Lipoxin A4 Attenuates Obesity-Induced Adipose Inflammation and Associated Liver and Kidney Disease
作者： Emma Börgeson , Andrew M.F. Johnson , Yun Sok Lee , Andreas Till , Gulam Hussain Syed
DOI: 10.1016/J.CMET.2015.05.003
关键词: Urinary system 、 Inflammation 、 Adipose tissue 、 Fatty liver 、 Internal medicine 、 Autophagy 、 Impaired glucose tolerance 、 Endocrinology 、 Kidney disease 、 Adiponectin 、 Medicine
摘要: The role of inflammation in obesity-related pathologies is well established. We investigated the therapeutic potential LipoxinA4 (LXA4:5(S),6(R),15(S)-trihydroxy-7E,9E,11Z,13E,-eicosatetraenoic acid) and a synthetic 15(R)-Benzo-LXA4-analog as interventions 3-month high-fat diet (HFD; 60% fat)-induced obesity model. Obesity caused distinct pathologies, including impaired glucose tolerance, adipose inflammation, fatty liver, chronic kidney disease (CKD). Lipoxins (LXs) attenuated obesity-induced CKD, reducing glomerular expansion, mesangial matrix, urinary H2O2. Furthermore, LXA4 reduced liver weight, serum alanine-aminotransferase, hepatic triglycerides. decreased attenuating TNF-α CD11c(+) M1-macrophages (MΦs), while restoring CD206(+) M2-MΦs increasing Annexin-A1. LXs did not affect renal or MΦs, suggesting protection occurred via attenuation inflammation. restored expression autophagy markers LC3-II p62. LX-mediated was demonstrable adiponectin(-/-) mice, that mechanism adiponectin independent. In conclusion, protect against systemic disease, these data support novel paradigm for treating associated pathologies.
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