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Original article
Treatment with camu camu (Myrciaria dubia) prevents obesity by altering the gut microbiota and increasing energy expenditure in diet-induced obese mice
  1. Fernando F Anhê1,2,
  2. Renato T Nachbar1,
  3. Thibault V Varin2,
  4. Jocelyn Trottier3,4,
  5. Stéphanie Dudonné2,
  6. Mélanie Le Barz1,2,
  7. Perrine Feutry2,
  8. Geneviève Pilon1,2,
  9. Olivier Barbier3,4,
  10. Yves Desjardins2,
  11. Denis Roy2,
  12. André Marette1,2
  1. 1 Department of Medicine, Faculty of Medicine, Cardiology Axis of the Québec Heart and Lung Institute, Laval University, Québec, Canada
  2. 2 Institute of Nutrition and Functional Foods, Laval University, Québec, Canada
  3. 3 Laboratory of Molecular Pharmacology, Endocrinology-Nephrology Axis, CHU-Québec Research Centre, Québec, Canada
  4. 4 Faculty of Pharmacy, Laval University, Québec, Canada
  1. Correspondence to Dr André Marette, Cardiology Axis of the Québec Heart and Lung Institute, Laval University, Québec QC G1V 0A6, Canada; andre.marette{at}criucpq.ulaval.ca

Abstract

Objective The consumption of fruits is strongly associated with better health and higher bacterial diversity in the gut microbiota (GM). Camu camu (Myrciaria dubia) is an Amazonian fruit with a unique phytochemical profile, strong antioxidant potential and purported anti-inflammatory potential.

Design By using metabolic tests coupled with 16S rRNA gene-based taxonomic profiling and faecal microbial transplantation (FMT), we have assessed the effect of a crude extract of camu camu (CC) on obesity and associated immunometabolic disorders in high fat/high sucrose (HFHS)-fed mice.

Results Treatment of HFHS-fed mice with CC prevented weight gain, lowered fat accumulation and blunted metabolic inflammation and endotoxaemia. CC-treated mice displayed improved glucose tolerance and insulin sensitivity and were also fully protected against hepatic steatosis. These effects were linked to increased energy expenditure and upregulation of uncoupling protein 1 mRNA expression in the brown adipose tissue (BAT) of CC-treated mice, which strongly correlated with the mRNA expression of the membrane bile acid (BA) receptor TGR5. Moreover, CC-treated mice showed altered plasma BA pool size and composition and drastic changes in the GM (eg, bloom of Akkermansia muciniphila and a strong reduction of Lactobacillus). Germ-free (GF) mice reconstituted with the GM of CC-treated mice gained less weight and displayed higher energy expenditure than GF-mice colonised with the FM of HFHS controls.

Conclusion Our results show that CC prevents visceral and liver fat deposition through BAT activation and increased energy expenditure, a mechanism that is dependent on the GM and linked to major changes in the BA pool size and composition.

  • brown adipose tissue
  • metabolic syndrome
  • insulin resistance
  • akkermansia muciniphila
  • polyphenols

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Footnotes

  • Contributors FFA, GP and AM conceived the study. FFA, MLB, TVV, JT, SD and RTN performed the experiments. FFA wrote the manuscript, prepared the figures and was responsible for data compilation and integration. All authors contributed to discuss the results and to research directions. All authors approved the manuscript.

  • Funding This work was funded by the Ministère du Développement Économique, de l’Innovation et de l’Exportation (MDEIE, PSR-SIIRI-444), J.A. deSève Foundation, by a joint grant from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-Agence Universitaire de la Francophonie (AUF) and by a Canadian Institutes of Health Research (CIHR) foundation grant (FDN#143247) to AM.

  • Competing interests None declared.

  • Patient consent Not required.

  • Ethics approval Laval University Animal Ethics Committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement All raw sequences from 16S rRNA gene-based analysis have been deposited in the public European Nucleotide Archive server under accession number PRJEB23031. Data sets generated and analysed during this study are available from the corresponding author on reasonable request.

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