Research

Hormonal

Activation of the nuclear receptor FXR in enteroendocrine L-cells inhibits GLP-1 production by suppressing glycolysis and proglucagon transcription, whereas FXR deactivation (via deficiency or bile acid sequestrants) increases GLP-1 and improves glucose tolerance.

This research highlights that the specific bile acid receptor targeted matters for glucose control. While TGR5 agonists increase GLP-1, FXR activation suppresses it. Therefore, therapies aiming to boost GLP-1 (like bile acid sequestrants) work partly by deactivating FXR, not just by activating TGR5. This suggests that optimal treatments might combine TGR5 activation with FXR inhibition to maximize GLP-1 production.

GoodQualifiesHIGH confidence
Here we show that FXR activation in L-cells decreases proglucagon expression by interfering with the glucose-responsive factor Carbohydrate-Responsive Element Binding Protein (ChREBP) and GLP-1 secretion by inhibiting glycolysis. In vivo, FXR-deficiency increases GLP-1 gene expression and secretion in response to glucose hence improving glucose metabolism.
Mohamed Trabelsi et al. · Nature Communications · 2015

Why this rating

Strong evidence from multiple models (in vitro, ex vivo human biopsies, and multiple mouse genotypes) with consistent mechanistic findings.

Source

Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells

Mohamed Trabelsi et al. · Nature Communications · 2015

DOI 10.1038/ncomms8629

mechanism_onlyCited 377×
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DOI resolved against Crossref · corpus check 2026-06-10

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