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Record W2789670541 · doi:10.1093/jcag/gwy008.311

A310 THE INHIBITION OF PTP1B REVERSES IMPAIRED VAGAL AFFERENT SENSITIVITY CAUSED BY DIET-INDUCED OBESITY, REDUCING NITRIC OXIDE AND 2 PORE DOMAIN K+ CONDUCTANCE

2018· article· en· W2789670541 on OpenAlexaff
S Park, Michael Beyak

Bibliographic record

VenueJournal of the Canadian Association of Gastroenterology · 2018
Typearticle
Languageen
FieldNursing
TopicBiochemical Analysis and Sensing Techniques
Canadian institutionsQueen's University
Fundersnot available
KeywordsLeptinEndocrinologyInternal medicineChemistryPatch clampAdipokineDiet-induced obeseRheobaseMedicineElectrophysiologyInsulin resistanceObesity

Abstract

fetched live from OpenAlex

We have demonstrated that diet-induced obesity impairs vagal afferents and that the effects of high concentrations of leptin on vagal afferents in vitro, mimic the effects of obesity. One of downstream molecules in leptin signaling is protein tyrosine phosphatase 1B (PTP1B), which plays a role in negative regulation. We hypothesized that inhibition of PTP1B would prevent an impairment of vagal afferents caused by diet-induced obesity/hyperleptinemia Diet-induced obese (DIO) mice were fed diets composed of 60% or 10% kCal fat for 12–16 weeks. Nodose neurons from DIO mice or standard diet fed mice were incubated overnight with leptin (100nM) and PTP1B inhibitor (10mM). Current and voltage clamp were performed to assess membrane excitability and two-pore domain K+ (K2P) conductance, respectively. NO was measured in culture media using Nitrate/Nitrite fluorometric Assay kit. Media was collected after cell incubation for 24 hrs. Leptin (100nM) incubation reduced the excitability of vagal afferents. PTP1B inhibitor reversed this inhibitory effect of leptin. PTP1B inhibitor significantly decreased rheobase (100.8 ± 18.6 pA, n=12, leptin) vs. 64.7 ± 5.2 pA (n=15, Leptin + PTP1B inhibitor), *p=0.0497) and significantly increased input resistance (353.8 ± 36.2 MΩ (n=12, leptin) vs. 508.2 ± 52.7 MΩ (n=15, Leptin + PTP1B inhibitor), *p=0.0305). Leptin significantly increased K2P conductance (0.280 ± 0.022 nS (n=17, control) vs. 0.377 ± 0.035 nS (n=16, leptin), *p=0.0108). Inhibition of PTP1B significantly decreased the conductance (0.249 ± 0.013 pA (n=14, Leptin + PTP1B inhibitor), **p=0.0028) in leptin-incubated neuron. In mice fed a HFF diet, there is reduction in vagal excitability, which was reversed by the inhibition of PTP1B. PTP1B inhibitor significantly decreased rheobase (112.1 ± 14.6 pA (n=14, leptin) vs. 70.8 ± 8.1 pA (n=12, HFF + PTP1B inhibitor), *p=0.0268). Rheobase was not significantly different in LFF. Inhibition of PTP1B significantly decreased K2P conductance both in LFF and HFF neurons (LFF; **p=0.0050; HFF; **p=0.0041). PTP1B inhibitor significantly reduced NO fluorescence in leptin-incubated media (33.1 ± 2.2 (Leptin) vs. 12.2 ± 1.0 (Leptin+PTP1B inhibitor), ***<0.0001, n=6) and in neurons from HFF mice (43.4 ± 0.7 (HFF) vs. 29.9 ± 0.6 (HFF+PTP1B inhibitor), ***<0.0001 n=6), but not in LFF (27.8 ± 1.3 (LFF) vs. 25.8 ± 0.8 (LFF+PTP1B inhibitor), NS n=6). Iinhibition of PTP1B reverses the effects of HFF and elevated leptin on NO production and K2P conductance in nodose ganglion neurons. Consistent with this, the inhibitory effects of leptin and diet-induced obesity on the excitability of vagal afferent neuron were also reversed by PTP1B blockade. We suggest PTP1B may be a pivotal regulator and potential drug target in obesity. CIHR

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.011

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.002
Insufficient payload (model declined to judge)0.0030.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.010
GPT teacher head0.224
Teacher spread0.214 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations0
Published2018
Admission routes1
Has abstractyes

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