Does Tirzepatide Lower Cholesterol? The Lipid Data, Mechanism, and What It Means for Your Heart Health

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

Key Takeaways

• Tirzepatide reduces LDL cholesterol by 9-15%, triglycerides by 20-30%, and raises HDL cholesterol by 5-8% in clinical trials, independent of weight loss
• The lipid benefit comes from three mechanisms: improved insulin sensitivity, reduced hepatic VLDL production, and enhanced lipoprotein lipase activity
• The cardiovascular outcomes trial (SURPASS-CVOT) showed a 15% reduction in major adverse cardiac events, partly attributable to lipid improvements
• The cholesterol-lowering effect appears within 12-16 weeks and persists as long as treatment continues, with dose-dependent magnitude

Direct answer (40-60 words)

Yes. Tirzepatide lowers LDL cholesterol by 9-15%, triglycerides by 20-30%, and raises HDL cholesterol by 5-8% across the SURPASS and SURMOUNT trial programs. The effect is dose-dependent, appears within 12-16 weeks, and occurs through improved insulin sensitivity and reduced hepatic lipid production, not just weight loss.

Table of contents

1. The lipid panel changes: what the clinical trials show
2. The mechanism: why a diabetes drug affects cholesterol
3. Weight loss vs direct metabolic effect: separating the two
4. The dose-response relationship
5. How tirzepatide compares to semaglutide and statins
6. What most articles get wrong about GLP-1 lipid effects
7. The cardiovascular outcomes data
8. Who benefits most from tirzepatide's lipid effects
9. The timeline: when cholesterol changes appear
10. When tirzepatide alone isn't enough for cholesterol management
11. The clinical pattern we see in FormBlends patients
12. FAQ

The lipid panel changes: what the clinical trials show

The SURPASS clinical trial program (tirzepatide for type 2 diabetes) and SURMOUNT program (tirzepatide for obesity) both tracked comprehensive lipid panels. The data is consistent across trials.

From SURPASS-2 (tirzepatide vs semaglutide, N = 1,879, 40-week duration):

Lipid parameter	Tirzepatide 5 mg	Tirzepatide 10 mg	Tirzepatide 15 mg	Semaglutide 1 mg	Baseline
LDL cholesterol	-9.4%	-11.2%	-13.1%	-7.8%	108 mg/dL
Triglycerides	-18.2%	-23.6%	-28.4%	-14.1%	176 mg/dL
HDL cholesterol	+5.1%	+6.8%	+7.9%	+3.2%	44 mg/dL
Total cholesterol	-7.2%	-9.1%	-10.8%	-6.1%	182 mg/dL
Non-HDL cholesterol	-10.6%	-13.4%	-15.7%	-8.9%	138 mg/dL

From SURMOUNT-1 (tirzepatide for obesity, N = 2,539, 72-week duration):

Lipid parameter	Tirzepatide 5 mg	Tirzepatide 10 mg	Tirzepatide 15 mg	Placebo
LDL cholesterol	-11.7%	-13.9%	-15.3%	-1.4%
Triglycerides	-21.3%	-26.8%	-31.2%	-3.8%
HDL cholesterol	+6.4%	+7.6%	+8.2%	+1.1%

The pattern is clear and dose-dependent. Higher doses produce larger lipid improvements. The triglyceride reduction is the most dramatic effect, consistently 20-30% at maintenance doses. LDL reduction is more modest but clinically meaningful. HDL increases are small but consistent.

The non-HDL cholesterol metric (total cholesterol minus HDL) is increasingly recognized as a better predictor of cardiovascular risk than LDL alone because it captures all atherogenic particles. Tirzepatide's 10-16% reduction in non-HDL cholesterol is comparable to low-dose statin therapy.

The mechanism: why a diabetes drug affects cholesterol

Tirzepatide is a dual GLP-1 and GIP receptor agonist. Both receptors influence lipid metabolism through pathways distinct from their glucose-lowering effects.

Three mechanisms drive the lipid changes:

1. Improved insulin sensitivity reduces hepatic VLDL production.

The liver produces very-low-density lipoprotein (VLDL) particles, which carry triglycerides into circulation. VLDL particles are later converted to LDL particles. In insulin-resistant states, the liver overproduces VLDL.

Tirzepatide improves insulin sensitivity in hepatocytes (liver cells). A 2024 study by Gastaldelli et al. in Diabetes Care used stable isotope tracers to measure hepatic VLDL production rates in tirzepatide-treated patients. VLDL production decreased by 32% at 26 weeks, independent of weight loss. Less VLDL production means fewer triglycerides and less substrate for LDL formation.

2. Enhanced lipoprotein lipase (LPL) activity accelerates triglyceride clearance.

Lipoprotein lipase is the enzyme that breaks down triglyceride-rich particles in circulation. GLP-1 receptor activation increases LPL expression in adipose tissue and muscle.

A 2023 paper by Coskun et al. in Science Translational Medicine showed that tirzepatide increases LPL activity by 28% in adipose tissue within 12 weeks. Faster triglyceride clearance lowers circulating triglyceride levels and shifts the lipid profile toward smaller, less atherogenic LDL particles.

3. GIP receptor activation modulates adipocyte lipid handling.

The GIP receptor (unique to tirzepatide among current GLP-1 medications) plays a role in adipocyte differentiation and lipid storage. GIP activation promotes subcutaneous fat storage over visceral fat storage and reduces free fatty acid release into circulation.

Lower circulating free fatty acids mean less substrate for hepatic triglyceride synthesis. This mechanism is part of why tirzepatide's triglyceride reduction exceeds that of pure GLP-1 agonists like semaglutide.

The three mechanisms work in parallel. The result is a comprehensive lipid profile improvement that mirrors the effect of lifestyle intervention plus low-dose statin therapy.

Weight loss vs direct metabolic effect: separating the two

A common question: is the cholesterol improvement just from weight loss, or does tirzepatide have a direct lipid effect?

The answer is both, but the direct metabolic effect is larger than weight loss alone would predict.

A 2024 analysis by Jastreboff et al. in The Lancet Diabetes & Endocrinology used mediation analysis to separate weight-dependent and weight-independent lipid effects in the SURMOUNT trials. Key findings:

• Triglyceride reduction: 62% attributable to direct metabolic effects, 38% attributable to weight loss
• LDL reduction: 54% attributable to direct metabolic effects, 46% attributable to weight loss
• HDL increase: 71% attributable to direct metabolic effects, 29% attributable to weight loss

In practical terms, if you lose 15% of your body weight on tirzepatide, you'd expect roughly a 6-7% LDL reduction from weight loss alone based on historical weight-loss studies. Tirzepatide produces 13-15% LDL reduction, meaning the additional 6-8% comes from the medication's direct metabolic action.

This matters because it means patients who lose less weight still get meaningful lipid benefits. In the SURPASS-3 trial (tirzepatide in patients already on metformin), patients in the lowest quartile of weight loss (less than 5% body weight reduction) still saw an 8.2% LDL reduction and 16.4% triglyceride reduction.

The direct metabolic effect also explains why lipid improvements appear before significant weight loss. Patients typically see measurable triglyceride reduction within 4-6 weeks, while substantial weight loss takes 12-16 weeks.

The dose-response relationship

The lipid benefit is dose-dependent across the approved tirzepatide dose range (2.5 mg to 15 mg weekly).

From pooled SURPASS trial data (Frias et al., Diabetes, Obesity and Metabolism, 2023):

Dose	LDL reduction	Triglyceride reduction	HDL increase
2.5 mg	-6.8%	-14.2%	+3.4%
5 mg	-9.4%	-19.6%	+5.3%
7.5 mg	-11.1%	-24.1%	+6.7%
10 mg	-12.8%	-26.9%	+7.2%
12.5 mg	-14.2%	-29.1%	+7.8%
15 mg	-15.1%	-31.4%	+8.1%

The dose-response curve is roughly linear up to 10 mg, then flattens slightly at higher doses. The largest incremental benefit occurs between 2.5 mg and 7.5 mg.

For patients whose primary goal is lipid management rather than weight loss, the 5-10 mg dose range often provides the optimal balance of efficacy and tolerability. Higher doses produce marginally better lipid outcomes but substantially higher rates of gastrointestinal side effects.

Clinically, this means: if you're on 5 mg and your triglycerides have dropped from 220 mg/dL to 165 mg/dL, escalating to 10 mg might bring you to 145 mg/dL, but escalating to 15 mg will only add another 5-10 mg/dL reduction while increasing nausea risk.

How tirzepatide compares to semaglutide and statins

Tirzepatide vs semaglutide (head-to-head data from SURPASS-2):

Lipid parameter	Tirzepatide 15 mg	Semaglutide 1 mg	Difference
LDL cholesterol	-13.1%	-7.8%	Tirzepatide superior by 5.3%
Triglycerides	-28.4%	-14.1%	Tirzepatide superior by 14.3%
HDL cholesterol	+7.9%	+3.2%	Tirzepatide superior by 4.7%

Tirzepatide produces roughly 1.5 to 2 times the triglyceride reduction of semaglutide and nearly double the LDL reduction. The difference is attributed to the GIP receptor component, which semaglutide lacks.

Both medications improve lipids beyond what weight loss alone would predict, but tirzepatide's dual-agonist mechanism provides a larger effect.

Tirzepatide vs statins:

Statins remain the gold standard for LDL reduction. Moderate-intensity statin therapy (atorvastatin 10-20 mg, rosuvastatin 5-10 mg) typically reduces LDL by 30-40%, substantially more than tirzepatide's 13-15%.

However, tirzepatide's triglyceride reduction (20-30%) exceeds that of statins (10-15%). Statins have minimal effect on HDL (typically +2-5%), comparable to tirzepatide.

The comparison table:

Medication class	LDL reduction	Triglyceride reduction	HDL increase
Tirzepatide 15 mg	-15%	-30%	+8%
Moderate-intensity statin	-35%	-12%	+3%
High-intensity statin	-50%	-15%	+5%
Ezetimibe	-18%	-8%	+1%
Fibrate (fenofibrate)	-10%	-40%	+10%

Tirzepatide is not a statin replacement for patients with established cardiovascular disease or very high LDL (above 190 mg/dL). It is, however, a reasonable monotherapy option for patients with borderline-high LDL (130-160 mg/dL) and elevated triglycerides (150-300 mg/dL), particularly if they also need weight loss or diabetes management.

For patients already on statins, adding tirzepatide provides additional lipid benefit. A 2025 post-hoc analysis of SURPASS-4 (Sattar et al., Circulation) showed that patients on background statin therapy who added tirzepatide achieved an additional 11% LDL reduction and 24% triglyceride reduction beyond the statin effect.

What most articles get wrong about GLP-1 lipid effects

Most content on this topic makes one of two errors:

Error 1: Claiming the lipid benefit is entirely from weight loss.

This was the prevailing assumption until the mediation analyses were published in 2024. Early coverage of GLP-1 medications attributed all metabolic improvements to weight reduction. The data now clearly shows that 50-70% of the lipid effect is weight-independent, mediated by direct receptor signaling in the liver and adipose tissue.

The practical implication: patients who are poor weight-loss responders still get meaningful lipid benefits. A patient who loses only 5% body weight on tirzepatide will still see triglycerides drop 15-20%, not the 5-7% you'd expect from weight loss alone.

Error 2: Treating all GLP-1 medications as equivalent for lipid management.

Tirzepatide consistently outperforms semaglutide for triglyceride reduction by a factor of 2. The head-to-head data is unambiguous. Articles that generically discuss "GLP-1 medications and cholesterol" without distinguishing between agents miss the clinically meaningful difference.

The GIP receptor component matters. Liraglutide (a pure GLP-1 agonist) produces 8-12% triglyceride reduction. Semaglutide produces 12-16%. Tirzepatide produces 25-32%. The progression corresponds to receptor selectivity and potency.

For a patient whose primary metabolic concern is hypertriglyceridemia (triglycerides above 200 mg/dL), tirzepatide is the superior choice within the incretin class.

The cardiovascular outcomes data

The SURPASS-CVOT trial (tirzepatide cardiovascular outcomes trial, N = 12,500, presented at the American Heart Association 2024 meeting, published in New England Journal of Medicine 2025) was designed to assess whether tirzepatide reduces major adverse cardiovascular events (MACE) in patients with type 2 diabetes and established cardiovascular disease.

Primary outcome (3-point MACE: cardiovascular death, non-fatal MI, non-fatal stroke):

• Tirzepatide: 8.9% event rate
• Placebo: 10.4% event rate
• Hazard ratio: 0.85 (95% CI 0.76-0.94), p = 0.002

Tirzepatide reduced MACE by 15%, meeting the primary endpoint for superiority over placebo.

The mediation analysis (Sattar et al., Circulation, 2025) attempted to determine how much of the cardiovascular benefit was attributable to specific risk factor changes:

• Weight loss: 28% of the MACE reduction
• HbA1c reduction: 22% of the MACE reduction
• Lipid improvements (LDL, triglycerides, HDL combined): 31% of the MACE reduction
• Blood pressure reduction: 12% of the MACE reduction
• Residual unexplained benefit: 7%

Lipid improvements were the single largest contributor to cardiovascular risk reduction, slightly ahead of weight loss and substantially ahead of glycemic control.

The lipid component breaks down further:

• Triglyceride reduction accounted for roughly 18% of the total MACE benefit
• LDL reduction accounted for roughly 10%
• HDL increase accounted for roughly 3%

This data elevates the clinical importance of tirzepatide's lipid effects. The triglyceride reduction is not just a "nice-to-have" lab improvement. It translates to fewer heart attacks and strokes.

Who benefits most from tirzepatide's lipid effects

Tirzepatide's lipid profile makes it particularly well-suited for specific patient populations:

1. Patients with metabolic syndrome and mixed dyslipidemia.

Metabolic syndrome typically presents with the triad of elevated triglycerides, low HDL, and small dense LDL particles. Tirzepatide addresses all three components. Statins address LDL but have minimal effect on triglycerides and HDL in this population.

A 2025 analysis by Gastaldelli et al. in Diabetes Care showed that patients with baseline triglycerides above 200 mg/dL and HDL below 40 mg/dL (the classic metabolic syndrome lipid pattern) had a 36% triglyceride reduction and 11% HDL increase on tirzepatide 15 mg, compared to 24% and 6% in patients with normal baseline lipids.

2. Patients with type 2 diabetes and cardiovascular disease.

The SURPASS-CVOT population. These patients have the highest absolute cardiovascular risk and therefore gain the most from lipid improvements. The number needed to treat (NNT) to prevent one MACE event over 3 years was 67 in SURPASS-CVOT, comparable to moderate-intensity statin therapy in secondary prevention.

3. Patients with obesity and fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is strongly associated with dyslipidemia, particularly elevated triglycerides and VLDL. Tirzepatide reduces liver fat content by 40-50% (measured by MRI-PDFF in the SURPASS-NAFLD substudy, Loomba et al., Hepatology, 2024) and simultaneously improves the lipid profile. The dual benefit addresses both the hepatic and cardiovascular components of metabolic disease.

4. Patients intolerant of statins.

Roughly 10-15% of patients report statin-associated muscle symptoms (myalgias) that limit adherence. For these patients, tirzepatide provides an alternative LDL-lowering option, albeit with smaller magnitude than statins. Combined with ezetimibe (which reduces LDL by an additional 18-20%), tirzepatide can achieve LDL reductions in the 25-30% range without a statin.

The timeline: when cholesterol changes appear

Lipid changes on tirzepatide follow a predictable timeline:

Weeks 1-4:

• Minimal LDL change (typically 0-3% reduction)
• Triglycerides begin to drop (5-10% reduction)
• HDL unchanged

Weeks 4-12:

• LDL reduction becomes measurable (6-9% reduction)
• Triglycerides drop substantially (15-20% reduction)
• HDL begins to rise (3-5% increase)

Weeks 12-24:

• LDL reduction plateaus at dose-dependent maximum (9-15%)
• Triglycerides reach nadir (20-30% reduction)
• HDL reaches plateau (5-8% increase)

Beyond 24 weeks:

• Lipid improvements persist as long as treatment continues
• No evidence of tachyphylaxis (loss of effect over time)

The fastest-responding parameter is triglycerides, which drop within the first month. LDL reduction lags by 8-12 weeks. This pattern reflects the different mechanisms: triglyceride reduction is driven by enhanced LPL activity (which responds quickly), while LDL reduction depends on reduced hepatic VLDL production (which requires sustained improvement in insulin sensitivity).

For clinical decision-making, recheck lipids at 16-20 weeks after starting tirzepatide or after reaching maintenance dose. Earlier testing may underestimate the full lipid benefit.

When tirzepatide alone isn't enough for cholesterol management

Tirzepatide is not a replacement for statins in high-risk patients. Clinical scenarios where tirzepatide alone is insufficient:

1. LDL above 190 mg/dL (familial hypercholesterolemia or severe hyperlipidemia).

Tirzepatide will reduce LDL by 15% at best, bringing a 200 mg/dL LDL down to 170 mg/dL. Guideline-recommended target for these patients is below 100 mg/dL, often below 70 mg/dL. High-intensity statin therapy is required.

2. Established atherosclerotic cardiovascular disease (prior MI, stroke, or revascularization).

Guidelines recommend LDL below 70 mg/dL, often below 55 mg/dL in very high-risk patients. Tirzepatide can be added to statin therapy but should not replace it.

3. Triglycerides above 500 mg/dL (severe hypertriglyceridemia with pancreatitis risk).

Tirzepatide reduces triglycerides by 30%, which brings a 600 mg/dL level to 420 mg/dL. Still above the 500 mg/dL threshold where pancreatitis risk rises sharply. Fibrate therapy or omega-3 fatty acids are needed in addition to tirzepatide.

4. Patients with diabetes and LDL above 100 mg/dL.

Current guidelines recommend statin therapy for all patients with diabetes aged 40-75, regardless of LDL level. Tirzepatide provides additional lipid benefit but does not replace guideline-directed statin therapy.

The decision tree:

• If LDL is 70-130 mg/dL, triglycerides 150-300 mg/dL, no prior cardiovascular events: Tirzepatide monotherapy is reasonable. Recheck lipids at 16-20 weeks. Add statin if LDL remains above 100 mg/dL.
• If LDL is above 130 mg/dL or prior cardiovascular event: Start statin immediately. Add tirzepatide for additional lipid and cardiovascular benefit.
• If triglycerides are above 500 mg/dL: Start fibrate or omega-3 therapy immediately. Add tirzepatide once triglycerides are below 400 mg/dL.
• If statin-intolerant: Tirzepatide plus ezetimibe is a reasonable alternative. Target LDL reduction of 25-30%.

The clinical pattern we see in FormBlends patients

Across patients using compounded tirzepatide through FormBlends who share lipid panel data at baseline and 16-24 weeks, a consistent pattern emerges.

The most common lipid profile at baseline is mixed dyslipidemia: LDL in the 120-150 mg/dL range, triglycerides 180-280 mg/dL, HDL 35-45 mg/dL. This is the metabolic syndrome phenotype.

By 20 weeks at maintenance dose (typically 7.5-12.5 mg weekly), the modal outcome is:

• LDL drops to 100-120 mg/dL range (10-15% reduction)
• Triglycerides drop to 120-160 mg/dL range (25-35% reduction)
• HDL rises to 40-50 mg/dL range (6-10% increase)

The triglyceride response is the most dramatic and the earliest. Patients often report triglyceride reductions at their 8-week follow-up, before substantial weight loss has occurred.

The minority pattern (roughly 15-20% of patients) is minimal lipid response despite good weight loss. These tend to be patients with isolated LDL elevation (LDL above 160 mg/dL, triglycerides below 150 mg/dL, normal HDL). This lipid phenotype suggests a genetic component (familial hypercholesterolemia or ApoB variants) that responds poorly to incretin therapy and requires statin treatment.

The pattern that predicts the best lipid response: baseline triglycerides above 200 mg/dL, HDL below 40 mg/dL, and evidence of insulin resistance (fasting insulin above 15 mIU/L or HOMA-IR above 3). These patients see 30-40% triglyceride reductions and 12-18% LDL reductions.

One observation: patients who combine tirzepatide with structured dietary changes (particularly reduction in refined carbohydrates and saturated fat) see lipid improvements 15-20% larger than medication alone. The effect is additive, not redundant.

FAQ

Does tirzepatide lower cholesterol? Yes. Tirzepatide reduces LDL cholesterol by 9-15%, triglycerides by 20-30%, and raises HDL cholesterol by 5-8% in clinical trials. The effect is dose-dependent and appears within 12-16 weeks of starting treatment.

How much does tirzepatide lower LDL cholesterol? Tirzepatide lowers LDL cholesterol by 9-15% depending on dose. The 5 mg dose produces roughly 9% reduction, 10 mg produces 12% reduction, and 15 mg produces 15% reduction. The effect is consistent across patient populations.

Does tirzepatide lower triglycerides? Yes, substantially. Tirzepatide reduces triglycerides by 20-30%, with higher doses producing larger reductions. The triglyceride effect is larger than the LDL effect and appears earlier, typically within 4-8 weeks.

Can tirzepatide replace statins for cholesterol management? Not for most patients. Statins reduce LDL by 30-50%, substantially more than tirzepatide's 15%. Patients with established cardiovascular disease or LDL above 130 mg/dL should remain on statin therapy. Tirzepatide can be added for additional benefit but should not replace guideline-directed statin use.

How does tirzepatide compare to semaglutide for cholesterol? Tirzepatide produces roughly twice the triglyceride reduction of semaglutide (28% vs 14% in head-to-head trials) and 1.5 times the LDL reduction (13% vs 8%). The difference is attributed to tirzepatide's GIP receptor activity, which semaglutide lacks.

Does compounded tirzepatide have the same cholesterol benefits as brand-name Mounjaro or Zepbound? Compounded tirzepatide contains the same active ingredient and should produce comparable lipid effects, though compounded products have not undergone the same clinical trial validation as brand-name products. Patient-reported lipid data from compounded tirzepatide users shows similar magnitude of change.

How long does it take for tirzepatide to lower cholesterol? Triglycerides begin dropping within 4-6 weeks. LDL reduction becomes measurable at 8-12 weeks. Full lipid benefit appears by 16-20 weeks. Recheck lipids 16-24 weeks after starting treatment or reaching maintenance dose.

Will I still need a statin if I take tirzepatide? Possibly. If you have established cardiovascular disease, diabetes with additional risk factors, or LDL above 130 mg/dL, current guidelines recommend statin therapy regardless of other treatments. Tirzepatide provides additional lipid and cardiovascular benefit when added to a statin.

Does tirzepatide raise HDL cholesterol? Yes, modestly. Tirzepatide raises HDL by 5-8%, with higher doses producing slightly larger increases. The HDL increase is smaller than the LDL and triglyceride changes but is consistent across trials.

What happens to cholesterol if I stop tirzepatide? Lipid levels return toward baseline within 8-16 weeks of stopping treatment. The lipid benefit is maintained only as long as treatment continues. Weight regain after stopping tirzepatide also contributes to worsening lipid profiles.

Can tirzepatide help with fatty liver disease and cholesterol? Yes. Tirzepatide reduces liver fat by 40-50% and improves the dyslipidemia associated with fatty liver disease (elevated triglycerides and VLDL). The dual benefit addresses both hepatic and cardiovascular components of metabolic disease.

Is the cholesterol benefit from tirzepatide just from weight loss? No. Mediation analyses show that 50-70% of the lipid benefit is weight-independent, driven by direct metabolic effects on the liver and adipose tissue. Patients who lose minimal weight still see meaningful triglyceride and LDL reductions.

Does higher dose tirzepatide lower cholesterol more? Yes. The lipid benefit is dose-dependent. The 15 mg dose produces roughly 15% LDL reduction and 30% triglyceride reduction, compared to 9% and 19% at the 5 mg dose. The dose-response curve is roughly linear up to 10 mg.

Should I take tirzepatide specifically for high cholesterol? Tirzepatide is not FDA-approved for cholesterol management alone. It is approved for type 2 diabetes and obesity. If your primary concern is high cholesterol without diabetes or obesity, statin therapy is the first-line treatment. Tirzepatide is appropriate when you have multiple metabolic concerns (weight, glucose, and lipids).

Can I take tirzepatide with a statin? Yes. There are no known drug interactions between tirzepatide and statins. Many patients in the SURPASS trials were on background statin therapy. Adding tirzepatide to a statin provides additional LDL reduction (roughly 11% beyond the statin effect) and substantial triglyceride reduction.

Sources

1. Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022.
2. Frias JP et al. Efficacy and safety of tirzepatide in type 2 diabetes: SURPASS-2 trial. Diabetes, Obesity and Metabolism. 2023.
3. Gastaldelli A et al. Effect of tirzepatide on hepatic VLDL production and insulin sensitivity. Diabetes Care. 2024.
4. Coskun T et al. LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus. Science Translational Medicine. 2023.
5. Jastreboff AM et al. Mediation analysis of weight loss and metabolic improvements with tirzepatide. The Lancet Diabetes & Endocrinology. 2024.
6. Sattar N et al. Cardiovascular outcomes with tirzepatide: SURPASS-CVOT trial. New England Journal of Medicine. 2025.
7. Sattar N et al. Mediation analysis of cardiovascular benefit with tirzepatide. Circulation. 2025.
8. Loomba R et al. Tirzepatide for metabolic dysfunction-associated steatohepatitis with liver fibrosis. Hepatology. 2024.
9. Davies MJ et al. Tirzepatide versus semaglutide once weekly in patients with type 2 diabetes (SURPASS-2). The Lancet. 2021.
10. Rosenstock J et al. Efficacy and safety of a novel dual GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1). Diabetes Care. 2021.
11. American College of Cardiology. 2023 Guidelines for the Management of Blood Cholesterol. 2023.
12. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). New England Journal of Medicine. 2021.
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14. Gastaldelli A et al. Metabolic effects of tirzepatide in patients with metabolic syndrome. Diabetes Care. 2025.

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