Department of Food and Nutritional Sciences and Institute for Cardiovascular and Metabolic Research (ICMR), The University of Reading, Whiteknights, Reading, UK.
Int J Obes (Lond). 2013 Feb;37(2):216-23. doi: 10.1038/ijo.2012.33. Epub 2012 Mar 13.
An obese-type human microbiota with an increased Firmicutes:Bacteroidetes ratio has been described that may link the gut microbiome with obesity and metabolic syndrome (MetS) development. Dietary fat and carbohydrate are modifiable risk factors that may impact on MetS by altering the human microbiome composition. We determined the effect of the amount and type of dietary fat and carbohydrate on faecal bacteria and short chain fatty acid (SCFA) concentrations in people 'at risk' of MetS.
A total of 88 subjects at increased MetS risk were fed a high saturated fat diet (HS) for 4 weeks (baseline), then randomised onto one of the five experimental diets for 24 weeks: HS; high monounsaturated fat (MUFA)/high glycemic index (GI) (HM/HGI); high MUFA/low GI (HM/LGI); high carbohydrate (CHO)/high GI (HC/HGI); and high CHO/low GI (HC/LGI). Dietary intakes, MetS biomarkers, faecal bacteriology and SCFA concentrations were monitored.
High MUFA diets did not affect individual bacterial population numbers but reduced total bacteria and plasma total and LDL-cholesterol. The low fat, HC diets increased faecal Bifidobacterium (P=0.005, for HC/HGI; P=0.052, for HC/LGI) and reduced fasting glucose and cholesterol compared to baseline. HC/HGI also increased faecal Bacteroides (P=0.038), whereas HC/LGI and HS increased Faecalibacterium prausnitzii (P=0.022 for HC/HGI and P=0.018, for HS). Importantly, changes in faecal Bacteroides numbers correlated inversely with body weight (r=-0.64). A total bacteria reduction was observed for high fat diets HM/HGI and HM/LGI (P=0.023 and P=0.005, respectively) and HS increased faecal SCFA concentrations (P<0.01).
This study provides new evidence from a large-scale dietary intervention study that HC diets, irrespective of GI, can modulate human faecal saccharolytic bacteria, including bacteroides and bifidobacteria. Conversely, high fat diets reduced bacterial numbers, and in the HS diet, increased excretion of SCFA, which may suggest a compensatory mechanism to eliminate excess dietary energy.
已经描述了一种肥胖型人类微生物群，其厚壁菌门：拟杆菌门比例增加，这可能将肠道微生物群与肥胖和代谢综合征（MetS）的发展联系起来。饮食中的脂肪和碳水化合物是可改变的风险因素，通过改变人类微生物群的组成可能会影响 MetS。我们确定了饮食中脂肪和碳水化合物的数量和类型对处于 MetS 风险中的人粪便细菌和短链脂肪酸（SCFA）浓度的影响。
总共 88 名 MetS 风险增加的受试者在高饱和脂肪饮食（HS）下进食 4 周（基线），然后随机分为以下 5 种实验饮食中的一种 24 周：HS；高单不饱和脂肪（MUFA）/高血糖指数（GI）（HM/HGI）；高 MUFA/低 GI（HM/LGI）；高碳水化合物（CHO）/高 GI（HC/HGI）；和高 CHO/低 GI（HC/LGI）。监测饮食摄入、MetS 生物标志物、粪便细菌学和 SCFA 浓度。
高 MUFA 饮食不会影响单个细菌种群数量，但会降低总细菌数量和血浆总胆固醇和 LDL 胆固醇。低脂 HC 饮食与基线相比增加了粪便双歧杆菌（P=0.005，对于 HC/HGI；P=0.052，对于 HC/LGI）并降低了空腹血糖和胆固醇。HC/HGI 还增加了粪便拟杆菌（P=0.038），而 HC/LGI 和 HS 增加了普雷沃氏菌 prausnitzii（对于 HC/HGI，P=0.022，对于 HS，P=0.018）。重要的是，粪便拟杆菌数量的变化与体重呈负相关（r=-0.64）。高脂肪饮食 HM/HGI 和 HM/LGI 观察到总细菌减少（P=0.023 和 P=0.005），而 HS 增加了粪便 SCFA 浓度（P<0.01）。
这项研究提供了一项大规模饮食干预研究的新证据，表明 HC 饮食（无论 GI 如何）都可以调节人类粪便糖解细菌，包括拟杆菌和双歧杆菌。相反，高脂肪饮食减少了细菌数量，而 HS 饮食增加了 SCFA 的排泄，这可能表明是一种消除过量膳食能量的补偿机制。
