Animal models indicate that butyrate might reduce motor symptoms in Parkinson’s disease. Some dietary fibers are butyrogenic, but in Parkinson’s disease patients their butyrate stimulating capacity is unknown. Therefore, we investigated different fiber supplements’ effects on short-chain fatty acid production, along with potential underlying mechanisms, in Parkinson’s patients and age-matched healthy controls. Finally, it was investigated if this butyrate production could be confirmed by using fiber-rich vegetables. Different fibers (n = 40) were evaluated by in vitro fermentation experiments with fecal samples of Parkinson’s patients (n = 24) and age-matched healthy volunteers (n = 39). Short-chain fatty acid production was analyzed by headspace solid-phase micro-extraction gas chromatography-mass spectrometry. Clostridium coccoides and C. leptum were quantified through 16S-rRNA gene-targeted group-specific qPCR. Factors influencing short-chain fatty acid production were investigated using linear mixed models. After fiber fermentation, butyrate concentration varied between 25.6 ± 16.5 µmol/g and 203.8 ± 91.9 µmol/g for Parkinson’s patients and between 52.7 ± 13.0 µmol/g and 229.5 ± 42.8 µmol/g for controls. Inulin had the largest effect, while xanthan gum had the lowest production. Similar to fiber supplements, inulin-rich vegetables, but also fungal β-glucans, stimulated butyrate production most of all vegetable fibers. Parkinson’s disease diagnosis limited short-chain fatty acid production and was negatively associated with butyrate producers. Butyrate kinetics during 48 h fermentation demonstrated a time lag effect in Parkinson’s patients, especially in fructo-oligosaccharide fermentation. Butyrate production can be stimulated in Parkinson’s patients, however, remains reduced compared to healthy controls. This is a first step in investigating dietary fiber’s potential to increase short-chain fatty acids in Parkinson’s disease.

动物模型表明，丁酸盐可能会减轻帕金森病的运动症状。一些膳食纤维具有丁酸作用，但在帕金森病患者中，它们的丁酸盐刺激能力尚不清楚。因此，我们在帕金森病患者和年龄匹配的健康对照中研究了不同纤维补充剂对短链脂肪酸产生的影响，以及潜在的潜在机制。最后，研究了是否可以通过使用富含纤维的蔬菜来确认这种丁酸盐的产生。不同的纤维 ( n  = 40) 通过体外发酵实验对帕金森病患者 ( n  = 24) 和年龄匹配的健康志愿者 ( n = 39）。通过顶空固相微萃取气相色谱-质谱法分析短链脂肪酸的产生。球状梭菌和C. leptum通过 16S-rRNA 基因靶向组特异性 qPCR 定量。使用线性混合模型研究影响短链脂肪酸生产的因素。纤维发酵后，帕金森氏症患者的丁酸盐浓度在 25.6 ± 16.5 µmol/g 和 203.8 ± 91.9 µmol/g 之间变化，而对照的丁酸盐浓度在 52.7 ± 13.0 µmol/g 和 229.5 ± 42.8 µmol/g 之间变化。菊粉的影响最大，而黄原胶的产量最低。与纤维补充剂类似，富含菊粉的蔬菜以及真菌 β-葡聚糖可刺激丁酸盐的产生，这是所有植物纤维中的大部分。帕金森氏病的诊断限制了短链脂肪酸的产生，并且与丁酸盐生产者呈负相关。48 小时发酵过程中的丁酸盐动力学证明了帕金森病患者的时间滞后效应，尤其是在低聚果糖发酵中。可以刺激帕金森病患者的丁酸盐产生，但与健康对照相比，丁酸盐的产生仍然减少。这是研究膳食纤维在帕金森病中增加短链脂肪酸的潜力的第一步。