Medical School of Ningbo University, Ningbo 315211, China.
Ningbo College of Health Sciences, Ningbo 315100, China.
Theranostics. 2020 Sep 15;10(25):11497-11506. doi: 10.7150/thno.50953. eCollection 2020.
Light pollution leads to high risk of obesity but the underlying mechanism is not known except for the influence of altered circadian rhythm. Peroxisome proliferator-activated receptor α (PPARα) regulates lipid metabolism, but its role in circadian-related obesity is not clear. Wild-type (WT) and null (KO) mice on a high-fat diet (HFD) were treated with neon light at night for 6 weeks. Body weights were recorded and diet consumption measured. The hypothalamus, liver, adipose and serum were collected for mechanism experimentation. WT mice on a HFD and exposed to night neon light gained about 19% body weight more than the WT control mice without light exposure and KO control mice on a HFD and exposed to night neon light. The increase in adipose tissue weight and adipocyte size led to the differences in body weights. Biochemical analysis suggested increased hepatic lipid accumulated and increased transport of lipid from the liver to peripheral tissues in the WT mice that gained weight under neon light exposure. Unlike KO mice, the expression of genes involved in lipid metabolism and the circadian factor circadian locomotor output cycles kaput (CLOCK) in both liver and adipose tissues were elevated in WT mice under neon light exposure. PPARα mediated weight gain of HFD-treated mice exposed to night neon light. More lipids were synthesized in the liver and transported to peripheral tissue leading to adaptive metabolism and lipid deposition in the adipose tissue. These data revealed an important mechanism of obesity induced by artificial light pollution where PPARα was implicated.
光污染会导致肥胖风险增加，但除了昼夜节律改变的影响外，其潜在机制尚不清楚。过氧化物酶体增殖物激活受体α（PPARα）调节脂代谢，但它在与昼夜节律相关的肥胖中的作用尚不清楚。在高脂肪饮食（HFD）中，野生型（WT）和缺失型（KO）小鼠接受夜间氖灯照射 6 周。记录体重并测量饮食消耗。收集下丘脑、肝脏、脂肪组织和血清进行机制实验。在 HFD 下的 WT 小鼠在夜间暴露于氖灯下，体重比未暴露于光的 WT 对照组小鼠和在 HFD 下暴露于夜间氖光的 KO 对照组小鼠增加了约 19%。脂肪组织重量和脂肪细胞大小的增加导致了体重的差异。生化分析表明，在氖灯下体重增加的 WT 小鼠中，肝脏脂质积累增加，脂质从肝脏向外周组织的转运增加。与 KO 小鼠不同，WT 小鼠在肝脏和脂肪组织中，与脂质代谢和昼夜节律因子昼夜运动输出周期 kaput（CLOCK）相关的基因表达在氖灯下均升高。PPARα介导了 HFD 处理的小鼠在夜间氖光暴露下的体重增加。肝脏合成的更多脂质并转运到外周组织，导致适应性代谢和脂肪组织中的脂质沉积。这些数据揭示了人工光污染导致肥胖的一个重要机制，其中涉及 PPARα。
