Wu, C.-F.C.-F.WuHou, P.-H.P.-H.HouMao, F.C.F.C.MaoSu, Y.-C.Y.-C.SuWu, C.-Y.C.-Y.WuWEI-CHENG YANGCHEN-SI LINTsai, H.-P.H.-P.TsaiLiao, H.-J.H.-J.LiaoChang, G.-R.G.-R.Chang2021-03-042021-03-042020https://www.scopus.com/inward/record.url?eid=2-s2.0-85089668642&partnerID=40&md5=e1b97c9990b8f8203032fc236bcbb825https://scholars.lib.ntu.edu.tw/handle/123456789/550729Metabolic syndrome is known to engender type 2 diabetes as well as some cardiac, cerebrovascular, and kidney diseases. Mirtazapine—an atypical second-generation antipsychotic drug with less severe side effects than atypical first-generation antipsychotics—may have positive effects on blood glucose levels and obesity. In our executed study, we treated male high-fat diet (HFD)-fed C57BL/6J mice with mirtazapine (10 mg/kg/day mirtazapine) for 4 weeks to understand its antiobesity effects. We noted these mice to exhibit lower insulin levels, daily food efficiency, body weight, serum triglyceride levels, aspartate aminotransferase levels, liver and epididymal fat pad weight, and fatty acid regulation marker expression when compared with their counterparts (i.e., HFD-fed control mice). Furthermore, we determined a considerable drop in fatty liver scores and mean fat cell size in the epididymal white adipose tissue in the treated mice, corresponding to AMP-activated protein kinase expression activation. Notably, the treated mice showed lower glucose tolerance and blood glucose levels, but higher glucose transporter 4 expression. Overall, the aforementioned findings signify that mirtazapine could reduce lipid accumulation and thus prevent HFD-induced increase in body weight. In conclusion, mirtazapine may be useful in body weight control and antihyperglycemia therapy. ? 2020 by the authors. Licensee MDPI, Basel, Switzerland.Adipocyte; Blood glucose; Insulin; Mirtazapine; Obesity[SDGs]SDG3aspartate aminotransferase; fatty acid synthase; glucose transporter; glucose transporter 4; mirtazapine; triacylglycerol; AMPK signaling; animal experiment; animal model; animal tissue; Article; body weight; controlled study; diet-induced obesity; enzyme linked immunosorbent assay; epididymis fat; fatty acid blood level; fatty liver; food intake; gastrocnemius muscle; glucose blood level; glucose homeostasis; glucose metabolism; glucose tolerance test; histology; homeostasis model assessment; hyperglycemia; hypertrophy; insulin blood level; insulin resistance; insulin sensitivity; lipid diet; lipid storage; liver weight; male; morphometry; mouse; non insulin dependent diabetes mellitus; nonhuman; obesity; protein expression; Western blottingjournal article10.3390/ani10081423328240022-s2.0-85089668642WOS:000565544100001