脂肪组织
脂肪变性
胰岛素抵抗
内科学
内分泌学
脂肪细胞
炎症
医学
脂肪肝
脂肪组织巨噬细胞
肥胖
2型糖尿病
糖尿病
疾病
作者
Claudia Sardi,Elisa Martini,Tommaso Mello,Simone Camelliti,Lucia Sfondrini,Fabrizio Marcucci,Marinos Kallikourdis,Michele Sommariva,Cristiano Rumio
出处
期刊:Life Sciences
[Elsevier]
日期:2021-01-01
卷期号:264: 118618-118618
被引量:7
标识
DOI:10.1016/j.lfs.2020.118618
摘要
Obesity represents a global health problem. Excessive caloric intake promotes the release of inflammatory mediators by hypertrophic adipocytes and obesity-induced inflammation is now recognized as a risk factor for the development of several diseases, such as cardiovascular diseases, insulin resistance, type-II diabetes, liver steatosis and cancer. Since obesity causes inflammation, we tested the ability of acetylsalicylic acid (ASA), a potent anti-inflammatory drug, in counteracting this inflammatory process and in mitigating obesity-associated health complications. Mice were fed with standard (SD) or high fat diet (HFD) for 3 months and then treated with acetylsalicylic acid for the subsequent two months. We then analyzed the metabolic and inflammatory status of their adipose and liver tissue by histological, molecular and biochemical analysis. Although ASA did not exert any effect on body weight, quantification of adipocyte size revealed that the drug slightly reduced adipocyte hypertrophy, however not sufficient so as to induce weight loss. Most importantly, ASA was able to improve insulin resistance. Gene expression profiles of pro- and anti-inflammatory cytokines as well as the expression of macrophage and lymphocyte markers revealed that HFD led to a marked macrophage accumulation in the adipose tissue and an increase of several pro-inflammatory cytokines, a situation almost completely reverted after ASA administration. In addition, liver steatosis caused by HFD was completely abrogated by ASA treatment. ASA can efficiently ameliorate pathological conditions usually associated with obesity by inhibiting the inflammatory process occurring in the adipose tissue.
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