Evidence map›Paper›PMID 33048307›Full record

ArticleJournal of endocrinological investigation2021

Decreased Sestrin levels in patients with type 2 diabetes and dyslipidemia and their association with the severity of atherogenic index.

S Sundararajan, I Jayachandran, S C Subramanian, R M Anjana, M Balasubramanyam, V Mohan, B Venkatesan, N Manickam

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Article in Journal of endocrinological investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  9. Review
  10. Sestrin2 in diabetes and diabetic complications.Frontiers in endocrinology · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Article
  19. Sestrin2 in hypoxia and hypoxia-related diseases.Redox report : communications in free radical research · 2021
    Review
  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

8 authors at 2 institutions in 1 country.

S SundararajanDepartment of Vascular Biology, Madras Diabetes Research Foundation and ICMR Centre for Advanced Research On Diabetes, Chennai, India.
I JayachandranDepartment of Vascular Biology, Madras Diabetes Research Foundation and ICMR Centre for Advanced Research On Diabetes, Chennai, India.
S C SubramanianClinical Epidemiology, Madras Diabetes Research Foundation, Chennai, India.
R M AnjanaMadras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialities Centre, Who Collaborating Centre for Non-Communicable Diseases Prevention and Control, Chennai, India.
M BalasubramanyamDepartment of Cell and Molecular Biology, Madras Diabetes Research Foundation, Chennai, India.
V MohanMadras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialities Centre, Who Collaborating Centre for Non-Communicable Diseases Prevention and Control, Chennai, India.
B VenkatesanDepartment of Vascular Biology, Madras Diabetes Research Foundation and ICMR Centre for Advanced Research On Diabetes, Chennai, India. venkatesanbalachandar@gmail.com.
N ManickamDepartment of Vascular Biology, Madras Diabetes Research Foundation and ICMR Centre for Advanced Research On Diabetes, Chennai, India. nagaraj@mdrf.in.ORCID http://orcid.org/0000-0002-0049-777X
Madras Diabetes Research Foundation · INScience and Engineering Research Board · IN

Funding

Department of Biotechnology, India BT/PR6550/GBD/27/451/2012Indian Counsil of Medical Research, India 2017-2773/CMB-BMS
6 · The paper itself

Abstract

purposeWe earlier reported that Sestrin2 regulates monocyte activation and atherogenic events through AMPK-mTOR nexus under high-glucose and dyslipidemic conditions. However, the statuses of Sestrins in diabetes and dyslipidemia are not known. We report here on the status of Sestrins and their association with diabetic dyslipidemia and atherosclerosis.

methodsIndividuals with normal glucose tolerance (NGT) (n = 46), dyslipidemia (n = 42), and patients with Type 2 diabetes with (n = 41) and without dyslipidemia (n = 40) were recruited from a tertiary diabetes centre, Chennai, India to study the mRNA expression levels of Sestrins (1, 2, and 3) in monocytes by RT-qPCR. Serum levels of Sestrins were measured using ELISA. Atherogenic index of plasma was calculated as log (triglyceride/HDL).

resultsmRNA expressions of Sestrin1 and Sestrin3 were significantly reduced in monocytes under dyslipidemic conditions but not in diabetes condition. Interestingly, Sestrin2 mRNA expression was significantly reduced in all disease conditions including dyslipidemia, and diabetes with and without dyslipidemia. Sestrin2 mRNA levels were negatively correlated with glycemic and lipid parameters and plasma atherogenic index. Furthermore, circulatory Sestrin2 was also found to be significantly decreased in dyslipidemia (415.2 ± 44.7 pg/ml), diabetes (375 ± 45 pg/ml), and diabetes with dyslipidemia (319.2 ± 26.3 pg/ml) compared to NGT (706.3 ± 77 pg/ml) and negatively correlated with glycemic, lipid parameters, and plasma atherogenic index.

conclusionWe report for the first time that Sestrins levels are significantly decreased in diabetes and dyslipidemic conditions. More strikingly, Sestrin2 had a strong association with atherogenic risk factors and severity of atherogenic index and we suggest that Sestrin2 may be used as a biomarker for assessing atherogenesis.

Indexed as

AdultAtherosclerosisBiomarkersDiabetes Mellitus, Type 2DyslipidemiasFemaleFollow-Up StudiesHumansMaleMiddle AgedMonocytesNuclear ProteinsPilot ProjectsPrognosisRisk FactorsSestrinsBiomarkersNuclear ProteinsSESN2 protein, humanSestrinsAtherogenesisCVDDiabetesDyslipidemiaMonocyteSestrins

Identifiers

PMID33048307
OpenAlexW3092432150

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.