{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T12:30:43Z","timestamp":1790771443983,"version":"4.1.0"},"reference-count":41,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,9,14]],"date-time":"2025-09-14T00:00:00Z","timestamp":1757808000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Anim Models and Exp Med"],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Type 2 Diabetes (T2D) is a growing global health issue, often aggravated by excessive sugar intake. Chronic high\u2010sucrose diets contribute to insulin resistance, oxidative stress, and pancreatic dysfunction, worsening metabolic health. Sodium\u2010glucose co\u2010transporter 2 (SGLT2) inhibitors, like empagliflozin, show potential in improving glycemic control and metabolic parameters, but their effects on pancreatic efficiency in sugar\u2010induced T2D are not well understood. This study aimed to explore the effects of empagliflozin on metabolic and pancreatic protection in a high\u2010sucrose diet\u2010induced T2D model. Male Wistar rats were divided into four groups: normal, normal\u2010treated, diabetic, and diabetic\u2010treated (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20098 per group). Diabetes was induced with a 35% sucrose solution for 8\u2009weeks, followed by a low\u2010dose streptozotocin (STZ) injection. Treated groups received empagliflozin (15\u2009mg\/kg\/day) for the duration. Biochemical markers, including fasting blood sugar (FBS), lipid profile, insulin levels, and oxidative stress markers, were measured. Insulin resistance (HOMA\u2010IR) and pancreatic function (HOMA\u2010B) were assessed. Histological analysis of pancreatic tissues was performed. The high\u2010sucrose diet increased FBS, insulin resistance, and oxidative stress, while decreasing pancreatic function and islet diameter. Empagliflozin treatment lowered FBS (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001), improved insulin sensitivity (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001), reduced triglycerides (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001), and LDL (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.05). It also enhanced antioxidant enzymes, reduced lipid peroxidation (MDA,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001), and preserved pancreatic islet structure (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001). A high\u2010sucrose diet negatively affects metabolic health and pancreatic function. Empagliflozin mitigates these effects by improving metabolism, reducing oxidative stress, and preserving pancreatic integrity, suggesting its potential as a therapeutic agent in diabetes related to excessive sugar consumption.\n                  <\/jats:p>","DOI":"10.1002\/ame2.70081","type":"journal-article","created":{"date-parts":[[2025,9,15]],"date-time":"2025-09-15T06:30:49Z","timestamp":1757917849000},"page":"2091-2098","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Innovative insights into the effects of a high\u2010sucrose diet on pancreatic health and the therapeutic role of empagliflozin in type 2 diabetes: An experimental study"],"prefix":"10.1002","volume":"8","author":[{"given":"Emad","family":"Gholami","sequence":"first","affiliation":[{"name":"Research Center of Physiology Semnan University of Medical Sciences  Semnan 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