Evidence map›Paper›PMID 27288421›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2016

High-fat diet-induced obesity alters nitric oxide-mediated neuromuscular transmission and smooth muscle excitability in the mouse distal colon.

Yogesh Bhattarai, David Fried, Brian Gulbransen, Mark Kadrofske, Roxanne Fernandes, Hui Xu, James Galligan

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  10. Oxidative medicine and cellular longevity · 2021
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  19. GASTROINTESTINAL MOTILITY DISORDERS IN OBESITY.Acta endocrinologica (Bucharest, Romania : 2005)
    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

7 authors at 1 institution in 1 country.

Yogesh BhattaraiThe Neuroscience Program, Michigan State University, East Lansing, Michigan;
David FriedDepartment of Physiology, Michigan State University, East Lansing, Michigan; and.
Brian GulbransenThe Neuroscience Program, Michigan State University, East Lansing, Michigan; Department of Physiology, Michigan State University, East Lansing, Michigan; and.ORCID 0000-0003-1145-3227
Mark KadrofskeDepartment of Pediatrics and Human Development, Michigan State University, East Lansing, Michigan.
Roxanne FernandesDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan;
Hui XuThe Neuroscience Program, Michigan State University, East Lansing, Michigan; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan;
James GalliganThe Neuroscience Program, Michigan State University, East Lansing, Michigan; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan; galliga1@msu.edu.
Michigan State University · US

Funding

SIGNALING MECHANISMS IN ARTERIES AND VEINS IN HYPERTENSIONP01HL070687 · NHLBI · MICHIGAN STATE UNIVERSITY · PI WATTS, STEPHANIE W · 2003 to 2019
$22.8M
Purinergic neurotransmission in the gutR01DK094932 · NIDDK · MICHIGAN STATE UNIVERSITY · PI GALLIGAN, JAMES J. · 2012 to 2016
$1.5M
NHLBI NIH HHS P01 HL070687NIDDK NIH HHS R01 DK094932
6 · The paper itself

Abstract

We tested the hypothesis that colonic enteric neurotransmission and smooth muscle cell (SMC) function are altered in mice fed a high-fat diet (HFD). We used wild-type (WT) mice and mice lacking the β1-subunit of the BK channel (BKβ1 (-/-)). WT mice fed a HFD had increased myenteric plexus oxidative stress, a 28% decrease in nitrergic neurons, and a 20% decrease in basal nitric oxide (NO) levels. Circular muscle inhibitory junction potentials (IJPs) were reduced in HFD WT mice. The NO synthase inhibitor nitro-l-arginine (NLA) was less effective at inhibiting relaxations in HFD compared with control diet (CD) WT mice (11 vs. 37%, P < 0.05). SMCs from HFD WT mice had depolarized membrane potentials (-47 ± 2 mV) and continuous action potential firing compared with CD WT mice (-53 ± 2 mV, P < 0.05), which showed rhythmic firing. SMCs from HFD or CD fed BKβ1 (-/-) mice fired action potentials continuously. NLA depolarized membrane potential and caused continuous firing only in SMCs from CD WT mice. Sodium nitroprusside (NO donor) hyperpolarized membrane potential and changed continuous to rhythmic action potential firing in SMCs from HFD WT and BKβ1 (-/-) mice. Migrating motor complexes were disrupted in colons from BKβ1 (-/-) mice and HFD WT mice. BK channel α-subunit protein and β1-subunit mRNA expression were similar in CD and HFD WT mice. We conclude that HFD-induced obesity disrupts inhibitory neuromuscular transmission, SMC excitability, and colonic motility by promoting oxidative stress, loss of nitrergic neurons, and SMC BK channel dysfunction.

Indexed as

Diet, High-FatGastrointestinal MotilitySynaptic TransmissionAction PotentialsAnimalsColonDisease Models, AnimalGenotypeKineticsLarge-Conductance Calcium-Activated Potassium Channel beta SubunitsMice, Inbred C57BLMice, KnockoutMuscle, SmoothMyenteric PlexusMyoelectric Complex, MigratingNeural InhibitionLarge-Conductance Calcium-Activated Potassium Channel beta SubunitsNitric Oxideenteric nervous systemgastrointestinal motilitylarge conductance calcium-activated K+ channelobesity

Identifiers

PMID27288421
PMCPMC5007291
OpenAlexW2414419248

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.