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Adult male rats (10 rats\/group) were divided into four groups: control fed standard diet (<jats:styled-content style=\"fixed-case\">STD<\/jats:styled-content>) (3.82\u00a0kcal\/g, 9.4% fat), <jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content> (5.4\u00a0kcal\/g, 40% fat), T1<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> fed <jats:styled-content style=\"fixed-case\">STD<\/jats:styled-content>, and T1<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content> and T1<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> alone or in combination impaired systolic and diastolic functions of rats and significantly reduced levels of <jats:styled-content style=\"fixed-case\">GSH<\/jats:styled-content> and the activity of <jats:styled-content style=\"fixed-case\">SOD<\/jats:styled-content>, enhanced lipid peroxidation, increased protein levels of P53, Bax, cleaved caspase\u20103, and <jats:styled-content style=\"fixed-case\">ANF<\/jats:styled-content> and decreased levels of Bcl\u20102 in their atria. Concomitantly, atrial cells exhibited fragmentation of the myofibrils, disorganized mitochondria, decreased number of atrionatriuretic factor (<jats:styled-content style=\"fixed-case\">ANF<\/jats:styled-content>) granules, and loss of gap junctions accompanied by changes in capillary walls. Among all treatments, the severity of all these findings was more severe in T1<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> and most profound in the atria of T1<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>. In conclusion, chronic consumption of <jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content> by T1<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>\u2010induced rats elicits significant biochemical and ultrastructural damage to rat atrial cells accompanied by elevated oxidative stress and mitochondria\u2010mediated cell death.<\/jats:p>","DOI":"10.1111\/1440-1681.13158","type":"journal-article","created":{"date-parts":[[2019,8,9]],"date-time":"2019-08-09T17:18:32Z","timestamp":1565371112000},"page":"1111-1123","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Chronic consumption of a high\u2010fat diet rich in corn oil activates intrinsic cell death pathway and induces several ultrastructural changes in the atria of healthy and type 1 diabetic 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