Evidence map›Paper›PMID 26311627›Full record

ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2015

Protection by beta-Hydroxybutyric acid against insulin glycation, lipid peroxidation and microglial cell apoptosis.

Manijheh Sabokdast, Mehran Habibi-Rezaei, Ali Akbar Moosavi-Movahedi, Maryam Ferdousi, Effat Azimzadeh-Irani, Najmeh Poursasan

Open access · hybridAbstract read
In one paragraph

Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Nutrients · 2019
    Article
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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

6 authors at 1 institution in 1 country.

Manijheh SabokdastSchool of Biology, College of Science, University of Tehran, Tehran, Iran. sabokdast@ut.ac.ir.
Mehran Habibi-RezaeiSchool of Biology, College of Science, University of Tehran, Tehran, Iran. mhabibi@ut.ac.ir.
Ali Akbar Moosavi-MovahediInstitute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran. moosavi@ut.ac.ir.
Maryam FerdousiSchool of Biology, College of Science, University of Tehran, Tehran, Iran. maryam.ferdousi@gmail.com.
Effat Azimzadeh-IraniSchool of Biology, College of Science, University of Tehran, Tehran, Iran. eazimirani@gmail.com.
Najmeh PoursasanInstitute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran. poursasan_n@ibb.ut.ac.ir.
University of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the formation of insulin-AGE, insulin glycation derived liposomal lipid peroxidation and insulin-AGE toxicity in microglial cells.

methodsThe inhibitory effect of BHB was monitored as a result of insulin incubation in the presence of glucose or fructose using AGE-dependent fluorescence, Tyr fluorescence as well as anilinonaphthalenesulfonate (ANS) andthioflavin T (ThT) binding, and circular dichroism (CD) investigations. To study lipid peroxidation induced by insulin glycation, thiobarbituric acid (TBA) assay and thiobarbituric acid reactive substance (TBARS) monitoring were used. The effect of insulin-AGE on microglial viability was investigated by 3-(4, 5 dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide (MTT) cell assay and Annexin V/propidium iodide (PI) staining.

resultsHere we are reporting the inhibitory effect of BHB on insulin glycation and generation of insulin-AGE as a possible explanation for insulin resistance. Moreover, the protective effect of BHB on consequential glycation derived liposomal lipid peroxidation as a causative event in microglial apoptosis is reported.

conclusionThe reduced insulin fibril formation, structural inertia to glycation involved conformational changes, anti-lipid peroxidation effect, and increasing microglia viability indicated the protective effect of BHB that disclose insight on the possible preventive effect of BHB on Alzheimer's disease.

Indexed as

3-Hydroxybutyric AcidAnimalsApoptosisCircular DichroismGlycosylationInsulinLipid PeroxidationLiposomesMicrogliaRats, Wistar3-Hydroxybutyric AcidInsulinLiposomes

Identifiers

PMID26311627
PMCPMC4551523
OpenAlexW1910405214

What OpenQuestion holds

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LicenceCC BY
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.