{"title":"维生素D与非酒精性脂肪肝之间的分子串扰","authors":"Subendu Sarkar","doi":"10.14218/erhm.2023.00019","DOIUrl":null,"url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver disease. The worldwide increasing prevalence of NAFLD has become a cause of concern for clinicians. Furthermore, the molecular mechanism of NAFLD pathogenesis remains poorly understood. Moreover, therapeutic interventions are presently limited. Balanced diet, physical exercise and lifestyle modifications have been recommended. Several studies have revealed that vitamin D deficiency is correlated with NAFLD, and it’s supplementation may play a vital role in this regard. Sufficient information was obtained from full articles written in the English language, and accessible in PubMed, Google Scholar, Web of Science, and Scopus. The increasing prevalence of vitamin D deficiency remains as a global health risk factor, and this is linked to NAFLD pathogenesis. In vitro and in vivo studies, and clinical trials have revealed the beneficial role of vitamin D supplementation to control NAFLD. Vitamin D potentially regulates the molecular pathways associated with NAFLD risk factors, such as obesity, insulin resistance, and diabetes. It acts on adipocytes to control free fatty acid (FFA) trafficking, lipogenesis, and inflammation. Similarly, vitamin D acts on hepatocytes to reduce de novo lipogenesis and cellular FFA trafficking. Furthermore, it acts on pancreatic β-cells to im - prove insulin secretion, cell survival, and cellular functions. Vitamin D supplementation improves glucose uptake and insulin sensitivity. In addition, it decreases inflammation and liver injury, and acts on mitochondria to control reactive oxygen species (ROS)-mediated cellular toxicity. Vitamin D deficiency is a major risk factor for NAFLD pathogenesis. Thus, there is an urgent need to conduct molecular level analysis for further discernments","PeriodicalId":12074,"journal":{"name":"Exploratory Research and Hypothesis in Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Molecular Crosstalk Between Vitamin D and Non-alcoholic Fatty Liver Disease\",\"authors\":\"Subendu Sarkar\",\"doi\":\"10.14218/erhm.2023.00019\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver disease. The worldwide increasing prevalence of NAFLD has become a cause of concern for clinicians. Furthermore, the molecular mechanism of NAFLD pathogenesis remains poorly understood. Moreover, therapeutic interventions are presently limited. Balanced diet, physical exercise and lifestyle modifications have been recommended. Several studies have revealed that vitamin D deficiency is correlated with NAFLD, and it’s supplementation may play a vital role in this regard. Sufficient information was obtained from full articles written in the English language, and accessible in PubMed, Google Scholar, Web of Science, and Scopus. The increasing prevalence of vitamin D deficiency remains as a global health risk factor, and this is linked to NAFLD pathogenesis. In vitro and in vivo studies, and clinical trials have revealed the beneficial role of vitamin D supplementation to control NAFLD. Vitamin D potentially regulates the molecular pathways associated with NAFLD risk factors, such as obesity, insulin resistance, and diabetes. It acts on adipocytes to control free fatty acid (FFA) trafficking, lipogenesis, and inflammation. Similarly, vitamin D acts on hepatocytes to reduce de novo lipogenesis and cellular FFA trafficking. Furthermore, it acts on pancreatic β-cells to im - prove insulin secretion, cell survival, and cellular functions. Vitamin D supplementation improves glucose uptake and insulin sensitivity. In addition, it decreases inflammation and liver injury, and acts on mitochondria to control reactive oxygen species (ROS)-mediated cellular toxicity. Vitamin D deficiency is a major risk factor for NAFLD pathogenesis. 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引用次数: 0
摘要
非酒精性脂肪性肝病(NAFLD)是慢性肝病的主要原因之一。全球范围内NAFLD患病率的上升已经成为临床医生关注的一个原因。此外,NAFLD发病的分子机制尚不清楚。此外,治疗干预目前是有限的。建议均衡饮食、体育锻炼和改变生活方式。几项研究表明,维生素D缺乏与NAFLD有关,补充维生素D可能在这方面起着至关重要的作用。充分的信息是从用英语撰写的完整文章中获得的,并且可以在PubMed, Google Scholar, Web of Science和Scopus中访问。维生素D缺乏症的日益流行仍然是一个全球健康风险因素,这与NAFLD的发病机制有关。体外和体内研究以及临床试验显示,补充维生素D对控制NAFLD有有益作用。维生素D可能调节与NAFLD风险因素相关的分子途径,如肥胖、胰岛素抵抗和糖尿病。它作用于脂肪细胞,控制游离脂肪酸(FFA)的运输、脂肪生成和炎症。同样,维生素D作用于肝细胞,减少新生脂肪生成和细胞游离脂肪酸运输。此外,它还作用于胰腺β细胞,改善胰岛素分泌、细胞存活和细胞功能。补充维生素D可以改善葡萄糖摄取和胰岛素敏感性。此外,它还能减少炎症和肝损伤,并作用于线粒体来控制活性氧(ROS)介导的细胞毒性。维生素D缺乏是NAFLD发病的主要危险因素。因此,迫切需要进行分子水平分析以进一步鉴别
Molecular Crosstalk Between Vitamin D and Non-alcoholic Fatty Liver Disease
Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver disease. The worldwide increasing prevalence of NAFLD has become a cause of concern for clinicians. Furthermore, the molecular mechanism of NAFLD pathogenesis remains poorly understood. Moreover, therapeutic interventions are presently limited. Balanced diet, physical exercise and lifestyle modifications have been recommended. Several studies have revealed that vitamin D deficiency is correlated with NAFLD, and it’s supplementation may play a vital role in this regard. Sufficient information was obtained from full articles written in the English language, and accessible in PubMed, Google Scholar, Web of Science, and Scopus. The increasing prevalence of vitamin D deficiency remains as a global health risk factor, and this is linked to NAFLD pathogenesis. In vitro and in vivo studies, and clinical trials have revealed the beneficial role of vitamin D supplementation to control NAFLD. Vitamin D potentially regulates the molecular pathways associated with NAFLD risk factors, such as obesity, insulin resistance, and diabetes. It acts on adipocytes to control free fatty acid (FFA) trafficking, lipogenesis, and inflammation. Similarly, vitamin D acts on hepatocytes to reduce de novo lipogenesis and cellular FFA trafficking. Furthermore, it acts on pancreatic β-cells to im - prove insulin secretion, cell survival, and cellular functions. Vitamin D supplementation improves glucose uptake and insulin sensitivity. In addition, it decreases inflammation and liver injury, and acts on mitochondria to control reactive oxygen species (ROS)-mediated cellular toxicity. Vitamin D deficiency is a major risk factor for NAFLD pathogenesis. Thus, there is an urgent need to conduct molecular level analysis for further discernments