Aims The catabolism products of the fermentation process of selected hydroxycinnamic acids initiated by different species of Lactobacillus strains were identified. Methods and Results Three dietary supplements (Sanprobi IBS^®, BioGaia ProTectis Baby^® and Dicoflor 60^®) were used to isolate the Lactobacillus strains. The overnight bacterial cultures (18 h) were diluted and grown in a microaerophilic atmosphere at 37°C. Then, each phenolic acid was added to bacterial cultures and incubated for 24 h at 37°C. Samples were collected at specific intervals for a further 24 h of incubation. LC‐MS/MS was used for the identification of metabolism products of selected phenolic acids. Conclusions The phenolic acids were resistant to the Lactobacillus rhamnosus GG. Lactobacillus plantarum 299v caused degradation of caffeic and ferulic acids. The former was degraded either to dihydrocaffeic acid or to 4‐vinylcatechol and 4‐ethylcatechol. Ferulic acid was degraded only to dihydroferulic acid. Lactobacillus reuteri DSM 17938 caused only the degradation of chlorogenic acid (5‐caffeoylquinic acid, referred to IUPAC nomenclature) to caffeic acid. Significance and Impact of the Study Using of Lactobacilli as food additive should be taken into account that phenolic acids metabolism rate depends on not only the specific bacterial strain but also the structural properties of the acid.

We showed recently that the adenosine system and nitric oxide (NO) can interact differently in the control of renal function in normoglycaemia (NG) versus streptozotocin-induced diabetes (DM). Herein, we investigated if this relationship is modulated by dietary betaine (Bet, food compound possessing antioxidant and anti-inflammatory properties), to examine if adenosine receptor signalling in NG and DM females is altered by chronic Bet supplementation. The effects of intravenous infusion of theophylline, non-selective adenosine receptor antagonist, were examined in anaesthetised Sprague–Dawley female rats, pretreated for 2 weeks with Bet alone or combined with 4-day NO synthesis blockade with L-NAME (Bet + L-NAME). Renal blood flow (RBF, ultrasound artery probe), perfusion of the cortex, outer (OM-BF) and inner medulla (IM-BF; laser-Doppler technique), and tissue NO signal (selective electrode) were determined along with renal excretion. Bet and Bet + L-NAME decreased baseline RBF irrespective of glycaemia, whereas Bet lowered (NG) or elevated (DM) basal OM-BF; Bet + L-NAME treatment abolished these effects. Baseline sodium excretion decreased after Bet and Bet + L-NAME in NG only. Bet modified theophylline effects: IM-BF was lowered in DM rats, while tissue NO changes shown in the control were modified: NO increased in NG and decreased in DM. In NG, these effects were abolished by Bet + L-NAME. Bet pretreatment did not alter diuresis, natriuresis and kaliuresis, but after Bet + L-NAME these parameters increased (NG) or decreased (DM). Dietary Bet has the potential to affect renal medullary blood circulation; however, the eventual effect depends on glycaemia. Bet can modify renal functional changes induced by the interplay of the adenosine and NO systems, both in rats with normoglycaemia and streptozotocin diabetes.