
doi: 10.1002/oby.70059
pmid: 41140006
ABSTRACT Objective Acid‐sensing ion channels are proton‐activated ion channels predominantly found in the nervous system. They are well known to affect metabolic and neurological health, yet their role in obesity and gut physiology remains unclear. This study investigates how systemic deletion of Asic1a influences obesity, metabolic, and gut‐based outcomes. Methods Employing male and female rats with systemic Asic1a deletion ( Asic1a −/− ), metabolic, gut, and fecal microbiota (16S rRNA sequencing) measures were assessed following chow diet or high‐fat diet administration for 8 weeks. Fecal microbiota transplantation into germ‐free mice was carried out as a proof‐of‐concept approach to assess the gut microbiota's direct impact. Results On a chow diet, Asic1a deletion resulted in significant gains in body weight, fat mass, glucose intolerance, and insulin resistance in both male and female rats compared to wild‐type controls. These effects were exacerbated with high‐fat diet administration. Asic1a −/− reshaped the gut microbiota, characterized by the enrichment of Bacteroides and Akkermansia . Microbiota transplantation from Asic1a −/− rats to recipient germ‐free mice increased body weight gain relative to those from wild‐type rats, implicating the potential role of gut microbiota. Conclusions Results provide evidence that ASIC1a plays a role in regulating metabolic homeostasis and the gut microbiota impacting body composition.
Male, Mice, Knockout, Fecal Microbiota Transplantation, Diet, High-Fat, Gastrointestinal Microbiome, Rats, Acid Sensing Ion Channels, Mice, Feces, Animals, Female, Obesity, Insulin Resistance, ORIGINAL ARTICLE
Male, Mice, Knockout, Fecal Microbiota Transplantation, Diet, High-Fat, Gastrointestinal Microbiome, Rats, Acid Sensing Ion Channels, Mice, Feces, Animals, Female, Obesity, Insulin Resistance, ORIGINAL ARTICLE
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