Camu-camu decreases steatosis and markers of liver injury (16S sequencing).

Non-alcoholic fatty liver disease (NAFLD) affects approximately 25% of the adult population, making it the most prevalent liver disease worldwide. As of today, no effective drug treatments against NAFLD are available. Previous animal studies reported that a polyphenol-rich extract from the Amazonian berry camu-camu (CC) prevented hepatic steatosis in a mouse model of diet-induced obesity in association with changes in gut microbiota composition, but no clinical trial has investigated whether CC has beneficial effects on these parameters. Objective: The primary outcome of this study was to determine the impact of CC on hepatic steatosis and the exploratory outcomes were to evaluate changes in metabolic and gut microbiota profiles following CC supplementation. Methods: A randomized, double-blind, placebo-controlled crossover trial was con-ducted on 30 adults with overweight and hypertriglyceridemia. Participants were instructed to consume daily 1.5 g of CC capsules or maltodextrin (placebo) for 12 weeks. Metabolic phenotypes (anthropometric measurements, blood profiles, and indices of glucose homeostasis) and fecal microbiota composition were assessed before and after each intervention phase. Results: CC treatment was found to decrease liver fat (%HFF) by 7.43% as com-pared to baseline, as measured by magnetic resonance imaging. Liver fat in-creased by 8.42% from baseline during the placebo intervention, corresponding to a significant difference of 15.85% (P=0.003) in relative liver fat change between the CC and placebo arms. Moreover, CC significantly (P<0.05) decreased circu-lating levels of aspartate (AST) and alanine aminotransferases (ALT), which are markers of liver injury. When comparing the fecal microbiota composition at base-line and post-supplementation, we found that CC promoted taxonomic and func-tional changes in the gut microbiota, as revealed by both 16S-rRNA and meta-genomic analyses.. Conclusion: This is the first human clinical trial to report that CC supplementation decreases hepatic steatosis and plasma AST and ALT levels in subjects with over-weight and hypertriglyceridemia. These changes were associated with a shift in the gut microbiota composition and function. These studies support that polyphe-nol-rich prebiotic supplements may be used to reduce liver fat in overweight adults thus reducing the risk to develop NAFLD.

非酒精性脂肪性肝病（Non-alcoholic fatty liver disease, NAFLD）影响全球约25%的成年人群，是目前全球范围内最流行的肝脏疾病。截至目前，尚无针对NAFLD的有效药物治疗方案。既往动物研究显示，源自亚马逊浆果卡姆果（camu-camu, CC）的富含多酚提取物可在饮食诱导肥胖小鼠模型中预防肝脂肪变性，且该作用与肠道菌群组成改变相关，但目前尚无临床试验探讨CC对相关指标是否具有有益影响。

本研究的主要结局为明确CC对肝脂肪变性的影响，探索性结局为评估CC补充干预后代谢特征与肠道菌群谱的变化。

本研究针对30名合并超重与高甘油三酯血症的成年受试者开展了一项随机双盲安慰剂对照交叉试验。受试者被要求每日服用1.5g CC胶囊或麦芽糖糊精（安慰剂），干预周期共12周。在每一轮干预阶段前后，均对受试者的代谢表型（人体测量学指标、血液学指标及葡萄糖稳态相关指数）与粪便菌群组成进行检测评估。

研究结果显示，通过磁共振成像检测，CC干预组的肝脏脂肪含量（%HFF）较基线水平降低7.43%；而安慰剂干预组的肝脏脂肪含量较基线升高8.42%，两组相对肝脏脂肪变化量的差异达15.85%（P=0.003），具有统计学显著性。此外，CC干预可显著降低血清天冬氨酸转氨酶（aspartate aminotransferases, AST）与丙氨酸转氨酶（alanine aminotransferases, ALT）水平——这二者均为肝损伤标志物（P<0.05）。对比干预前后的粪便菌群组成，通过16S核糖体RNA（16S-rRNA）与宏基因组学分析均可发现，CC干预可促使肠道菌群在分类学与功能层面发生改变。

本研究是首项针对合并超重与高甘油三酯血症人群的临床试验，证实CC补充干预可降低受试者的肝脂肪变性程度与血清AST、ALT水平。上述变化与肠道菌群组成及功能的重塑密切相关。本研究结果支持富含多酚的益生元补充剂可用于降低超重成年人群的肝脏脂肪含量，从而降低其罹患NAFLD的风险。