{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T12:42:41Z","timestamp":1791895361679,"version":"4.3.4"},"reference-count":65,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2020,9,4]],"date-time":"2020-09-04T00:00:00Z","timestamp":1599177600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Pineal Research"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Palmitic acid (PA), the main component of dietary saturated fat, has been known to increase in patients with obesity, and PA\u2010induced lipotoxicity may contribute to obesity\u2010related male infertility. Melatonin has beneficial effects on reproductive processes; however, the effect and the underlying molecular mechanism of melatonin's involvement in PA\u2010induced cytotoxicity in the testes are poorly understood. Our findings showed that lipotoxicity was observed in mouse testes after long\u2010term PA treatment and that melatonin therapy restored spermatogenesis and fertility in these males. Moreover, melatonin therapy suppressed PA\u2010induced apoptosis by modulating apoptosis\u2010associated proteins such as Bcl2, Bax, C\u2010Caspase3, C\u2010Caspase12, and CHOP in type B spermatogonial stem cells. Changes in the expression of endoplasmic reticulum (ER) stress markers (p\u2010IRE1, p\u2010PERK, ATF4) and intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    levels showed that melatonin relieved PA\u2010induced ER stress. Mechanistically, melatonin stimulated the expression and nuclear translocation of SIRT1 through its receptors and prevented PA\u2010induced ROS production and mitochondrial dysfunction via SIRT1 signaling pathway. Furthermore, melatonin promoted SIRT1\u2010mediated p53 deacetylation, thereby relieving G2\/M arrest in response to PA\u2010stimulated DNA damage. Collectively, these findings indicate that melatonin protects the testes from PA\u2010induced lipotoxicity through the activation of SIRT1, which alleviates oxidative stress, ER stress, mitochondrial dysfunction, and DNA damage.\n                  <\/jats:p>","DOI":"10.1111\/jpi.12690","type":"journal-article","created":{"date-parts":[[2020,8,6]],"date-time":"2020-08-06T20:27:10Z","timestamp":1596745630000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":219,"title":["Melatonin protects mouse testes from palmitic acid\u2010induced lipotoxicity by attenuating oxidative stress and DNA damage in a SIRT1\u2010dependent manner"],"prefix":"10.1111","volume":"69","author":[{"given":"Dejun","family":"Xu","sequence":"first","affiliation":[{"name":"College of Animal Science and Technology Southwest University  Chongqing China"},{"name":"College of Animal Science and Technology Northwest A&amp;F University  Yangling 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