Saroglitazar, a Dual PPAR α/γ Agonist, Improves Atherogenic Dyslipidemia in Patients With Non-Cirrhotic Nonalcoholic Fatty Liver Disease: A Pooled Analysis.


Journal

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
ISSN: 1542-7714
Titre abrégé: Clin Gastroenterol Hepatol
Pays: United States
ID NLM: 101160775

Informations de publication

Date de publication:
09 2023
Historique:
received: 31 08 2022
revised: 23 11 2022
accepted: 17 01 2023
medline: 28 8 2023
pubmed: 3 2 2023
entrez: 2 2 2023
Statut: ppublish

Résumé

Cardiovascular disease is the leading cause of mortality in nonalcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the effects of saroglitazar, a dual peroxisome proliferator-activated receptor α/γ agonist, on serum lipids in patients with NAFLD. A total of 221 patients (saroglitazar, 130; placebo, 91) with NAFLD from phase 2 and 3 double-blinded placebo-controlled randomized clinical trials were pooled to assess the impact of saroglitazar magnesium 4 mg on traditional lipids, very low density lipoprotein cholesterol (VLDL-C), and small dense LDL-C (sdLDL-C). Change from baseline in lipid parameters was performed by using analysis of covariance including treatment as fixed effect and baseline value, diabetes, hypertension, and statin use as covariates. Treatment with saroglitazar significantly improved total cholesterol (-17 mg/dL, 95% confidence interval [CI], -24 to 9; P < .001), triglyceride (-45 mg/dL, 95% CI, -60 to 31; P < .001), low-density lipoprotein cholesterol (-8 mg/dL, 95% CI, -15 to -1; P = .01), and VLDL-C (-8 mg/dL, -14 to -3; P < .001). Saroglitazar improved serum lipids as early as 4-6 weeks of initiation of therapy, and these effects persisted for duration of therapy. Saroglitazar also improved the highly atherogenic sdLDL-C (-10 mg/dL, -17 to -2; P = .01). In subgroup analysis of patients with either diabetes or hypertension, saroglitazar significantly improved serum lipids. Saroglitazar improved the serum atherogenic lipoprotein profile in patients with NAFLD, irrespective of comorbid conditions and statin use. Saroglitazar has the potential to not only positively affect liver disease but also reduce cardiovascular risk in patients with NAFLD. (Trials registrations: CTRI 2015/10/006236, CTRI 173300410A0106, NCT03863574, and NCT03061721).

Sections du résumé

BACKGROUND & AIMS
Cardiovascular disease is the leading cause of mortality in nonalcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the effects of saroglitazar, a dual peroxisome proliferator-activated receptor α/γ agonist, on serum lipids in patients with NAFLD.
METHODS
A total of 221 patients (saroglitazar, 130; placebo, 91) with NAFLD from phase 2 and 3 double-blinded placebo-controlled randomized clinical trials were pooled to assess the impact of saroglitazar magnesium 4 mg on traditional lipids, very low density lipoprotein cholesterol (VLDL-C), and small dense LDL-C (sdLDL-C). Change from baseline in lipid parameters was performed by using analysis of covariance including treatment as fixed effect and baseline value, diabetes, hypertension, and statin use as covariates.
RESULTS
Treatment with saroglitazar significantly improved total cholesterol (-17 mg/dL, 95% confidence interval [CI], -24 to 9; P < .001), triglyceride (-45 mg/dL, 95% CI, -60 to 31; P < .001), low-density lipoprotein cholesterol (-8 mg/dL, 95% CI, -15 to -1; P = .01), and VLDL-C (-8 mg/dL, -14 to -3; P < .001). Saroglitazar improved serum lipids as early as 4-6 weeks of initiation of therapy, and these effects persisted for duration of therapy. Saroglitazar also improved the highly atherogenic sdLDL-C (-10 mg/dL, -17 to -2; P = .01). In subgroup analysis of patients with either diabetes or hypertension, saroglitazar significantly improved serum lipids.
CONCLUSIONS
Saroglitazar improved the serum atherogenic lipoprotein profile in patients with NAFLD, irrespective of comorbid conditions and statin use. Saroglitazar has the potential to not only positively affect liver disease but also reduce cardiovascular risk in patients with NAFLD. (Trials registrations: CTRI 2015/10/006236, CTRI 173300410A0106, NCT03863574, and NCT03061721).

Identifiants

pubmed: 36731585
pii: S1542-3565(23)00077-0
doi: 10.1016/j.cgh.2023.01.018
pii:
doi:

Substances chimiques

saroglitazar E0YMX3S4JD
PPAR alpha 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
PPAR-gamma Agonists 0
Triglycerides 0
Cholesterol 97C5T2UQ7J

Banques de données

ClinicalTrials.gov
['NCT03863574', 'NCT03061721']

Types de publication

Meta-Analysis Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2597-2605.e2

Informations de copyright

Copyright © 2023 AGA Institute. Published by Elsevier Inc. All rights reserved.

Auteurs

Mohammad Shadab Siddiqui (MS)

Virginia Commonwealth University, Richmond, Virginia. Electronic address: mohammad.siddiqui@vcuhealth.org.

Deven Parmar (D)

Zydus Therapeutics Inc USA, Pennington, NJ. Electronic address: dparmar@zydustherapeutics.com.

Farheen Sheikh (F)

Zydus Therapeutics Inc USA, Pennington, NJ.

Shiv Kumar Sarin (SK)

Department of Hepatology, Institute of Liver & Biliary Sciences, New Delhi, India.

Laura Cisneros (L)

Christus Muguerza Alta Especialidad, Monterrey, Mexico.

Samer Gawrieh (S)

Indiana University School of Medicine, Indianapolis, Indiana.

Taufik Momin (T)

Zydus Therapeutics Inc USA, Pennington, NJ.

Ajay Duseja (A)

Postgraduate Institute of Medical Education & Research, Chandigarh, India.

Arun J Sanyal (AJ)

Virginia Commonwealth University, Richmond, Virginia.

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Classifications MeSH