ArticleCell discovery2026
GV-971 remodels the gut microbiota-bile acid-FXR axis to ameliorate obesity and metabolic dysfunction.
Article in Cell discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity and its associated metabolic complications represent a global health crisis, yet effective microbiota-targeted pharmacotherapies remain limited. Here, we report that GV-971 (sodium oligomannate), a marine-derived oligosaccharide originally developed for Alzheimer's disease, exerts potent anti-obesity and metabolic benefits by reprogramming gut microbial and host signaling networks. In high-fat diet-induced obese mice, GV-971 reduced adiposity, improved glucose homeostasis, and alleviated hepatic steatosis without affecting food intake. Multi-omics and causal intervention experiments revealed that GV-971 selectively decreased the abundance of Clostridium scindens, a keystone bacterium responsible for secondary bile acid synthesis. This decrease downregulated the expression of the baiF gene encoding 7α-hydroxysteroid dehydrogenase, leading to reduced intestinal deoxycholic acid (DCA) levels and inhibition of intestinal farnesoid X receptor (FXR) signaling. Restoration of C. scindens abundance, baiF expression, or DCA supplementation abrogated the metabolic benefits of GV-971, confirming the causal role of the C. scindens-DCA-FXR axis. Mechanistically, inhibition of intestinal FXR promoted thermogenic gene expression and white adipose tissue browning, thus enhancing systemic energy expenditure. These findings uncover a bacterium-metabolite-host signaling pathway underlying the effects of GV-971 and establish microbiota-directed FXR modulation as a promising therapeutic approach for obesity and metabolic disease.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.