Evidence map›Paper›PMID 24722905›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014

Intestinal alkaline phosphatase promotes gut bacterial growth by reducing the concentration of luminal nucleotide triphosphates.

Madhu S Malo, Omeed Moaven, Nur Muhammad, Brishti Biswas, Sayeda N Alam, Konstantinos P Economopoulos, Sarah Shireen Gul, Sulaiman R Hamarneh, Nondita S Malo, Abeba Teshager and 8 more

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% of its field
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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Intestinal Alkaline Phosphatase Expression in Response toAnimals : an open access journal from MDPI · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Anti-Antibiotics (Basel, Switzerland) · 2023
    Article
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  18. Review
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 3 institutions in 1 country.

Madhu S MaloDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Omeed MoavenDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Nur MuhammadDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Brishti BiswasDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Sayeda N AlamDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Konstantinos P EconomopoulosDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Sarah Shireen GulDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Sulaiman R HamarnehDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Nondita S MaloDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Abeba TeshagerDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Mussa M Rafat MohamedDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Qingsong TaoDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;
Sonoko NarisawaSanford Children's Health Research Center, Sanford-Burnham Medical Research Institute, La Jolla, California;
José Luis MillánSanford Children's Health Research Center, Sanford-Burnham Medical Research Institute, La Jolla, California;
Elizabeth L HohmannInfectious Disease Unit, Departments of Pediatrics and Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and.
H Shaw WarrenInfectious Disease Unit, Departments of Pediatrics and Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and.
Simon C RobsonDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Richard A HodinDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; rhodin@mgh.harvard.edu.
Harvard University · USSanford Burnham Prebys Medical Discovery Institute · USBeth Israel Deaconess Medical Center · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHRISTOPHER P DUGGAN · 1994 to 2026
$31.6M
THYROID HORMONE AND THE GUTR01DK050623 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HODIN, RICHARD A. · 1996 to 2010
$3.4M
MOLECULAR MECHANISMS OF INTESTINAL ATROPHY/HYPERPLASIAR01DK047186 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HODIN, RICHARD A. · 2000 to 2011
$3.4M
NIDDK NIH HHS P30 DK043351NIDDK NIH HHS P30DK40561NIDDK NIH HHS R01DK047186NIDDK NIH HHS R01DK050623
6 · The paper itself

Abstract

The intestinal microbiota plays a pivotal role in maintaining human health and well-being. Previously, we have shown that mice deficient in the brush-border enzyme intestinal alkaline phosphatase (IAP) suffer from dysbiosis and that oral IAP supplementation normalizes the gut flora. Here we aimed to decipher the molecular mechanism by which IAP promotes bacterial growth. We used an isolated mouse intestinal loop model to directly examine the effect of exogenous IAP on the growth of specific intestinal bacterial species. We studied the effects of various IAP targets on the growth of stool aerobic and anaerobic bacteria as well as on a few specific gut organisms. We determined the effects of ATP and other nucleotides on bacterial growth. Furthermore, we examined the effects of IAP on reversing the inhibitory effects of nucleotides on bacterial growth. We have confirmed that local IAP bioactivity creates a luminal environment that promotes the growth of a wide range of commensal organisms. IAP promotes the growth of stool aerobic and anaerobic bacteria and appears to exert its growth promoting effects by inactivating (dephosphorylating) luminal ATP and other luminal nucleotide triphosphates. We observed that compared with wild-type mice, IAP-knockout mice have more ATP in their luminal contents, and exogenous IAP can reverse the ATP-mediated inhibition of bacterial growth in the isolated intestinal loop. In conclusion, IAP appears to promote the growth of intestinal commensal bacteria by inhibiting the concentration of luminal nucleotide triphosphates.

Indexed as

Adenosine TriphosphateAlkaline PhosphataseAmpicillinAnimalsDeoxyribonucleotidesDrug Resistance, BacterialEnterococcus faecalisEscherichia coliFecesIntestinesMiceMice, Inbred C57BLMice, KnockoutMorganella morganiiPhenylalanineStarvationAdenosine TriphosphateAlkaline PhosphataseAmpicillinDeoxyribonucleotidesPhenylalanineStreptomycinCpG DNAdysbiosisflagellingut floraintestinal loop modellipopolysaccharidesmicrobiotal homeostasis

Identifiers

PMID24722905
PMCPMC4024727
OpenAlexW2098996610

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.