Evidence map›Paper›PMID 40186075›Full record

ArticleNature metabolism2025

Alterations in intestinal bile acid transport provide a therapeutic target in patients with post-bariatric hypoglycaemia.

Snehal N Chaudhari, Yingjia Chen, Rafael Ferraz-Bannitz, Cameron Cummings, Amanda Sheehan, Pilar Casanova Querol, Berkcan Ozturk, Hanna Wang, Gabriel D'Agostino, Fei Ye and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Observational
  4. Article
  5. Inulin andFrontiers in endocrinology · 2025
    Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Snehal N ChaudhariDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.
Yingjia ChenLaboratory for Surgical and Metabolic Research, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Rafael Ferraz-BannitzDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0003-4496-4883
Cameron CummingsDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Amanda SheehanDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Pilar Casanova QuerolDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0009-0006-0227-6096
Berkcan OzturkDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Hanna WangDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Gabriel D'AgostinoDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.
Fei YeDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.
Eric G SheuLaboratory for Surgical and Metabolic Research, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0003-2707-1768
A Sloan DevlinDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA. sloan_devlin@hms.harvard.edu.ORCID http://orcid.org/0000-0001-5598-3751
Mary-Elizabeth PattiDepartment of Integrative Physiology and Metabolism, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. maryelizabeth.patti@joslin.harvard.edu.ORCID http://orcid.org/0000-0002-8163-3429

Funding

PILOT STUDY--SECRETORY TARGETING IN PANCREATIC B CELLSP30DK036836 · JOSLIN DIABETES CENTER · 1986 to 2025
$12.1M
"A microbiome-dependent bile acid metabolite improves type 2 diabetes."R01DK126855 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · 2022 to 2025
$2.5M
Human microbiome metabolites in health and diseaseR35GM128618 · HARVARD MEDICAL SCHOOL · 2025 to 2025
$530k
Elucidating the role of the microbiome in inducing gut permeability and inflammationR00DK128503 · UNIVERSITY OF WISCONSIN-MADISON · 2025 to 2025
$242k
Elucidating the role of the microbiome in inducing gut permeability and inflammationK99DK128503 · NIDDK · HARVARD MEDICAL SCHOOL · PI Snehal N. Chaudhari · 2023 to 2023
$90k
NIDDK NIH HHS K99 DK128503NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R00 DK128503NIDDK NIH HHS R01 DK121995NIDDK NIH HHS R01 DK126855NIGMS NIH HHS R35 GM128618
6 · The paper itself

Abstract

While Roux-en-Y gastric bypass is an effective treatment for obesity and type 2 diabetes, up to one-third of patients develop post-bariatric hypoglycaemia (PBH). Individuals with PBH exhibit increased postprandial secretion of the intestinal hormone fibroblast growth factor 19 (FGF19, Fgf15 in mice). However, the underlying mechanisms contributing to PBH remain uncertain. Here we demonstrate that faecal and plasma bile acid (BA) profiles are significantly altered in postoperative individuals with PBH versus those without hypoglycaemia. Furthermore, altered BAs in PBH induce FGF19 secretion in intestinal cells in a manner dependent on the apical sodium-dependent BA transporter (ASBT). We demonstrate that ASBT inhibition reduces Fgf15 expression and increases postprandial glucose in hypoglycaemic mice. Our data suggest that dysregulation of luminal BA profiles and transport may contribute to PBH and provide proof of concept that ASBT inhibition could be developed as a new therapeutic strategy for PBH.

Indexed as

Bariatric SurgeryBile Acids and SaltsHypoglycemiaIntestinal MucosaAnimalsBiological TransportFemaleFibroblast Growth FactorsGastric BypassHumansMaleMiceMice, Inbred C57BLMiddle AgedOrganic Anion Transporters, Sodium-DependentSymportersBile Acids and SaltsFGF19 protein, humanfibroblast growth factor 15, mouseFibroblast Growth FactorsOrganic Anion Transporters, Sodium-Dependentsodium-bile acid cotransporterSymporters

Identifiers

PMID40186075
PMCPMC12476230

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.