Evidence map›Paper›PMID 23007523›Full record

ArticleMolecular and cellular biochemistry2013

Excess aldosterone-induced changes in insulin signaling molecules and glucose oxidation in gastrocnemius muscle of adult male rat.

Jayaraman Selvaraj, Sampath Sathish, Chinnaiyan Mayilvanan, Karundevi Balasubramanian

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Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-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, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Recent progress in unraveling cardiovascular complications associated with primary aldosteronism: a succinct review.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  6. Article
  7. The Effect of Aldosterone on Cardiorenal and Metabolic Systems.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Mineralocorticoid receptors in the pathogenesis of insulin resistance and related disorders: from basic studies to clinical disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Jayaraman SelvarajDepartment of Endocrinology, Dr.ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Sekkizhar Campus, Taramani, Chennai 600113, India.
Sampath Sathish
Chinnaiyan Mayilvanan
Karundevi Balasubramanian
University of Madras · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidences demonstrate that excess aldosterone and insulin interact at target tissues. It has been shown that increased levels of aldosterone contribute to the development of insulin resistance and thus act as a risk factor for the development of type-2 diabetes mellitus. However, the molecular mechanisms involved in this scenario are yet to be identified. This study was designed to assess the dose-dependent effects of aldosterone on insulin signal transduction and glucose oxidation in the skeletal muscle (gastrocnemius) of adult male rat. Healthy adult male albino rats of Wistar strain (Rattus norvegicus) weighing 180-200 g were used in this study. Rats were divided into four groups. Group I: control (treated with 1 % ethanol only), group II: aldosterone treated (10 μg /kg body weight, twice daily for 15 days), group III: aldosterone treated (20 μg /kg body weight, twice daily for 15 days), and group IV: aldosterone treated (40 μg/kg body weight, twice daily for 15 days). Excess aldosterone caused glucose intolerance in a dose-dependent manner. Serum insulin and aldosterone were significantly increased, whereas serum testosterone was decreased. Aldosterone treatment impaired the rate of glucose uptake, oxidation, and insulin signal transduction in the gastrocnemius muscle through defective expression of IR, IRS-1, Akt, AS160, and GLUT4 genes. Phosphorylation of IRS-1, β-arrestin-2, and Akt was also reduced in a dose-dependent manner. Excess aldosterone results in glucose intolerance as a result of impaired insulin signal transduction leading to decreased glucose uptake and oxidation in skeletal muscle. In addition to this, it is inferred that excess aldosterone may act as one of the causative factors for the onset of insulin resistance and thus increased incidence of type-2 diabetes.

Indexed as

Signal TransductionAldosteroneAnimalsArrestinsbeta-Arrestin 2beta-ArrestinsBlood GlucoseCSK Tyrosine-Protein KinaseDiabetes Mellitus, Type 2Glucose IntoleranceGlucose Transporter Type 4GlycogenGTPase-Activating ProteinsInsulinInsulin Receptor Substrate ProteinsLipid PeroxidationAldosteroneArrb2 protein, ratArrestinsbeta-Arrestin 2beta-ArrestinsBlood GlucoseCSK Tyrosine-Protein KinaseGlucose Transporter Type 4GlycogenGTPase-Activating ProteinsInsulinInsulin Receptor Substrate ProteinsIrs1 protein, ratProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptor, InsulinRNA, MessengerSlc2a4 protein, ratsrc-Family KinasesTBC1D4 protein, ratTestosterone

Identifiers

PMID23007523
OpenAlexW2017166689

What OpenQuestion holds

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Registered trials

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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.