The gut microbiota strongly influences digestive and metabolic health. A study recently published in Nature Metabolism reports a link between hydrogen sulfide released by the gut microbiota and GLP-1 production in the intestines. The findings might have implications for treatment and prevention of the metabolic syndrome.

To elucidate the mechanism behind this response, the researchers studied interactions between mouse enteroendocrine L cells and Desulfovibrio. They found that exposing cultured L cells to Desulfovibrio culture supernatant inhibited GLP-1 production in response to glucose. As Desulfovibrio is a major producer of hydrogen sulfide (H₂S), the researchers tested the hypothesis that H₂S inhibits L-cell GLP-1 production by treating the cells with the H₂S donor sodium hydrosulfide (NaHS). In line with the hypothesis, the cells produced less GLP-1 when exposed to NaHS than when NaHS was not present. The investigators also treated the cells with bismuth salicylate (an over-the-counter drug that sequesters H₂S) along with the Desulfovibrio supernatant and demonstrated that this treatment rescued GLP-1 production in a dose-dependent manner.

肠道微生物群强烈影响消化和代谢健康。最近发表在Nature Metabolism上的一项研究报告了肠道微生物群释放的硫化氢与肠道中 GLP-1 的产生之间的联系。这些发现可能对代谢综合征的治疗和预防有影响。

为了阐明这种反应背后的机制，研究人员研究了小鼠肠内分泌 L 细胞和脱硫弧菌之间的相互作用。他们发现，将培养的 L 细胞暴露于Desulfovibrio培养物上清液中，可抑制响应葡萄糖的 GLP-1 产生。由于脱硫弧菌是硫化氢 (H ₂ S) 的主要产生者，研究人员通过用 H ₂ S 供体硫氢化钠 (NaHS) 处理细胞来测试 H ₂ S 抑制 L 细胞 GLP-1 产生的假设。与假设一致，当细胞暴露于 NaHS 时产生的 GLP-1 比不存在 NaHS 时要少。研究人员还用水杨酸铋（一种隔离 H ₂ S 的非处方药）和脱硫弧菌上清液处理细胞，并证明这种处理以剂量依赖性方式挽救了 GLP-1 的产生。