Treatment with camu camu (Myrciaria dubia) prevents obesity by altering the gut microbiota and increasing energy expenditure in diet-induced obese mice.

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. In the present study 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. Treatment of HFHS-fed mice with CC prevented weight gain, lowered fat accumulation and blunted metabolic inflammation and endotoxemia as compared to vehicle-treated HFHS-fed animals. 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 protein1 (UCP1) mRNA expression in the brown adipose tissue of CC-mice, which strongly correlated with the mRNA expression of the bile acid (BA) receptor TGR5. Moreover, CC-treated mice showed altered plasma BA pool and drastic changes in the GM (e.g, bloom of Barnesiella and A. muciniphila and a strong reduction of Lactobacillus). Germ-free (GF) mice reconstituted with the fecal microbiota (FM) of CC-treated mice gained less weight and displayed higher energy expenditure than GF-mice colonized with the FM of HFHS controls. 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.