Kaliannan K, Wang B, Li X-Y, Bhan A K, Kang J X
Laboratory for Lipid Medicine and Technology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Int J Obes (Lond). 2016 Jun;40(6):1039-42. doi: 10.1038/ijo.2016.27. Epub 2016 Feb 15.
Early-life antibiotic exposure can disrupt the founding intestinal microbial community and lead to obesity later in life. Recent studies show that omega-3 fatty acids can reduce body weight gain and chronic inflammation through modulation of the gut microbiota. We hypothesize that increased tissue levels of omega-3 fatty acids may prevent antibiotic-induced alteration of gut microbiota and obesity later in life. Here, we utilize the fat-1 transgenic mouse model, which can endogenously produce omega-3 fatty acids and thereby eliminates confounding factors of diet, to show that elevated tissue levels of omega-3 fatty acids significantly reduce body weight gain and the severity of insulin resistance, fatty liver and dyslipidemia resulting from early-life exposure to azithromycin. These effects were associated with a reversal of antibiotic-induced dysbiosis of gut microbiota in fat-1 mice. These results demonstrate the beneficial effects of omega-3 fatty acids on antibiotic-induced gut dysbiosis and obesity, and suggest the potential utility of omega-3 supplementation as a safe and effective means for the prevention of obesity in children who are exposed to antibiotics.
生命早期接触抗生素会破坏肠道微生物群落的建立,并导致日后肥胖。最近的研究表明,ω-3脂肪酸可通过调节肠道微生物群来减轻体重增加和慢性炎症。我们假设,组织中ω-3脂肪酸水平的升高可能会预防抗生素诱导的肠道微生物群改变及日后肥胖。在此,我们利用fat-1转基因小鼠模型,该模型可内源性产生ω-3脂肪酸,从而消除饮食的混杂因素,结果表明,组织中升高的ω-3脂肪酸水平可显著减轻生命早期接触阿奇霉素所致的体重增加以及胰岛素抵抗、脂肪肝和血脂异常的严重程度。这些效应与fat-1小鼠中抗生素诱导的肠道微生物群失调的逆转有关。这些结果证明了ω-3脂肪酸对抗生素诱导的肠道菌群失调和肥胖的有益作用,并表明补充ω-3作为预防接触抗生素儿童肥胖的安全有效手段具有潜在用途。