Intestinal, adipose, and liver inflammation in diet-induced obese mice

Intestinal, adipose, and liver inflammation in diet-induced obese mice
复制标题

DOI:
10.1016/j.metabol.2008.07.029
复制
发表时间:
2008-12-01
影响因子:
9.8
通讯作者:
Michaelsson, Erik
Michaelsson, Erik
中科院分区:
医学1区
文献类型:
--
作者:
Li, Hong;Lelliott, Christopher;Michaelsson, Erik

文献摘要

被引文献

相似文献

慢性炎症和内脏脂肪组织(VAT)增加是代谢综合征的关键因素。两者都被认为在肝脏脂肪变性和胰岛素抵抗的发展中起致病作用。本研究的目的是调查的假设,即发炎的肠道,诱导饮食和化学刺激,可以诱导持续性炎症的增值税。使用雌性C57 BL/6 JO 1aHsd小鼠。在研究1中,给予小鼠组(每组n = 6)诱导肥胖的自助餐饮食(饮食诱导的肥胖)或仅常规食物(对照)14周。在研究11中,小鼠结肠炎(n = 8)诱导的3%葡聚糖硫酸钠自来水5天,然后21天的自来水单独。健康对照小鼠(n = 8)仅饮用自来水。在研究结束时,杀死所有小鼠;并对血液和组织进行采样和处理以进行分析。饮食诱导的肥胖小鼠的体重大大增加,有全身炎症、胰岛素抵抗和肝脏脂肪变性的证据。在肝脏、肠系膜脂肪和近端结肠/远端回肠中记录了以促炎细胞因子表达为指数的组织炎症,但在皮下或性腺周围脂肪中未记录。在葡聚糖硫酸钠诱导的结肠炎小鼠中,肠系膜脂肪的炎症甚至比结肠更严重,而肝脏和皮下脂肪的炎症要轻得多。研究表明,饮食和结肠炎都引起了肠系膜脂肪的炎症。与肠相邻的脂肪库及其对肠屏障功能受损的条件的夸大炎症反应的能力可能是VAT在肥胖诱导的代谢紊乱中的特别致病作用的原因。(C)2008年爱思唯尔公司All rights reserved.
Chronic inflammation and increased visceral adipose tissue (VAT) are key elements of the metabolic syndrome. Both are considered to play a pathogenic role in the development of liver steatosis and insulin resistance. The aim of the present study was to investigate the hypothesis that an inflamed intestine, induced both by diet and chemical irritation, could induce persistent inflammation in VAT. Female C57BL/6JO1aHsd mice were used. In study 1, groups of mice (n = 6 per group) were given an obesity-inducing cafeteria diet (diet-induced obesity) or regular chow only (control) for 14 weeks. In study 11, colitis in mice (n = 8) was induced by 3% dextran Sulfate sodium in tap water for 5 days followed by 2 1 days of tap water alone. Healthy control mice (n = 8) had tap water only. At the end of the studies, all mice were killed; and blood and tissues were sampled and processed for analysis. Body weight of diet-induced obese mice was greatly increased, with evidence of systemic inflammation, insulin resistance, and liver steatosis. Tissue inflammation indexed by proinflammatory cytokine expression was recorded in liver, mesenteric fat, and proximal colon/distal ileum, but not in subcutaneous or perigonadal fat. In dextran sulfate sodium-induced colitis mice, mesenteric fat was even more inflamed than the colon, whereas a much milder inflammation was seen in liver and Subcutaneous fat. The studies showed both diet- and colitis-initiated inflammation in mesenteric fat. Fat depots contiguous with intestine and their capacity for exaggerated inflammatory responses to conditions of impaired gut barrier function may account for the particularly pathogenic role of VAT in obesity-induced metabolic disorders. (C) 2008 Elsevier Inc. All rights reserved.