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Additional file 6: Fig. S2. Morphometry. Morphometric measurement of renal (a) arteries and (b) arterioles in rats maintained either on tap water (control group) or low and high dose of TMA. Abbreviations: TMA, trimethylamine. Morphometric measurements of five arcuate arteries and five arterioles were performed for each individual. Four measurements were made for each vessel. All measurements are expressed as single points (n = 3–5); ANOVA followed by post-hoc Tuckey test; *P < 0.05

Additional file 1. Methods

Additional file 2: Table S1. List of oligonucleotide primers used for RT-qPCR

Additional file 3: Table S2. Echocardiographic parameters. IVSD, interventricular septum thickness at diastole; LVDD, left ventricular diastolic diameter; PWD, posterior wall thickness at diastole; IVSS, interventricular septum thickness at systole; LVDS, left ventricular systolic diameter; PWS, posterior wall thickness at systole; EF, ejection fraction; FS, fractional shortening, LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; AO, aortic root diameter; LA, left atrium diameter; CO; cardiac output; L group – TMA low-dose group; H group – TMA high-dose group. All data are expressed as the mean ± SD; ANOVA followed by post hoc Tuckey-test

Additional file 5: Fig. S1. Renin – angiotensin system. The genes of the renin-angiotensin system. RT-qPCR analysis of REN, AGT, AGTr1a, AGTr1b, AGTr2 transcript levels in the (A) renal cortex, (B) renal medulla, (C) liver in rats maintained either on tap water (control group) or low and high dose of TMA. Abbreviations: TMA, trimethylamine; REN, renin; AGT, angiotensinogen; AGTr1a, angiotensin II receptor, type 1a; AGTr1b, angiotensin II receptor, type 1b; AGTr2, angiotensin II receptor, type 2. All data are expressed as the median, Q1, Q3, MIN, MAX (n = 6; use arbitrary units); Kruskal–Wallis test followed by post-hoc Dunn’s test. **P < 0.01 vs control group

The gut microbiota produces a number of biologically active compounds that may have both, positive and negative effects on health. To enter the circulation, microbiota-derived molecules need to pass the gut-blood barrier (GBB), a complex multi-layer system that prevents the free passage form the gut lumen to the blood. The integrity and permeability of the GBB depends on numerous factors, and may be disturbed in gastrointestinal, metabolic, cardiovascular and other diseases. An increased permeability of the GBB results in easier access of gut-derived molecules to the circulation. This may exert a significant effect on the course of the underlying disease and may alter functioning of various organs. Here, we discuss physiological significance of the GBB and available methods of assessing the GBB permeability.