Hasan Sohel, Amin Md Aminul Islam, Mia Masum, Khatun Sumaiya, Arafat Yesir, Gofur Md Royhan, Islam Md Mahmudul, Hosen Md Eram, Almaary Khalid S, Fentahun Wondmie Gezahign, Islam Amirul, Rahman Matiar, Bourhia Mohammed
Molecular and Biomedical Research Lab (MBRL), Department of Biochemistry and Molecular Biology University of Rajshahi Rajshahi Bangladesh.
Department of Veterinary and Animal Sciences University of Rajshahi Rajshahi Bangladesh.
Food Sci Nutr. 2024 Dec 5;13(1):e4650. doi: 10.1002/fsn3.4650. eCollection 2025 Jan.
Hepatic steatosis/non-alcoholic fatty liver disease is a major public health delinquent caused by the excess deposition of lipid into lipid droplets (LDs) as well as metabolic dysregulation. Hepatic cells buildup with more fat molecules when a person takes high fat diet that is excessive than the body can handle. At present, millions of people in the world are affected by this problem. So, it is very important to know the effects of factors responsible for the disease. Here, the role of lipid droplet (LD) biogenesis and metabolism was analyzed and intended to investigate if defects in biogenesis/metabolic enzymes are responsible for the accumulation of lipids other than LDs in fatty liver disease in high-fat-induced conditions in mice model. To explore it, high-fat diet (HFD), fast food (FF), and soft drinks (SD) were administered to wild-type Swiss albino mice for 14 weeks following yogurt supplementation. After experimental period, glucose tolerance, enzyme function, lipid profile, plasma biochemistry, and other analytical tests were analyzed by auto-analyzer including different oxidative stress markers. Lipids from hepatic tissues were extracted, and purified by Floatation Assay and subsequently analyzed by different biochemical and chromatographic techniques. Histological architecture of hepatocytes was performed using Zeiss microscope. Finally, increased amount of lipids biogenesis/accumulation was found in liver tissues that causes Fatty liver disease. Significantly, HFD, FF, and SD were identified as factors for the increased LD biogenesis and or lipid metabolic disorder. Nevertheless, yogurt supplementation can homeostasis those LD formation and metabolic syndrome as it increases the down regulation of lipid biogenesis as well as lipid metabolic rate. So, yogurt supplementation was considered as a novel agent for decreasing LD biogenesis as well as excessive accumulation of fat in hepatocytes which can be used as therapeutics for the treatment of NAFLD.
肝脂肪变性/非酒精性脂肪性肝病是一种主要的公共卫生问题,它是由脂质过度沉积到脂滴(LDs)以及代谢失调引起的。当一个人摄入的高脂肪饮食超过身体所能承受的量时,肝细胞中会积累更多的脂肪分子。目前,世界上数百万人受此问题影响。因此,了解导致该疾病的因素的作用非常重要。在此,分析了脂滴(LD)生物发生和代谢的作用,并旨在研究在高脂诱导的小鼠模型中,生物发生/代谢酶的缺陷是否是导致脂肪肝疾病中除LDs之外的脂质积累的原因。为了探究这一点,在给野生型瑞士白化小鼠补充酸奶后,对其给予高脂饮食(HFD)、快餐(FF)和软饮料(SD),持续14周。实验期结束后,通过自动分析仪分析葡萄糖耐量、酶功能、血脂谱、血浆生化以及包括不同氧化应激标志物在内的其他分析测试。从肝组织中提取脂质,通过浮选法进行纯化,随后采用不同的生化和色谱技术进行分析。使用蔡司显微镜观察肝细胞的组织学结构。最后,在导致脂肪肝疾病的肝组织中发现脂质生物发生/积累量增加。值得注意的是,HFD、FF和SD被确定为导致LD生物发生增加和/或脂质代谢紊乱的因素。然而,补充酸奶可以使那些LD的形成和代谢综合征恢复稳态,因为它增加了脂质生物发生的下调以及脂质代谢率。因此,补充酸奶被认为是一种新型药物,可减少LD生物发生以及肝细胞中脂肪的过度积累,可用于治疗非酒精性脂肪性肝病。