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Metabolic & Cardiometabolic · Gut & Microbiome

secondary bile acids stimulates GLP-1

In plain terms: Do gut-bacteria bile acids boost your appetite-suppressing hormone GLP-1?

Leans support(preclinical) Metabolic & Cardiometabolic 🐭 Non-human evidence
RefutedContestedStrong support
consensus score 0.94
🔬 Capped to leans support — preclinical evidence only. The raw signal looked like strong support, but a claim about human health can't be graded that high on animal or lab evidence alone. It stays capped until human trials weigh in.

Yes as a mechanism, but only shown in animals so far — human evidence is correlational.

📅 Last reviewed: 2026-07-15

Evidence ladder

How far up the ladder this claim has climbed. A high consensus on a low rung means "consistent so far," not "proven in people."

Top evidence so far: Animal studies (Animal)

MechanismIn-vitroAnimalObservationalRCTMeta-analysis

How the studies fall

15 support 0 contradict 0 tested null 1 mixed · 16 sources, 15 independent groups

What the evidence shows

Microbe-generated secondary bile acids (DCA/LCA, taurine-conjugated) activate basolateral TGR5/GPBAR1 on L-cells to stimulate GLP-1 — robust in animal/ex-vivo models; the diet->microbe->secondary-BA->GLP-1 chain is causal in mice, human evidence is correlational only.

The evidence (16)

SourceGradeStanceQualityFinding
Meng Y et al
2026 · study_type: animal
animal mixed medium Oat β-glucan raised gut secondary bile acids (LCA, DCA) in obese mice, which the authors show promote GLP-1 secretion 'via inhibiting FXR' — TGR5 is not invoked as the mediating receptor for the GLP-1 rise in this study.
Zhu
2024 · Altern Ther Health Med
animal supports moderate Bile acid injection lowered glucose in T2DM rats via TGR5/GLP-1 rather than the FXR/FGF15 pathway.
Lv J et al
2026 · study_type: animal
animal supports medium L. salivarius XA1416 raised UDCA in mice, improving glucose/GLP-1. Oral UDCA replicated effect: acts as intestinal FXR antagonist + TGR5 (GPBAR1) agonist to stimulate GLP-1. HepG2 cells + molecular dynamics show UDCA directly activates GLP-
Wang
2026 · J Pharm Biomed Anal
animal supports moderate Liuwei Dihuang upregulated ileal TGR5 and enhanced GLP-1/PYY secretion via gut-microbiota-bile-acid axis in T2DM rats.
Zheng X, et al.
2021 · (HCA)
animal supports moderate [FT-verified] Zheng 2021 CellMetab hyocholic acids via TGR5+FXR mouse+human corr. ANIMAL/MECHANISM
Sun
2024 · J Agric Food Chem
animal supports moderate Mushroom polysaccharide raised conjugated ileal bile acids that stimulated TGR5, inducing GLP-1 release and better glucose metabolism.
Sun YH et al
2026 · study_type: animal
animal supports low Herbal formula LGZG in HFD mice enriched non-12α-OH secondary bile acids (hyocholic acid, 7-ketoLCA) — known TGR5 agonists/FXR antagonists — which elevated serum GLP-1 and activated adipose TGR5-cAMP/PKA/CREB signaling and thermogenesis.
Yue
2024 · Food & Function
animal supports moderate TGR5 agonist INT-777 restored ileal TGR5/proglucagon expression and serum GLP-1 suppressed by acrylamide in mice.
Stefela
2025 · Pharmacol Res
animal supports moderate Dual FXR-antagonist/TGR5-agonist bile-acid analogue enhanced GLP-1 secretion and improved glucose homeostasis in Western-diet mice.
Zhang
2025 · Sci Transl Med
animal supports high Intestinal TGR5-targeted deoxycholic-acid conjugate boosted GLP-1 secretion and glycemic control in mice and pigs.
Wang
2023 · Gut Microbes
animal supports high Gut-microbiota-derived ileal bile acids (wMCA, HCA) drive postprandial GLP-1 via TGR5, not FXR, in mice.
Yu
2023 · Endocrine Journal
mechanism supports moderate Review: intestinal GPBAR1/TGR5 activation by bile acids stimulates GLP-1, linking bile-acid signaling to glucose homeostasis.
Pathak P, et al.
2018 · (FXR/TauroLCA)
animal supports moderate [FT-verified] Pathak/Chiang 2018 mouse microbiota+FXR activate TGR5 to improve metabolism. ANIMAL-only
Hui
2020 · FASEB J
animal supports moderate Capsaicin raised lithocholic acid (LCA) via microbiota remodeling, an endogenous TGR5 agonist enhancing L-cell GLP-1 secretion.
Brighton CA, et al.
2015 · Endocrinology
mechanism supports moderate [FT-verified] Brighton/Gribble 2015 murine/ex-vivo L-cell BA->GLP-1 via basolateral TGR5. ANIMAL/MECHANISM-only
Ma H et al
2026 · study_type: animal
animal supports high Obesity-prone humans/mice show depleted GDCA (secondary bile acid). GDCA supplementation in obese mice improved weight/steatosis and stimulated ileal GLP-1 secretion by activating TGR5 signaling, alongside BAT thermogenesis; FMT recapitulat

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