Camu-camu decreases hepatic steatosis and liver injury markers in overweight, hypertriglyceridemic individuals: A randomized crossover trial

Abstract

Non-alcoholic fatty liver disease (NAFLD) affects 25% of the adult population with no effective drug treatments 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. This study aims to determine the impact of CC on hepatic steatosis (primary outcome) and evaluate changes in metabolic and gut microbiota profiles (exploratory outcomes). A randomized, double-blind, placebo-controlled crossover trial is conducted on 30 adults with overweight and hypertriglyceridemia, who consume 1.5 g of CC capsules or placebo daily for 12 weeks. CC treatment decreases liver fat by 7.43%, while it increases by 8.42% during the placebo intervention, showing a significant difference of 15.85%. CC decreases plasma aspartate and alanine aminotransferases levels and promotes changes in gut microbiota composition. These findings support that polyphenol-rich prebiotic may reduce liver fat in adults with overweight, reducing the risk of developing NAFLD.

Keywords: aminotransferases; camu-camu; gut microbiota; non-alcoholic fatty liver disease; polyphenols.

Graphical abstract

Figure 1

Graphical representation of the study protocol See also Figure S1.

Figure 2

Effects of treatment on MRI-measured hepatic and abdominal fat distribution (A) Δ hepatic fat fraction (HFF) for CC: n = 20 and placebo: n = 25; p = 0.003. (B) Δ volume of subcutaneous adipose tissue (SAT) for CC: n = 20 and placebo: n = 24. (C) Δ volume of visceral adipose tissue (VAT) for CC: n = 20 and placebo: n = 25. (D) Individual relative change of percentage of HFF from baseline after CC (left) or placebo (right) phases. Results are presented as raw means ± SD. Analyses were conducted with SAS Studio and comparisons were made using the MIXED procedure adjusted for age, gender, BMI, baseline, sequence, interaction between treatment and sequence. See also Tables S1, S2, S3, and S4.

Figure 3

Effects of treatment on liver steatosis and hepatic health markers (A) Δ aspartate aminotransferase (AST) for CC: n = 22 and placebo: n = 23; p = 0.04. (B) D alanine aminotransferase (ALT) for CC: n = 29 and placebo: n = 30; p = 0.0006. Results are presented as raw means ± SD. Analyses were conducted with SAS Studio and comparisons were made using the MIXED procedure adjusted for age, gender, BMI, baseline, sequence, and interaction between treatment and sequence. See also Table S3.

Figure 4

Effects of treatment of gut microbiota composition (A) Shannon index. (B) Simpson’s reciprocal index. (C) Principal component analysis of fecal microbial diversity. (D) Linear discriminant analysis (LDA) effect size (LEfSe) was calculated to explore the taxa that most strongly discriminated between all participants after the intervention (post-placebo vs. post-CC). (E) LEfSe was also calculated to explore the changes induced by CC following the 12 weeks intervention (pre-CC vs. post-CC). (F) DESeq2 analysis on shotgun sequencing data was performed to explore the taxa or pathways (G) that were significantly different between the gut microbiota before and after CC consumption (pre-CC vs. post-CC). For plots A–C: CC: n = 30; placebo: n = 30. See also Figure S2.