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Ahlqvist, K.

Publications and source records attributed to Ahlqvist, K..

2 recordsLinked to original sources

Impact of gestational antibiotics on maternal and offspring gut microbiota and growth in pigs

Maternal microbiota modulates the development of the microbiota in the offspring. Effects of gestational antibiotics are not well understood, as most studies have focused on the perinatal period. We treated sows with penicillin, tetracycline or saline on days 78-80 of the 114-119-day gestation, a critical period in the fetal immune system development. Microbiotas were analyzed by 16S rRNA gene amplicon sequencing in sow feces and vagina at days 77 and 113, in colostrum, and in piglet feces at three days, three weeks and ten weeks of age. Sow fecal microbiota changed during pregnancy, but less in antibiotic groups. No significant effects on sow microbiota remained on day 113. The piglets of the antibiotic-treated sows had lower Firmicutes+Actinobacteriota to Bacteroidota+Proteobacteria ratio, lower alpha diversity and higher relative abundance of Escherichia at three days. At ten weeks, they exhibited higher alpha diversity, had higher of Prevotella and Clostridium sp. CAG-127, and smaller increase of Limosilactobacillus than the control. Increased alpha diversity at 10 weeks was associated with lower weight gain during nursing. Oliverpabstia and Mitsuokella were positively associated with growth, while CAG-127 and Campylobacter B were negatively associated. Sow antibiotic treatment decreased the positive effect of Oliverpabstia and Mitsuokella and increased the negative effects of CAG-127 and Campylobacter B. Gestational antibiotics may have had adverse effects on microbiota and growth of the offspring, even if their effects on maternal microbiota were undetectable by parturition.

microbiology↗

NAD+ precursor treatment prevents cardiomyopathybut disrupts erythroid maturation in mitochondrial progeria

Nicotinamide adenine dinucleotide (NAD+) plays a central role in energy metabolism, and its decline is linked to various degenerative diseases. While NAD+ restoration holds therapeutic promise, its long term, tissue-specific consequences remain poorly understood. We investigated effects of nicotinamide riboside (NR) supplementation for "mutator" mice manifesting mitochondrial progeria. Our results reveal strikingly divergent outcomes: in proliferative bone marrow, NR-treated mutators show reductive stress with accumulation of NADH/NADPH, altered amino acid, nucleotide, folate levels and impaired heme biosynthesis. In blood, erythrocyte maturation defects are aggravated, exacerbating anemia. Conversely, in postmitotic cardiac tissue, NR enhanced contractility, reduces stress response markers and normalized metabolic profile. These findings indicate that while being beneficial for heart, chronic NAD+ boosting can compromise erythrocyte maturation in the context of mitochondrial disease. The data emphasize importance of evaluating systemic effects of NAD+ boosting therapies beyond the primary affected tissues and development of tissue-specific metabolic interventions for degenerative diseases. HighlightsO_LIChronic nicotinamide riboside supplementation exacerbates anemia and disrupts erythroid maturation in progeric mice. C_LIO_LIIn proliferative bone marrow cells, NR induces redox imbalance and drives profound metabolic dysregulation. C_LIO_LINR suppresses heme biosynthesis and iron transport pathways in the bone marrow. C_LIO_LIIn the heart, NR restores NAD+ levels, enhances cardiac function, and reduces metabolic stress. C_LI

physiology↗