Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Department of Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan.
PLoS One. 2018 Apr 23;13(4):e0194867. doi: 10.1371/journal.pone.0194867. eCollection 2018.
Vitamin D deficiency and up-regulated TNFα-related signals are reported to be involved in abnormalities including intestinal hyper-permeability, bacterial translocation, systemic/portal endotoxemia, intestinal/adipose tissue/hepatic inflammation, and hepatic steatosis in nonalcoholic steatohepatitis (NASH). This study aims to explore the molecular mechanisms and effects of chronic calcitriol [1,25-(OH)2D3, hormonal form of vitamin D] on gut-adipose tissue-liver axis abnormalities using a high-fat diet (HFD)-fed rat model of NASH. In HFD-fed obese rats on a 10-week calcitriol (0.3 μg/kg/TIW) or vehicle treatment (NASH-vit. D and NASH-V rats) reigme, various in vivo and in vitro experiments were undertaken. Through anti-TNFα-TNFR1-NFκB signaling effects, chronic calcitriol treatment significantly restored plasma calcitriol levels and significantly improved vitamin D receptor (VDR) expression in monocytes and the small intestine of NASH-vit. D rats. Significantly, plasma and portal endotoxin/TNFα levels, bacterial translocation to mesenteric lymph nodes, plasma DX-4000-FITC, fecal albumin-assessed intestinal hyper-permeability, over-expression of TNFα-related immune profiles in monocytes, inflammation of intestinal/mesenteric adipose tissue (MAT)/liver and hepatic steatosis were improved by chronic calcitriol treatment of NASH rats. Additionally, in vitro experiments with acute calcitriol co-incubation reversed NASH-V rat monocyte supernatant/TNFα-induced monolayer barrier dysfunction in caco-2 cells, cytokine release from MAT-derived adipocytes, and triglyceride synthesis by lean-V rat hepatocytes. Using in vivo and in vitro experiments, our study reported calcitriol signaling in the gut as well as in adipose tissue. Meanwhile, our study suggests that restoration of systemic and intestinal vitamin D deficiency using by chronic vitamin D treatment effectively reduces TNFα-mediated immunological abnormalities associated with the gut-adipose tissue-liver axis and hepatic steatosis in NASH rats.
维生素 D 缺乏和上调的 TNFα 相关信号被报道与非酒精性脂肪性肝炎 (NASH) 中的异常有关,包括肠道通透性增加、细菌易位、全身/门脉内毒素血症、肠道/脂肪组织/肝脏炎症和肝脂肪变性。本研究旨在使用高脂肪饮食 (HFD) 喂养的 NASH 大鼠模型探索慢性骨化三醇 [1,25-(OH)2D3,维生素 D 的激素形式] 对肠道-脂肪组织-肝脏轴异常的分子机制和影响。在 HFD 喂养的肥胖大鼠上进行了为期 10 周的骨化三醇 (0.3μg/kg/TIW) 或载体处理 (NASH-vit.D 和 NASH-V 大鼠) 实验。通过抗 TNFα-TNFR1-NFκB 信号作用,慢性骨化三醇治疗显著恢复了 NASH-vit.D 大鼠的血浆骨化三醇水平,并显著改善了单核细胞和小肠中的维生素 D 受体 (VDR) 表达。显著地,血浆和门脉内毒素/TNFα 水平、细菌易位至肠系膜淋巴结、血浆 DX-4000-FITC、粪便白蛋白评估的肠道通透性、单核细胞中 TNFα 相关免疫谱的过度表达、肠道/肠系膜脂肪组织 (MAT)/肝脏的炎症和肝脂肪变性均通过慢性骨化三醇治疗 NASH 大鼠得到改善。此外,体外急性骨化三醇共孵育实验逆转了 NASH-V 大鼠单核细胞上清液/TNFα 诱导的 caco-2 细胞单层屏障功能障碍、MAT 来源脂肪细胞的细胞因子释放以及 lean-V 大鼠肝细胞的甘油三酯合成。通过体内和体外实验,我们的研究报告了肠道和脂肪组织中的骨化三醇信号。同时,我们的研究表明,通过慢性维生素 D 治疗恢复全身和肠道维生素 D 缺乏可有效减少 TNFα 介导的与肠道-脂肪组织-肝脏轴和 NASH 大鼠肝脂肪变性相关的免疫异常。