High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice.
High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice.
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高脂饮食在C57BL/6J小鼠的肝脏之前诱导脂肪组织中的肥胖症炎症。
DOI：
10.18632/aging.100738
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发表时间：
2015-04
期刊：
影响因子：
--
通讯作者：
Heeringa P
中科院分区：
文献类型：
--
作者：
van der Heijden RA;Sheedfar F;Morrison MC;Hommelberg PP;Kor D;Kloosterhuis NJ;Gruben N;Youssef SA;de Bruin A;Hofker MH;Kleemann R;Koonen DP;Heeringa P
在人类和啮齿动物的研究中，经常观察到脂肪组织和肝脏中的代谢性炎症是饮食引起的肥胖的结果。尽管脂肪组织和肝脏都容易因长期肥胖而发生慢性炎症，但它们各自对代谢性炎症发展的贡献仍是推测性的。因此，我们旨在阐明脂肪和肝脏组织中的炎症事件序列，以确定它们在饮食诱导的肥胖中代谢炎症和胰岛素抵抗（IR）发展中的作用。为了证实我们的假设，脂肪组织（AT）炎症在肝脏炎症之前开始，C57BL/6J雄性小鼠被喂食低脂饮食（LFD； 10% kcal脂肪）或高脂饮食（HFD； 45% kcal脂肪）24、40或52周。测定AT和肝脏的脂质积累和炎症。在整个研究过程中，评估葡萄糖耐量，并测量血浆中葡萄糖、胰岛素、瘦素和脂联素的水平。对于HFD， C57BL/6j小鼠出现进行性肥胖表型，并在HFD第24周和第40周伴有IR，但在HFD第52周后IR减弱。HFD治疗24周后，小鼠出现冠状结构，促炎基因Tnf、il - 1β、Mcp1和F4/80表达上调。由于肝炎症直到HFD的40周才被检测到，我们发现AT炎症在肝炎症发展之前就已经建立了。因此，与肝脏炎症相比，AT炎症可能对IR的发展有更大的贡献。
Metabolic inflammation in adipose tissue and the liver is frequently observed as a result of diet-induced obesity in human and rodent studies. Although the adipose tissue and the liver are both prone to become chronically inflamed with prolonged obesity, their individual contribution to the development of metabolic inflammation remains speculative. Thus, we aimed to elucidate the sequence of inflammatory events in adipose and hepatic tissues to determine their contribution to the development of metabolic inflammation and insulin resistance (IR) in diet-induced obesity. To confirm our hypothesis that adipose tissue (AT) inflammation is initiated prior to hepatic inflammation, C57BL/6J male mice were fed a low-fat diet (LFD; 10% kcal fat) or high-fat diet (HFD; 45% kcal fat) for either 24, 40 or 52 weeks. Lipid accumulation and inflammation was measured in AT and liver. Glucose tolerance was assessed and plasma levels of glucose, insulin, leptin and adiponectin were measured at various time points throughout the study. With HFD, C57BL/6j mice developed a progressive obese phenotype, accompanied by IR at 24 and 40 weeks of HFD, but IR was attenuated after 52 weeks of HFD. AT inflammation was present after 24 weeks of HFD, as indicated by the increased presence of crown-like structures and up-regulation of pro-inflammatory genes Tnf, Il1β, Mcp1 and F4/80. As hepatic inflammation was not detected until 40 weeks of HFD, we show that AT inflammation is established prior to the development of hepatic inflammation. Thus, AT inflammation is likely to have a greater contribution to the development of IR compared to hepatic inflammation.
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