The Journal of nutrition · 2026
Persistent Benefits of Early Gestational Chenodeoxycholic Acid Supplementation on Late Pregnancy in Sows via Sustained Modulation of the Gut-Metabolism Axis.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhao Ying, Wang Xiaolong, Ma Qian, Liu En, Zhang Dongyan, Liu Hui, Cai Long, Wang Jing, Feng Tao, Schroyen Martine, Chen Meixia
Аннотация
BACKGROUND: Our previous studies in pigs have identified chenodeoxycholic acid (CDCA) as a potent metabolic regulator during early gestation, capable of enhancing embryo implantation by optimizing maternal metabolic status and gut microbiota-host interactions, whereas the long-term impacts of early gestational CDCA on late pregnancy remain largely unexplored.
OBJECTIVES: This study investigated whether supplementation with CDCA during early gestation (gestational day 0-28) exerts a sustained metabolic modulation effect on maternal health and reproductive outcomes in late gestation in a sow model.
METHODS: Multiparous sows (n = 24) were randomly assigned to receive either a control diet or a diet supplemented with 0.15% CDCA during early gestation. The reproductive performance, oxidative stress, inflammatory status, gut microbiome, and serum metabolome in late gestation were subsequently evaluated.
RESULTS: Results showed that early CDCA intervention significantly increased the total and live litter sizes (P < 0.05). Furthermore, CDCA treatment alleviated maternal oxidative stress and systemic inflammation and improved insulin sensitivity in late gestation (P < 0.05). Untargeted metabolomics revealed a distinct metabolic remodeling, characterized by the enrichment of beneficial metabolites, such as L-ornithine, and the depletion of proinflammatory and oxidative markers, including 1-palmitoylphosphatidylcholine, 2-lysophosphatidylcholine, 3-hydroxyanthranilic acid, and N-carboxymethyllysine. 16S rRNA sequencing indicated that CDCA exerted a targeted modulation rather than a global reconstruction of the gut microbiota. Specifically, CDCA suppressed potentially harmful bacteria, including NK4A214_group, Clostridium_sensu_stricto_1, and Turicibacter, whereas it enriched beneficial genera such as Subdoligranulum. Multiomics integration identified NK4A214_group as a key driver associated with exacerbated inflammatory status and unfavorable metabolic profiles.
CONCLUSIONS: Collectively, these findings demonstrate that early gestational CDCA supplementation elicits a long-term protective effect on maternal metabolism via optimizing specific gut microbe-metabolite interactions, thereby ensuring optimal gestational outcomes.
OBJECTIVES: This study investigated whether supplementation with CDCA during early gestation (gestational day 0-28) exerts a sustained metabolic modulation effect on maternal health and reproductive outcomes in late gestation in a sow model.
METHODS: Multiparous sows (n = 24) were randomly assigned to receive either a control diet or a diet supplemented with 0.15% CDCA during early gestation. The reproductive performance, oxidative stress, inflammatory status, gut microbiome, and serum metabolome in late gestation were subsequently evaluated.
RESULTS: Results showed that early CDCA intervention significantly increased the total and live litter sizes (P < 0.05). Furthermore, CDCA treatment alleviated maternal oxidative stress and systemic inflammation and improved insulin sensitivity in late gestation (P < 0.05). Untargeted metabolomics revealed a distinct metabolic remodeling, characterized by the enrichment of beneficial metabolites, such as L-ornithine, and the depletion of proinflammatory and oxidative markers, including 1-palmitoylphosphatidylcholine, 2-lysophosphatidylcholine, 3-hydroxyanthranilic acid, and N-carboxymethyllysine. 16S rRNA sequencing indicated that CDCA exerted a targeted modulation rather than a global reconstruction of the gut microbiota. Specifically, CDCA suppressed potentially harmful bacteria, including NK4A214_group, Clostridium_sensu_stricto_1, and Turicibacter, whereas it enriched beneficial genera such as Subdoligranulum. Multiomics integration identified NK4A214_group as a key driver associated with exacerbated inflammatory status and unfavorable metabolic profiles.
CONCLUSIONS: Collectively, these findings demonstrate that early gestational CDCA supplementation elicits a long-term protective effect on maternal metabolism via optimizing specific gut microbe-metabolite interactions, thereby ensuring optimal gestational outcomes.