期刊
AGING-US
卷 7, 期 4, 页码 256-268出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.100738
关键词
obesity; metabolic syndrome; insulin resistance; inflammation; adipose tissue; NASH; liver
资金
- Top Institute for Food and Nutrition (TIFN)
- Center for Translational Molecular Medicine (CTMM) project PREDICCt [01C-104]
- Dutch Heart Foundation
- Dutch Diabetes Research Foundation
- Dutch Kidney Foundation (PREDICCt)
- TNO research program Personalized Medicine (Therapie Op Maat)
- Graduate School for Drug Exploration (GUIDE), University of Groningen
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, Il1 beta, 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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