Loading
Life sciences · Journal article
EMBO Reports · October 5, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract Obesity is a chronic condition and is closely associated with various metabolic diseases. It has become a global health concern, and effective pharmacotherapies are urgently needed. Farnesoid X receptor (FXR) is widely regarded as a pivotal target for the treatment of metabolic diseases because of its many biological functions. To avoid the possible adverse side effects of systemic FXR agonism, intestinal-specific FXR agonists have been developed. They show excellent anti-obesity effects, but the underlying mechanism remains unclear. In this study, we demonstrate that intestinal-restricted FXR agonists exhibit marked anti-obesity effects in diet-induced obesity (DIO) and db/db mice, but not in ob/ob mice. Mechanistically, they suppress appetite to reduce obesity in leptin-dependent and secretin-dependent manners. Intestinal FXR agonism upregulates secretin (SCT) expression in the presence of leptin. Specifically, FXR agonism enhances histone H3K4 methylation at the Sct locus, while leptin per se suppresses DNA methylation at the same locus in a leptin-receptor independent manner. Collectively, the results of this study clarify the anti-obesity mechanism underlying intestinal FXR agonists.