Abstract
Aims: Circulating amino acid (AA) abnormalities serve as predictors of adverse outcomes in patients with heart failure (HF). However, the role of the gut microbiota in AA disturbances remains unknown. Thus, we investigated gut microbial functions and their associations with AA metabolic alterations in patients with HF.Methods and Results: We performed whole-genome shotgun sequencing of fecal samples and mass spectrometry-based profiling of AAs in patients with compensated HF. Plasma levels of total essential AAs (EAAs) and histidine were significantly lower in patients with HF than in control subjects. HF patients also displayed increased and decreased abundance of gut microbial genes involved in the degradation and biosynthesis, respectively, of EAAs, including branched-chain AAs (BCAAs) and histidine. Importantly, a significant positive correlation was observed between the abundance of microbial genes involved in BCAA biosynthesis and plasma BCAA levels in patients with HF, but not in controls. Moreover, network analysis revealed that the depletion of Eubacterium and Prevotella, which harbor genes for BCAA and histidine biosynthesis, contributed to decreased abundance of microbial genes involved in the biosynthesis of those EAAs in patients with HF.Conclusions: The present study demonstrated the relationship between gut microbiota and AA metabolic disturbances in patients with HF.
Highlights
Heart failure (HF) is currently recognized as a systemic disease that affects the heart, and other organs such as the liver, kidney, and gut
HF patients displayed increased and decreased abundance of gut microbial genes involved in the degradation and biosynthesis, respectively, of essential AAs (EAAs), including branched-chain amino acid (AA) (BCAAs) and histidine
A significant positive correlation was observed between the abundance of microbial genes involved in BCAA biosynthesis and plasma BCAA levels in patients with HF, but not in controls
Summary
Heart failure (HF) is currently recognized as a systemic disease that affects the heart, and other organs such as the liver, kidney, and gut. Patients with chronic HF display alterations in morphology, permeability, and specific absorption in the intestine. These abnormalities are partially attributable to intestinal microcirculatory injuries [1,2,3]. A recent study has shown that gut microbial biosynthesis of branched-chain AAs (BCAAs; include leucine, isoleucine, and valine) was positively correlated with circulating levels of BCAAs in a healthy population [9]. This suggests that AAs generated by the gut microbiota enter the bloodstream from the intestine and affect systemic AA levels in the host
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