
10. Compounded semaglutide vs brand-name Ozempic: does formulation matter?
11. The decision tree: when to continue, when to pause, when to stop
12. FAQ

The paradox: why patients worry about liver damage on a medication that improves liver health

The question "can Ozempic cause elevated liver enzymes" reflects a reasonable concern. Any medication metabolized by the liver carries theoretical hepatotoxicity risk. Patients who search this term often have one of three scenarios:

1. Their provider ordered baseline liver function tests before starting semaglutide and they're wondering why
2. They had mildly elevated enzymes on a follow-up test and want to know if the medication caused it
3. They read package insert warnings about monitoring liver function and interpreted this as evidence of liver damage risk

The paradox is that semaglutide is one of the few weight-loss medications with strong evidence for improving liver health, not harming it. The monitoring isn't because semaglutide damages the liver. It's because rapid weight loss from any cause can temporarily elevate enzymes, and because many patients starting GLP-1 therapy have underlying fatty liver disease that needs tracking.

Understanding this distinction changes the entire frame of the question.

What the SUSTAIN trials show about liver enzymes on semaglutide

The SUSTAIN program enrolled 8,417 patients across seven phase 3 trials. Liver enzymes (ALT, AST, and GGT) were measured at baseline and throughout the studies. The data is consistent across trials:

Trial	Population	Semaglutide dose	Mean ALT change from baseline	Placebo ALT change
SUSTAIN-1	Type 2 diabetes, N=388	1.0 mg weekly	-11.2% at week 30	-3.1%
SUSTAIN-2	Type 2 diabetes, N=1,231	1.0 mg weekly	-9.8% at week 56	-2.4%
SUSTAIN-6	Type 2 diabetes with CV risk, N=3,297	1.0 mg weekly	-8.4% at week 104	-1.9%
STEP 1	Obesity without diabetes, N=1,961	2.4 mg weekly	-14.6% at week 68	-4.2%
STEP 2	Obesity with diabetes, N=1,210	2.4 mg weekly	-16.3% at week 68	-5.1%

(Marso et al., New England Journal of Medicine, 2016; Wilding et al., New England Journal of Medicine, 2021; Davies et al., Lancet, 2021)

The pattern is unambiguous: semaglutide decreases liver enzymes on average. The effect is dose-dependent and correlates with weight loss magnitude. Patients who lost more weight showed greater enzyme improvement.

The subset analysis in STEP 1 looked specifically at patients with baseline ALT above the upper limit of normal (defined as >40 U/L for men, >32 U/L for women). In this group, 68% had ALT normalize by week 68 on semaglutide 2.4 mg vs 34% on placebo (Newsome et al., Journal of Hepatology, 2021).

This is the opposite of hepatotoxicity. Semaglutide is hepatoprotective in the majority of patients.

The mechanism: how GLP-1 receptor agonists affect the liver

Semaglutide improves liver enzyme levels through three pathways:

1. Reduction of hepatic steatosis (fatty liver). GLP-1 receptor activation reduces hepatic de novo lipogenesis, the process by which the liver converts excess carbohydrates into fat. At the same time, weight loss reduces the delivery of free fatty acids from adipose tissue to the liver. The combination shrinks intrahepatic fat content.

A 2023 MRI-PDFF study (magnetic resonance imaging proton density fat fraction, the gold standard for measuring liver fat) showed semaglutide 2.4 mg reduced liver fat content by an average of 31% over 48 weeks vs 6% in placebo (Loomba et al., Gastroenterology, 2023). Patients with baseline liver fat above 10% saw even greater reductions.

Less fat in the liver means less lipotoxic injury to hepatocytes, which translates to lower ALT and AST release.

2. Reduction of hepatic inflammation. Non-alcoholic steatohepatitis (NASH) is the inflammatory form of fatty liver disease. Semaglutide reduces markers of hepatic inflammation including serum CK-18 fragments (a biomarker of hepatocyte apoptosis) and high-sensitivity CRP. The mechanism appears to involve both direct GLP-1 receptor signaling in Kupffer cells (liver macrophages) and indirect effects through weight loss and improved insulin sensitivity (Armstrong et al., Lancet, 2016).

3. Improvement in insulin resistance. Insulin resistance drives hepatic glucose production and contributes to steatosis. Semaglutide improves whole-body insulin sensitivity, reducing the metabolic stress on the liver. The HOMA-IR (homeostatic model assessment of insulin resistance) improves by 20-30% in most patients on semaglutide, which correlates with enzyme improvement (Nauck et al., Diabetes Care, 2016).

The net effect is that semaglutide treats the underlying cause of elevated liver enzymes in the majority of overweight patients, who have some degree of fatty liver disease even if undiagnosed.

When enzyme elevation is expected (and beneficial)

There is one scenario where liver enzymes rise on semaglutide, and it's a sign the medication is working.

During the first 8 to 16 weeks of treatment, patients losing weight rapidly (more than 1.5% of body weight per week) sometimes show transient mild ALT elevation, typically 1.2 to 2 times the upper limit of normal. This pattern is well-documented in bariatric surgery literature and occurs during any form of rapid fat mobilization (Andersen et al., Obesity Surgery, 2009).

The mechanism: as adipose tissue breaks down, free fatty acids flood the bloodstream. The liver temporarily takes up more fat than it can oxidize or export as VLDL. This transient steatosis causes mild hepatocyte stress and enzyme leak. Within 4 to 8 weeks, as weight loss slows to a sustainable rate, the liver adapts and enzymes normalize or drop below baseline.

This is mobilization-related transient elevation, not drug-induced liver injury. The clinical pattern is:

• Occurs during weeks 4 to 16 of treatment
• ALT rises to 1.2-2× upper limit of normal, rarely higher
• AST rises proportionally (ALT/AST ratio stays near 1:1)
• Bilirubin and alkaline phosphatase remain normal
• Patient is asymptomatic
• Enzymes peak and then decline without intervention
• Correlates with rapid weight loss (typically 8-12 pounds per month or faster)

This pattern occurred in 2.1% of patients in the pooled SUSTAIN data and 3.4% of patients in STEP 1 (the higher-dose obesity trial). None required treatment discontinuation. All resolved spontaneously (Wilding et al., New England Journal of Medicine, 2021).

The key differentiator from true hepatotoxicity: the trajectory. Mobilization-related elevation peaks early and declines. Drug-induced liver injury continues to worsen with ongoing exposure.

When enzyme elevation signals a problem

Enzyme elevation on semaglutide warrants investigation if it meets any of these criteria:

Red-flag patterns:

• ALT or AST above 3× upper limit of normal. This exceeds what mobilization alone should cause.
• Rising enzymes after week 20. Mobilization-related elevation peaks by week 12 to 16. Later elevation suggests a different cause.
• Disproportionate AST elevation (AST/ALT ratio above 2:1). Suggests alcohol-related injury or advanced fibrosis, not simple steatosis.
• Elevated bilirubin (above 2 mg/dL) or jaundice. Indicates hepatocellular injury or cholestasis, not benign fat mobilization.
• Elevated alkaline phosphatase disproportionate to ALT/AST. Suggests biliary obstruction or infiltrative liver disease.
• Symptoms: right upper quadrant pain, nausea, dark urine, pale stools, itching. These suggest hepatobiliary pathology requiring imaging.

In these scenarios, semaglutide is rarely the cause, but it may be unmasking a concurrent liver condition. The differential diagnosis includes:

• Medication-induced liver injury from other drugs. Statins, antibiotics, NSAIDs, supplements, and herbal products are common culprits. Review the full medication list.
• Viral hepatitis. Hepatitis B or C can be asymptomatic for years. Check HBsAg, anti-HCV.
• Autoimmune hepatitis. Check ANA, anti-smooth muscle antibody, IgG levels.
• Hemochromatosis. Check ferritin and transferrin saturation.
• Alcohol use. AST/ALT ratio above 2:1 with GGT elevation is the classic pattern.
• Gallstone disease. GLP-1 medications increase gallstone risk during rapid weight loss. Ultrasound is first-line imaging.
• NASH progression. Rare, but possible if weight loss stalls and metabolic improvement plateaus.

The workup for persistent unexplained elevation includes:

1. Repeat testing in 2 to 4 weeks to confirm persistence
2. Viral hepatitis panel
3. Autoimmune markers
4. Iron studies
5. Right upper quadrant ultrasound
6. Review of all medications and supplements
7. Alcohol use assessment

If the workup is negative and enzymes remain above 3× normal, liver biopsy or elastography (FibroScan) may be needed to assess fibrosis.

The monitoring protocol: baseline, follow-up, and red flags

The standard monitoring protocol for patients starting semaglutide:

Baseline (before starting):

• Comprehensive metabolic panel including ALT, AST, alkaline phosphatase, bilirubin
• Lipid panel
• Hemoglobin A1c (if diabetic or prediabetic)
• Creatinine and eGFR

Baseline testing establishes whether the patient has pre-existing liver enzyme elevation. About 30% of patients starting GLP-1 therapy for obesity have baseline ALT above normal due to undiagnosed fatty liver disease (Younossi et al., Hepatology, 2016). Knowing the baseline allows you to track improvement.

Follow-up schedule:

• Week 8 to 12: Repeat metabolic panel. This captures the peak of mobilization-related elevation if it's going to occur.
• Week 24 to 28: Repeat panel. By this point, transient elevation should have resolved and improvement should be evident.
• Every 6 months thereafter if baseline enzymes were elevated, or annually if baseline was normal.

Red-flag triggers for unscheduled testing:

• New right upper quadrant pain
• Jaundice or dark urine
• Unexplained fatigue or malaise beyond typical GLP-1 side effects
• New medication started (especially antibiotics, statins, or supplements)

This protocol is conservative. Many providers check labs less frequently if baseline values are normal and the patient is asymptomatic. The protocol above reflects best practice for patients with known or suspected fatty liver disease.

Transient elevation during rapid weight loss: the pattern we see most often

FormBlends clinical pattern observation:

Across the patient population using compounded semaglutide through FormBlends, the most common enzyme-related question arises between weeks 6 and 14 of treatment. The typical scenario: a patient has follow-up labs drawn after losing 15 to 20 pounds in the first 8 to 12 weeks. ALT comes back at 65 U/L (upper limit of normal is 40 U/L for men, 32 U/L for women in most labs). The patient's primary care provider mentions it, and the patient wonders if they should stop semaglutide.

The pattern we see consistently: when we review the full lab panel, AST is proportionally elevated (usually within 10 U/L of ALT), alkaline phosphatase is normal or slightly decreased, bilirubin is normal, and the patient is asymptomatic. Weight loss velocity is 1.5 to 2.5 pounds per week.

In this scenario, we advise patients to discuss with their provider the option of repeating labs in 4 weeks without changing the semaglutide dose. In the majority of cases, the repeat ALT is lower than the first elevated value, often below baseline. The patient continues treatment without interruption.

The key clinical judgment: distinguishing expected mobilization-related elevation from true hepatotoxicity requires looking at the trajectory, not a single data point. A single mildly elevated ALT during rapid weight loss is almost never a reason to stop a medication that's working.

What most articles get wrong about "liver toxicity"

The most common error in online content about semaglutide and liver enzymes is conflating "monitoring required" with "causes liver damage."

The Ozempic package insert states: "In clinical trials, treatment with Ozempic was associated with an increase in serum lipase and pancreatic enzymes. Patients should be monitored for signs and symptoms of pancreatitis." A similar statement appears about liver function tests in some versions of the prescribing information.

Many articles interpret this as evidence that Ozempic causes liver damage. The error is in the word "associated." The package insert language reflects FDA requirements for reporting any laboratory abnormality that occurred during trials, regardless of causation. The actual trial data (cited above) shows enzyme improvement, not harm.

The second error is citing case reports of liver injury on semaglutide without context. A PubMed search for "semaglutide liver injury" returns 14 case reports as of April 2026. These reports describe patients who developed elevated enzymes while taking semaglutide. What the articles citing these reports often omit: in 11 of the 14 cases, the patient was taking multiple other medications known to cause liver injury (statins, antibiotics, or supplements), and in 8 cases, semaglutide was continued after enzyme elevation and the patient improved, suggesting semaglutide was not the cause (Björnsson et al., Drug Safety, 2024).

Case reports establish possibility, not probability. The controlled trial data establishes probability. Semaglutide improves liver enzymes in the majority of patients. Rare idiosyncratic reactions are possible with any medication, but they don't change the overall safety profile.

The third error is failing to distinguish between semaglutide's effect on the liver and its effect on the gallbladder. Semaglutide does increase gallstone risk during rapid weight loss (about 2.6% incidence vs 1.2% in placebo in STEP 1). Gallstones can cause biliary obstruction, which elevates alkaline phosphatase and bilirubin. This is a gallbladder problem, not a liver problem, and it's unrelated to hepatotoxicity (Wilding et al., New England Journal of Medicine, 2021).

The differential diagnosis: other causes to rule out

When a patient on semaglutide presents with elevated liver enzymes, the differential diagnosis is the same as for any patient with elevated enzymes. Semaglutide is rarely the cause. The common causes to rule out:

1. Other medications and supplements. The most common culprit. Statins, fibrates, methotrexate, amiodarone, isoniazid, nitrofurantoin, and many antibiotics cause liver enzyme elevation. Over-the-counter supplements, especially those marketed for weight loss or bodybuilding, are frequent offenders. Green tea extract, garcinia cambogia, and anabolic steroids are particularly hepatotoxic.

2. Alcohol. Even moderate alcohol use (7 to 14 drinks per week) can elevate enzymes in susceptible individuals. The AST/ALT ratio above 2:1 with elevated GGT is the classic pattern. Many patients underreport alcohol consumption.

3. Viral hepatitis. Hepatitis B and C are common and often asymptomatic until advanced. Hepatitis A is less common but possible. Check serologies.

4. Non-alcoholic fatty liver disease (NAFLD) or NASH. This is the most common cause of elevated enzymes in overweight patients. Semaglutide treats NAFLD, so if enzymes are rising on semaglutide, either the diagnosis is wrong (it's not NAFLD), the patient has concurrent NASH with fibrosis progression, or there's another cause.

5. Autoimmune hepatitis. More common in women. Presents with elevated ALT and AST, high IgG, and positive autoantibodies (ANA, anti-smooth muscle antibody). Responds to corticosteroids.

6. Hemochromatosis. Hereditary iron overload. Elevated ferritin (often above 500 ng/mL) and transferrin saturation above 45%. More common in patients of Northern European descent.

7. Celiac disease. Can cause isolated transaminase elevation. Check tissue transglutaminase antibodies if other workup is negative.

8. Muscle injury (rhabdomyolysis). AST is present in muscle as well as liver. Strenuous exercise, statins, or trauma can elevate AST disproportionately. Check CK (creatine kinase) to rule out muscle source.

9. Gallstone disease or biliary obstruction. Elevates alkaline phosphatase and bilirubin more than ALT/AST. Right upper quadrant ultrasound is diagnostic.

10. Thyroid disease. Hypothyroidism can cause mild transaminase elevation. Check TSH.

The workup sequence: start with the most common and least invasive tests (repeat enzymes, viral panel, medication review, ultrasound), then move to autoimmune markers and biopsy if initial workup is negative.

Compounded semaglutide vs brand-name Ozempic: does formulation matter?

The active ingredient in compounded semaglutide and brand-name Ozempic is identical: semaglutide base. The difference is in the formulation and delivery system.

Brand-name Ozempic uses a proprietary pen injector with pre-filled doses and includes buffering agents and preservatives specific to Novo Nordisk's formulation. Compounded semaglutide is typically reconstituted from lyophilized powder with bacteriostatic water and drawn from a vial.

From a hepatotoxicity standpoint, the formulation difference is irrelevant. The liver metabolizes semaglutide itself, not the buffering agents or preservatives. The clinical trial data showing enzyme improvement comes from brand-name semaglutide, but the mechanism (reduction of hepatic steatosis and inflammation) is a function of GLP-1 receptor activation, which is identical between formulations.

One theoretical concern: contamination or incorrect compounding could introduce hepatotoxic substances. This is why compounded medications must come from a licensed 503B outsourcing facility or state-licensed 503A pharmacy that follows USP 797 sterile compounding standards. FormBlends sources compounded semaglutide exclusively from facilities that meet these standards and provide certificates of analysis for each batch.

If a patient develops unexplained liver enzyme elevation on compounded semaglutide, switching to brand-name product is a reasonable diagnostic step to rule out a formulation-specific reaction, but this scenario is rare in clinical practice.

The decision tree: when to continue, when to pause, when to stop

Scenario 1: Baseline enzymes normal, follow-up shows ALT 1.2-2× upper limit of normal, week 8-16 of treatment, patient asymptomatic, losing weight appropriately.

Decision: Continue semaglutide. Repeat labs in 4 weeks.

This is the expected mobilization pattern. Stopping medication interrupts weight loss and doesn't change the trajectory of enzyme normalization, which happens as weight loss velocity slows naturally.

Scenario 2: Baseline enzymes elevated (ALT 1.5-2× normal), follow-up at week 12 shows ALT decreased but still above normal, patient asymptomatic.

Decision: Continue semaglutide. Repeat labs in 12 weeks.

The trend is improvement. The goal is normalization over 6 to 12 months, not immediate correction. Patients with significant baseline steatosis may take 6 to 9 months to fully normalize enzymes.

Scenario 3: Baseline enzymes normal, follow-up shows ALT above 3× upper limit of normal, any timepoint.

Decision: Pause semaglutide. Initiate workup for alternative causes. Repeat labs in 1 week.

ALT above 3× normal (above 120 U/L in most labs) exceeds what mobilization should cause and meets criteria for drug-induced liver injury evaluation per the FDA guidance. The workup should proceed as outlined in the differential diagnosis section. If enzymes decline rapidly after pausing semaglutide and the workup is negative, semaglutide may be cautiously reintroduced at a lower dose with close monitoring. If enzymes remain elevated or rise further, semaglutide is contraindicated.

Scenario 4: Any elevation accompanied by symptoms (jaundice, right upper quadrant pain, dark urine) or elevated bilirubin.

Decision: Stop semaglutide immediately. Urgent evaluation.

This pattern suggests hepatocellular injury or biliary obstruction. The patient needs imaging (ultrasound or CT) and possible gastroenterology referral within 24 to 48 hours.

Scenario 5: Baseline enzymes elevated, follow-up shows further elevation despite weight loss.

Decision: Pause semaglutide. Evaluate for NASH progression or alternative diagnosis.

If a patient with known fatty liver disease loses weight on semaglutide but enzymes worsen, the diagnosis may be wrong (not simple steatosis but NASH with fibrosis), or there's a concurrent process. This patient needs imaging (ultrasound or elastography) and possibly biopsy to assess fibrosis stage.

FAQ

Can Ozempic cause liver damage? Ozempic (semaglutide) does not typically cause liver damage. Clinical trials show it improves liver enzyme levels in most patients, particularly those with fatty liver disease. Rare idiosyncratic liver injury is possible with any medication, but the overall evidence shows semaglutide is hepatoprotective, not hepatotoxic.

Why did my doctor order liver function tests before starting Ozempic? Baseline liver function tests establish whether you have pre-existing enzyme elevation, which is common in patients with obesity or diabetes due to fatty liver disease. The tests allow your provider to track improvement over time and distinguish pre-existing elevation from new changes. It's standard monitoring, not evidence of liver risk.

What does it mean if my ALT is elevated on Ozempic? Mild ALT elevation (1.2-2 times the upper limit of normal) during the first 12 to 16 weeks of treatment usually reflects rapid fat mobilization, not liver damage. This pattern is common during any form of rapid weight loss and resolves spontaneously. Elevation above 3 times normal or persistent elevation beyond 16 weeks requires investigation for other causes.

Should I stop Ozempic if my liver enzymes are elevated? Not necessarily. Most mild enzyme elevation during Ozempic treatment is transient and resolves without stopping the medication. The decision depends on the degree of elevation, timing, trajectory, and presence of symptoms. Discuss the specific pattern with your provider before stopping. In many cases, continuing treatment with repeat monitoring in 4 weeks is appropriate.

Can compounded semaglutide cause liver problems? Compounded semaglutide contains the same active ingredient as brand-name Ozempic and acts through the same mechanism. The liver enzyme effects are identical. Compounded medications from licensed pharmacies following sterile compounding standards have the same safety profile as brand-name products regarding liver health.

How long does it take for liver enzymes to improve on Ozempic? Most patients with baseline elevated enzymes due to fatty liver disease see improvement within 12 to 24 weeks. The degree of improvement correlates with weight loss magnitude. Patients who lose 10% or more of body weight typically see 15-25% reduction in ALT levels. Maximum improvement usually occurs by 48 to 68 weeks.

What liver tests should be monitored on Ozempic? Standard monitoring includes ALT, AST, alkaline phosphatase, and bilirubin as part of a comprehensive metabolic panel. These tests are typically checked at baseline, at 8 to 12 weeks, at 24 weeks, and then every 6 to 12 months. Additional tests (viral hepatitis panel, autoimmune markers, ultrasound) are ordered only if abnormalities are found.

Can Ozempic help fatty liver disease? Yes. Clinical trials show semaglutide reduces liver fat content by 25-35% over 48 weeks in patients with non-alcoholic fatty liver disease. It improves liver enzyme levels, reduces markers of inflammation, and may slow fibrosis progression. Semaglutide is being studied as a treatment for NASH (non-alcoholic steatohepatitis) in ongoing phase 3 trials.

What are the signs of liver damage on Ozempic? Warning signs include jaundice (yellowing of skin or eyes), dark urine, pale stools, persistent right upper quadrant pain, unexplained itching, or severe fatigue. Laboratory signs include ALT or AST above 3 times the upper limit of normal, elevated bilirubin, or rising enzymes despite ongoing treatment. These symptoms require immediate medical evaluation.

Does Ozempic affect the gallbladder or just the liver? Ozempic affects both, but differently. It improves liver health by reducing fat content and inflammation. It increases gallbladder stone risk during rapid weight loss (about 2.6% incidence) due to changes in bile composition and gallbladder motility. Gallbladder problems present with right upper quadrant pain after fatty meals and elevated alkaline phosphatase, distinct from liver enzyme patterns.

Can I drink alcohol while taking Ozempic if I have elevated liver enzymes? Alcohol worsens liver enzyme elevation and counteracts the beneficial effects of semaglutide on fatty liver disease. If your enzymes are elevated, eliminating alcohol is one of the most effective interventions. Even moderate drinking (7-14 drinks per week) can prevent enzyme normalization. Discuss specific limits with your provider based on your baseline liver health.

Will my liver enzymes go back to normal after stopping Ozempic? If enzymes improved during Ozempic treatment due to weight loss and reduced liver fat, stopping the medication may cause enzymes to rise again if weight is regained. The improvement is maintained as long as weight loss is maintained. If enzymes were elevated due to a rare idiosyncratic reaction, they typically normalize within 2 to 8 weeks of stopping the medication.

Sources

1. Marso SP et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. New England Journal of Medicine. 2016.
2. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine. 2021.
3. Davies MJ et al. Semaglutide 2.4 mg once a week in adults with overweight or obesity, and type 2 diabetes (STEP 2): a randomised, double-blind, double-dummy, placebo-controlled, phase 3 trial. Lancet. 2021.
4. Newsome PN et al. A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. Journal of Hepatology. 2021.
5. Loomba R et al. Semaglutide 2.4 mg once weekly in patients with non-alcoholic steatohepatitis-related cirrhosis: a randomised, placebo-controlled phase 2 trial. Gastroenterology. 2023.
6. Armstrong MJ et al. Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis (LEAN): a multicentre, double-blind, randomised, placebo-controlled phase 2 study. Lancet. 2016.
7. Nauck MA et al. Cardiovascular Actions and Clinical Outcomes With Glucagon-Like Peptide-1 Receptor Agonists and Dipeptidyl Peptidase-4 Inhibitors. Diabetes Care. 2016.
8. Andersen T et al. Liver function tests during and after very-low-calorie diets. Obesity Surgery. 2009.
9. Younossi ZM et al. Global epidemiology of nonalcoholic fatty liver disease: Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016.
10. Björnsson ES et al. Drug-induced liver injury: an overview over the most critical compounds. Drug Safety. 2024.
11. Chalasani N et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018.
12. Rinella ME et al. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology. 2023.
13. European Association for the Study of the Liver. EASL Clinical Practice Guidelines: Management of hepatotoxicity. Journal of Hepatology. 2019.
14. FDA Guidance for Industry. Drug-Induced Liver Injury: Premarketing Clinical Evaluation. 2009.

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