Xu Jian Hui, Liu Xing Zhen, Pan Wei, Zou Da Jin
Department of Endocrinology, Changhai Hospital, The Second Military Medical University, Shanghai 200433, P.R. China.
The Out‑Patient Department, Hangzhou Sanatorium of Nanjing Military Command Region, Hangzhou, Zhejiang 310007, P.R. China.
Mol Med Rep. 2017 May;15(5):2765-2787. doi: 10.3892/mmr.2017.6321. Epub 2017 Mar 14.
Systemic inflammation, which can be induced by metabolic endotoxemia, and corresponding high‑fat diet‑mediated metabolic disorders are associated with gut microbiota. In the present study reverse transcription-polymerase chain reaction, immunofluorescence, pyrosequencing, ELISA and Oil Red O staining were performed to assess whether berberine can protect against diet-induced obesity, through modulating the gut microbiota and consequently improving metabolic endotoxemia and gastrointestinal hormone levels. Alterations in the gut microbiota induced by berberine resulted in a significant reduction in bacterial lipopolysaccharide levels in portal plasma. Levels of inflammatory and oxidative stress markers, as well as the mRNA expression levels of macrophage infiltration markers in visceral adipose tissue, were also reduced by berberine. Inhibition of the inflammatory response was associated with a reduction in intestinal permeability and an increase in the expression of tight junction proteins. In addition, berberine was reported to restore aberrant levels of gut hormones in the portal plasma, such as glucagon‑like peptide‑1 and ‑2, peptide YY, glucose‑dependent insulinotropic polypeptide and pancreatic polypeptide. The present findings indicated that berberine, through modulating gut microbiota, restored the gut barrier, reduced metabolic endotoxemia and systemic inflammation, and improved gut peptide levels in high‑fat diet‑fed rats. The present study suggests that berberine may be an effective therapeutic strategy for the treatment of obesity and insulin resistance.
由代谢性内毒素血症诱导的全身炎症以及相应的高脂饮食介导的代谢紊乱与肠道微生物群有关。在本研究中，进行了逆转录聚合酶链反应、免疫荧光、焦磷酸测序、酶联免疫吸附测定和油红O染色，以评估小檗碱是否可以通过调节肠道微生物群，进而改善代谢性内毒素血症和胃肠激素水平，来预防饮食诱导的肥胖。小檗碱诱导的肠道微生物群改变导致门静脉血浆中细菌脂多糖水平显著降低。小檗碱还降低了炎症和氧化应激标志物的水平，以及内脏脂肪组织中巨噬细胞浸润标志物的mRNA表达水平。炎症反应的抑制与肠道通透性降低和紧密连接蛋白表达增加有关。此外，据报道小檗碱可恢复门静脉血浆中异常的肠道激素水平，如胰高血糖素样肽-1和-2、肽YY、葡萄糖依赖性促胰岛素多肽和胰多肽。本研究结果表明，小檗碱通过调节肠道微生物群，恢复了肠道屏障，降低了代谢性内毒素血症和全身炎症，并改善了高脂饮食喂养大鼠的肠道肽水平。本研究表明，小檗碱可能是治疗肥胖和胰岛素抵抗的有效治疗策略。
