Evidence map›Paper›PMID 32042868›Full record

ArticleGenes & diseases2019

Association of a genetic variant in AKT1 gene with features of the metabolic syndrome.

Fateme Sadat Eshaghi, Hamideh Ghazizadeh, Sakine Kazami-Nooreini, Ameneh Timar, Habibollah Esmaeily, Mehrane Mehramiz, Amir Avan, Majid Ghayour-Mobarhan

Open access · diamondAbstract read
In one paragraph

Article in Genes & diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Genetic Variations ofRisk management and healthcare policy · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. A Network Pharmacology to Explore the Mechanism ofBioMed research international · 2021
    Article
  11. Article
  12. 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

8 authors at 2 institutions in 1 country.

Fateme Sadat EshaghiDepartment of Biochemistry, Faculty of Basic Sciences, Hakim Sabzevary University, Sabzevar, Iran.
Hamideh GhazizadehMetabolic Syndrome and Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Sakine Kazami-NooreiniDepartment of Biochemistry, Faculty of Basic Sciences, Hakim Sabzevary University, Sabzevar, Iran.
Ameneh TimarDepartment of Biochemistry, Faculty of Basic Sciences, Hakim Sabzevary University, Sabzevar, Iran.
Habibollah EsmaeilySocial Department of Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mehrane MehramizMetabolic Syndrome and Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Amir AvanStudent Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Majid Ghayour-MobarhanMetabolic Syndrome and Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mashhad University of Medical Sciences · IRHakim Sabzevari University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MetS) is a clustering of metabolic abnormalities that is associated with increased risk of developing cardiovascular disease and type 2 diabetes. There is growing body of data showing the associations of genetic variants of the genes involved in the PI3K/AKT/mTOR pathway with diabetes and obesity. We aimed to investigate the association between MetS and its components with the genetic polymorphism in AKT1, rs1130233 (T > C). Total of 618 participants, recruited from Mashhad stroke and heart atherosclerosis disorder cohort (MASHAD study). Patients with MetS were defined by using international diabetes federation (IDF) criteria (n = 326) and those without MetS (n = 261) were recruited. Anthropometric and biochemical parameters were measured in all subjects. Genetic analysis for the rs1130233 polymorphism was performed, using the ABI-StepOne instruments with SDS version-2.0 software. Individuals with MetS had a significantly higher levels of BMI, waist-circumference, total cholesterol, triglyceride, high sensitivity-c reactive protein (hs-CRP) and blood-pressure, and lower concentrations of high density lipoprotein (HDL-C), compared to non-MetS individuals (P < 0.05). The association between the rs1130233 and MetS was not significant. Subjects with a CC or CT genotypes had a significantly higher serum hs-CRP-level (OR: 1.5; 95% CI (1.05-2.1), P = 0.02). Additionally, subjects who carried the TC genotype had a higher BMI compared to the CC genotype (p value = 0.045). Our findings demonstrated that AKT1, rs1130233 (T > C) polymorphism was associated with major components of MetS such as hs-CRP, and BMI, indicating further investigation in a multi-center setting to explore its value as an emerging biomarker of risk stratification marker.

Indexed as

AKT1CRPGenetic variantMetSPI3K/AKT/mTOR pathwayrs1130233

Identifiers

PMID32042868
PMCPMC6997569
OpenAlexW2951111271

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.