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Diets rich in (poly)phenols are associated with a reduced reduction in the incidence of cardiovascular disorders. While the absorption and metabolism of (poly)phenols has been described, it is not clear how their metabolic fate is affected under pathological conditions. This study evaluated the metabolic fate of berry (poly)phenols in an in vivo model of hypertension as well as the associated microbiota response. Dahl salt-sensitive rats were fed either a low-salt diet (0.26% NaCl) or a high-salt diet (8% NaCl), with or without a berry mixture (blueberries, blackberries, raspberries, Portuguese crowberry and strawberry tree fruit) for 9 weeks. The salt-enriched diet promoted an increase in the urinary excretion of berry (poly)phenol metabolites, while the abundance of these metabolites decreased in faeces, as revealed by UPLC-MS/MS. Moreover, salt and berries modulated gut microbiota composition as demonstrated by 16S rRNA analysis. Some changes in the microbiota composition were associated with the high-salt diet and revealed an expansion of the families and . However, this effect was mitigated by the dietary supplementation with berries. Alterations in the metabolic fate of (poly)phenols occur in parallel with the modulation of gut microbiota in hypertensive rats. Thus, beneficial effects of (poly)phenols could be related with these interlinked modifications, between metabolites and microbiota environments.
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http://dx.doi.org/10.3390/nu11112634 | DOI Listing |
Trends Immunol
September 2025
Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, 10 Center Drive, 12N248C, Bethesda, MD 20892, USA. Electronic address:
Autoimmune diseases arise from genetic and environmental factors that disrupt immune tolerance. Recent studies highlight the role of myeloid cell immunometabolism, particularly mitochondrial dysfunction, in driving autoimmunity. Mitochondria regulate energy homeostasis and cell fate; their impairment leads to defective immune cell differentiation, abnormal effector activity, and chronic inflammation.
View Article and Find Full Text PDFStem Cell Reports
September 2025
Laboratory of Neural Stem Cells and Functional Neurogenetics, Farmington, CT 06030, USA; Departments of Neuroscience, Neurology, Genetics and Genome Sciences, UConn Health, Farmington, CT 06030, USA. Electronic address:
Intratumoral heterogeneity in glioblastoma is thought to underlie its remarkable ability to recur and resist therapies. Its origins, however, remain unknown. In this issue, Liu et al.
View Article and Find Full Text PDFStem Cell Reports
September 2025
Department of Biological Chemistry, Alexander Silberman Institute of Life Sciences, The Hebrew University, Jerusalem, Israel. Electronic address:
Ten-eleven translocation (TET) enzymes regulate neural stem cell development via distinct cytosine oxidation steps. This study, by Ebert et al. reveals that hydroxymethylation is crucial for neurogenesis, while formylation and carboxylation drive gliogenesis, offering insights into TET biology and therapeutic potential in neurodevelopmental and neurodegenerative disorders.
View Article and Find Full Text PDFStem Cell Reports
September 2025
Regenerative Neurophysiology, Lund Stem Cell Centre, MultiPark Strategic Area in Neuroscience, Department of Experimental Medical Science, Faculty of Medicine, Lund University, 221 84 Lund, Sweden. Electronic address:
Cortical interneuron deficiencies, particularly involving the somatostatin (SST) subtypes, contribute to neurological and neuropsychiatric disorders. These interneurons are difficult to derive in vitro from human embryonic stem cells (hESCs) due to their late embryonic development and dependence on glial interaction. To this end, we developed a three-dimensional co-culture model of hESC-derived neurons, enabling long-term development, functional maturity, and neuron-glial interaction.
View Article and Find Full Text PDFSci Transl Med
September 2025
Department of Medicine, Columbia University Irving Medical Center, New York, NY 10032, USA.
Hepatocyte apoptosis is a key feature of metabolic dysfunction-associated steatohepatitis (MASH), but the fate of apoptotic hepatocytes in MASH is poorly understood. Here, we explore the hypotheses that clearance of dead hepatocytes by liver macrophages (efferocytosis) is impaired in MASH because of low expression of the efferocytosis receptor T cell immunoglobulin and mucin domain containing 4 (TIM4; gene ) by MASH liver macrophages, which then drives liver fibrosis in MASH. We show that apoptotic hepatocytes accumulate in human and experimental MASH, using mice fed the fructose-palmitate-cholesterol (FPC) diet or the high-fat, choline-deficient amino acid-defined (HF-CDAA) diet.
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