Evidence map›Paper›PMID 25152027›Full record

ArticleActa pharmacologica Sinica2014

Alpha-lipoic acid attenuates insulin resistance and improves glucose metabolism in high fat diet-fed mice.

Yi Yang, Wang Li, Yang Liu, Yan Li, Ling Gao, Jia-jun Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Article
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  15. Oxidative medicine and cellular longevity · 2022
    Article
  16. Article
  17. α-Lipoic Acid Maintains Brain Glucose MetabolismFrontiers in aging neuroscience · 2020
    Article
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Yi Yang1] Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Ji-nan 250021, China [2] Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Yinchuan 750004, China.
Wang LiBiochemistry and Molecular Biology, Ningxia Medical University, Yinchuan 750004, China.
Yang LiuBiochemistry and Molecular Biology, Ningxia Medical University, Yinchuan 750004, China.
Yan LiBiochemistry and Molecular Biology, Ningxia Medical University, Yinchuan 750004, China.
Ling GaoCentral Lab Provincial Hospital Affiliated to Shandong University, Ji-nan 250021, China.
Jia-jun Zhao1] Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Ji-nan 250021, China [2] Institute of Endocrinology, Shandong Academy of Clinical Medicine, Ji-nan 250021, China.
Ningxia Medical University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate whether alpha-lipoic acid (ALA) could attenuate the insulin resistance and metabolic disorders in high fat diet-fed mice.

methodsMale mice were fed a high fat diet (HFD) plus ALA (100 and 200 mg·kg(-1)·d(-1)) or HFD plus a positive control drug metformin (300 mg·kg(-1)·d(-1)) for 24 weeks. During the treatments, the relevant physiological and metabolic parameters of the mice were measured. After the mice were euthanized, blood samples and livers were collected. The expression of proteins and genes related to glucose metabolism in livers were analyzed by immunoblotting and real time-PCR.

resultsHFD induced non-alcoholic fatty liver disease (NAFLD) and abnormal physiological and metabolic parameters in the mice, which were dose-dependently attenuated by ALA. ALA also significantly reduced HFD-induced hyperglycemia and insulin resistance in HFD-fed mice. Furthermore, ALA significantly upregulated the glycolytic enzymes GCK, HK-1 and PK, and the glycogen synthesis enzyme GS, and downregulated the gluconeogenic enzymes PEPCK and G6Pase, thus decreased glucose production, and promoted glycogen synthesis and glucose utilization in livers. Moreover, ALA markedly increased PKB/Akt and GSK3β phosphorylation, and nuclear carbohydrate response element binding protein (ChREBP) expression in livers. Metformin produced similar effects as ALA in HFD-fed mice.

conclusionALA is able to sustain glucose homeostasis and prevent the development of NAFLD in HFD-fed mice.

Indexed as

AnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsDiet, High-FatDown-RegulationGluconeogenesisGlucoseGlycogenGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGlycolysisHyperglycemiaInsulin ResistanceLiverMaleMetabolic DiseasesMiceBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsGlucoseGlycogenGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseMlxipl protein, mouseNuclear ProteinsProto-Oncogene Proteins c-aktThioctic AcidTranscription Factors

Identifiers

PMID25152027
PMCPMC4186984
OpenAlexW2028261226

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.