{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T20:00:02Z","timestamp":1791576002974,"version":"4.3.4"},"reference-count":41,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,6,16]],"date-time":"2025-06-16T00:00:00Z","timestamp":1750032000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2025,9]]},"abstract":"Abstract<\/jats:title>\n \n Aims<\/jats:title>\n Saroglitazar is a dual peroxisome proliferator\u2010activated receptor (PPAR), predominantly a PPAR\u2010\u03b1 agonist and a moderate PPAR\u2010\u03b3 agonist activity, which has shown positive effects in diabetic dyslipidaemia. However, its potential anti\u2010diabetic effect has not been thoroughly investigated, and the data have been inconsistent. Thus, we conducted a meta\u2010analysis to examine the impact of saroglitazar on glycaemic markers in patients with dyslipidaemia, type 2 diabetes and non\u2010alcoholic fatty liver disease.<\/jats:p>\n <\/jats:sec>\n \n Materials and Methods<\/jats:title>\n \n The search strategy was conducted in PubMed, Web of Science, Scopus,\n ClinicalTrials.gov<\/jats:ext-link>\n and Google Scholar databases. Randomized controlled trials reporting changes in glycaemic parameters after saroglitazar therapy were selected. The Cochrane risk\u2010of\u2010bias tool for randomized trials version 2 was used to assess the quality of the included studies. For meta\u2010analysis, a random\u2010effects model and the generic inverse variance method were conducted. Also, the leave\u2010one\u2010out method was applied for the sensitivity analysis.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n A total of 10 clinical trials (\n N<\/jats:italic>\n \u2009=\u20092077; mean age: 49.7\u2009years; 40% female) were included. Regarding the quality of the included studies, two trials had a low risk of bias, seven trials showed some concerns and one study exhibited a high risk of bias. The meta\u2010analysis of 10 randomized controlled trials showed that saroglitazar significantly reduces fasting glucose (weighted mean difference [WMD]: \u221212.11\u2009mg\/dL, 95% CI: \u221214.79, \u22129.43,\n p<\/jats:italic>\n \u2009<\u20090.0001,\n I<\/jats:italic>\n 2<\/jats:sup>\n \u2009=\u200940%), postprandial glucose (WMD: \u221216.17\u2009mg\/dL, 95% CI: \u221222.29, \u221210.04,\n p<\/jats:italic>\n \u2009<\u20090.0001,\n I<\/jats:italic>\n 2<\/jats:sup>\n \u2009=\u20090%) and HbA1c (WMD: \u22120.39%, 95% CI: \u22120.57, \u22120.22,\n p<\/jats:italic>\n \u2009<\u20090.0001,\n I<\/jats:italic>\n 2<\/jats:sup>\n \u2009=\u200972%) compared to active control or placebo. However, there was no significant effect on insulin levels (WMD: \u22121.03 \u03bcU\/mL, 95% CI: \u22124.12, 2.06,\n p<\/jats:italic>\n \u2009=\u20090.51,\n I<\/jats:italic>\n 2<\/jats:sup>\n \u2009=\u200937%), HOMA\u2010IR (WMD: \u20130.41, 95% CI: \u22120.86, 0.04,\n p<\/jats:italic>\n \u2009=\u20090.07,\n I<\/jats:italic>\n 2<\/jats:sup>\n \u2009=\u200941%) and C\u2010peptide (WMD: \u22120.30\u2009ng\/mL, 95% CI: \u22120.76, 0.15,\n p<\/jats:italic>\n \u2009=\u20090.19,\n I<\/jats:italic>\n 2<\/jats:sup>\n \u2009=\u20090%) after saroglitazar therapy.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Our results revealed that saroglitazar therapy improves glycaemic parameters through the reduction of fasting glucose, postprandial glucose and HbA1c.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/dom.16506","type":"journal-article","created":{"date-parts":[[2025,6,16]],"date-time":"2025-06-16T08:22:47Z","timestamp":1750062167000},"page":"4627-4642","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Effect of saroglitazar on glycaemic parameters: A systematic review and meta\u2010analysis of randomized controlled trials"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3617-4921","authenticated-orcid":false,"given":"Luis E.","family":"Simental\u2010Mend\u00eda","sequence":"first","affiliation":[{"name":"Unidad de Investigaci\u00f3n Biom\u00e9dica, Delegaci\u00f3n Durango Instituto Mexicano del Seguro Social Durango M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario","family":"Simental\u2010Mend\u00eda","sequence":"additional","affiliation":[{"name":"Department of Orthopedics and Traumatology, Hospital Universitario \u201cDr. Jos\u00e9 E. Gonz\u00e1lez\u201d, Facultad de Medicina Universidad Aut\u00f3noma de Nuevo Le\u00f3n Monterrey M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura Jazel","family":"Barrag\u00e1n\u2010Zu\u00f1iga","sequence":"additional","affiliation":[{"name":"Centro Estatal de Cancerolog\u00eda Durango Mexico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana","family":"Arce\u2010Qui\u00f1ones","sequence":"additional","affiliation":[{"name":"Unidad de Investigaci\u00f3n Biom\u00e9dica, Delegaci\u00f3n Durango Instituto Mexicano del Seguro Social Durango M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,6,16]]},"reference":[{"key":"e_1_2_9_2_1","unstructured":"IDF DIABETES ATLAS [Internet] \u2010 PubMed. 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