Department of Endocrinology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Department of Cardiology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
J Gastroenterol Hepatol. 2020 Nov;35(11):1978-1989. doi: 10.1111/jgh.15005. Epub 2020 Feb 23.
Non-alcoholic fatty liver disease (NAFLD) is a growing public health concern worldwide. With the progression of urbanization, light pollution is becoming an inevitable risk factor for NAFLD. However, the role of light pollution on NAFLD is insufficiently understood, and the underlying mechanism remains unclear. The present study explored effects of constant light exposure on NAFLD and elucidated its related mechanisms.
Thirty-two male Sprague Dawley rats were divided into four groups (n = 8 each): (i) rats on a normal diet exposed to standard light-dark cycle (ND-LD); (ii) rats on a normal diet exposed to constant light (ND-LL); (iii) rats on a high-fat diet exposed to standard light-dark cycle (HFD-LD); and (iv) and rats on a high-fat diet exposed to constant light (HFD-LL). After 12 weeks of treatment, rats were sacrificed and pathophysiological assessments were performed. Targeted lipidomics was used to measure sphingolipids, including ceramides, glucosylceramides, and lactosylceramides, sphingomyelins, and sphingosine-1-phosphates in plasma and liver tissues.
In normal chow rats, constant light exposure led to glucose abnormalities and dyslipidemia. In high-fat-fed rats, constant light exposure exacerbated glucose abnormalities, dyslipidemia, insulin resistance, and inflammation and aggravated steatohepatitis. Compared with HFD-LD rats, HFD-LL had decreased plasma sphingosine-1-phosphate and elevated liver concentrations of total ceramide and specific ceramide species (ceramide d18:0/24:0, ceramide d18:1/22:0, ceramide d18:1/24:0, and ceramide d18:1/24:1), which were associated with increased hepatocyte apoptosis.
Constant light exposure causes dysregulation of sphingolipids and promotes steatohepatitis in high-fat-fed rats.
非酒精性脂肪性肝病（NAFLD）是全球日益严重的公共卫生问题。随着城市化进程的推进，光污染正成为 NAFLD 的一个不可避免的风险因素。然而，光污染对 NAFLD 的作用尚未得到充分认识，其潜在机制尚不清楚。本研究探讨了持续光照暴露对 NAFLD 的影响，并阐明了其相关机制。
32 只雄性 Sprague Dawley 大鼠随机分为 4 组（n=8）：（i）正常饮食暴露于明暗周期正常的大鼠（ND-LD）；（ii）正常饮食暴露于持续光照的大鼠（ND-LL）；（iii）高脂肪饮食暴露于明暗周期正常的大鼠（HFD-LD）；和（iv）高脂肪饮食暴露于持续光照的大鼠（HFD-LL）。治疗 12 周后处死大鼠并进行病理生理评估。靶向脂质组学用于测量血浆和肝组织中的鞘脂，包括神经酰胺、葡糖脑苷脂和半乳糖脑苷脂、神经鞘磷脂和鞘氨醇-1-磷酸。
在正常饲料大鼠中，持续光照导致葡萄糖异常和血脂异常。在高脂肪喂养的大鼠中，持续光照加重了葡萄糖异常、血脂异常、胰岛素抵抗和炎症，并加重了脂肪性肝炎。与 HFD-LD 大鼠相比，HFD-LL 大鼠血浆鞘氨醇-1-磷酸降低，肝脏总神经酰胺和特定神经酰胺种类（神经酰胺 d18：0/24：0、神经酰胺 d18：1/22：0、神经酰胺 d18：1/24：0 和神经酰胺 d18：1/24：1）浓度升高，与肝细胞凋亡增加有关。
持续光照导致鞘脂失调，并促进高脂肪喂养大鼠的脂肪性肝炎。
