Corinthian Currants Supplementation Restores Serum Polar Phenolic Compounds, Reduces IL-1beta, and Exerts Beneficial Effects on Gut Microbiota in the Streptozotocin-Induced Type-1 Diabetic Rat
2023
Vasiliki Kompoura | Ioanna Prapa | Paraskevi B. Vasilakopoulou | Gregoria Mitropoulou | Grigorios Nelios | Evangelos Balafas | Nikolaos Kostomitsopoulos | Antonia Chiou | Vaios T. Karathanos | Eugenia Bezirtzoglou | Yiannis Kourkoutas | Amalia E. Yanni
The present study aimed at investigating the possible benefits of a dietary intervention with Corinthian currants, a rich source of phenolic compounds, on type 1 diabetes (T1D) using the animal model of the streptozotocin-(STZ)-induced diabetic rat. Male Wistar rats were randomly assigned into four groups: control animals, which received a control diet (CD) or a diet supplemented with 10% <i>w</i>/<i>w</i> Corinthian currants (CCD), and diabetic animals, which received a control diet (DCD) or a currant diet (DCCD) for 4 weeks. Plasma biochemical parameters, insulin, polar phenolic compounds, and inflammatory factors were determined. Microbiota populations in tissue and intestinal fluid of the caecum, as well as fecal microbiota populations and short-chain fatty acids (SCFAs), were measured. Fecal microbiota was further analyzed by 16S rRNA sequencing. The results of the study showed that a Corinthian currant-supplemented diet restored serum polar phenolic compounds and decreased interleukin-1b (IL-1b) (<i>p</i> < 0.05) both in control and diabetic animals. Increased caecal lactobacilli counts (<i>p</i> < 0.05) and maintenance of enterococci levels within normal range were observed in the intestinal fluid of the DCCD group (<i>p</i> < 0.05 compared to DCD). Higher acetic acid levels were detected in the feces of diabetic rats that received the currant diet compared to the animals that received the control diet (<i>p</i> < 0.05). Corinthian currant could serve as a beneficial dietary component in the condition of T1D based on the results coming from the animal model of the STZ-induced T1D rat.
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