CD36 fatty-acid-transporter gene variants-CD36 G/A (rs1761667) and CD36 C/T (rs75326924) as biomarkers for risk-prediction in gestational diabetes mellitus

doi:10.4331/wjbc.v16.i4.111104

Advanced Search

BPG is committed to discovery and dissemination of knowledge

Home / Archive / Volume 16, Issue 4

This Article

Academic Content and Language Evaluation of This Article

CrossCheck and Google Search of This Article

Academic Rules and Norms of This Article

Supplementary Materials of This Article

Citation of this article

Corresponding Author of This Article

Research Domain of This Article

Article-Type of This Article

Open-Access Policy of This Article

Times Cited Counts in Google of This Article

Number of Hits and Downloads for This Article

Total Article Views (112)

All Articles published online

The chart showing PDF series, HTML series, Figures (1-3) series, Tables (1-2) series.

Item

Count

PDF

HTML

Figures (1-3)

Tables (1-2)

Sum=44

Featured Article

The chart showing Browse series, Download series.

Item

Count

Browse

Download

Sum=80

Publishing Process of This Article

Item

Count

Browse

Download

Sum=1

Dec 5, 2025 (publication date) through Dec 6, 2025

Times Cited of This Article

Times Cited (0)

Journal Information of This Article

Publication Name

World Journal of Biological Chemistry

ISSN

1949-8454

Publisher of This Article

Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Case Control Study

World J Biol Chem. Dec 5, 2025; 16(4): 111104
Published online Dec 5, 2025. doi: 10.4331/wjbc.v16.i4.111104

CD36 fatty-acid-transporter gene variants-CD36 G/A (rs1761667) and CD36 C/T (rs75326924) as biomarkers for risk-prediction in gestational diabetes mellitus

Amreen Shamsad, Tanu Gautam, Renu Singh, Monisha Banerjee

Amreen Shamsad, Tanu Gautam, Monisha Banerjee, Molecular and Human Genetics Laboratory, Department of Zoology, University of Lucknow, Lucknow 226007, Uttar Pradesh, India

Renu Singh, Department of Obstetrics and Gynecology, King George’s Medical University, Lucknow 226003, Uttar Pradesh, India

Co-first authors: Amreen Shamsad and Tanu Gautam.

Author contributions: Shamsad A and Gautam T have performed the experiments, analysis and prepared the manuscript; Shamsad A and Gautam T designed the experiment, carried out data curation, validation and analysis; Shamsad A, Gautam T and Singh R helped in clinical data collection; Banerjee M supervised, conceptualized, edited, reviewed the manuscript and provided all laboratory facilities; All authors read and approved the final manuscript.

Supported by Maulana Azad National Fellowship, University Grants Commission, New Delhi, Department of Biotechnology, New Delhi, No. AS [82-27/2019 (SA III)]; DBT-BUILDER-University of Lucknow Interdisciplinary Life Science Programme for Advance Research and Education (Level II), No. TG (BT/INF/22/SP47623/2022); and Department of Science and Technology -SERB Power Grant Scheme, No. SPG/2021/00545.

Institutional review board statement: The study was reviewed and approved by the King George’s Medical University (KGMU), Lucknow, India. Institutional Ethical Committee (No. 101st ECM II A/P18 dated May 18, 2020).

Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.

Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.

STROBE statement: The authors have read the STROBE Statement—checklist of items, and the manuscript was prepared and revised according to the STROBE Statement—checklist of items.

Data sharing statement: No additional data are available.

Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

Corresponding author: Monisha Banerjee, PhD, Professor, Molecular and Human Genetics Laboratory, Department of Zoology, University of Lucknow, University Road, Lucknow 226007, Uttar Pradesh, India. monishabanerjee30@gmail.com

Received: June 24, 2025
Revised: August 12, 2025
Accepted: November 7, 2025
Published online: December 5, 2025
Processing time: 164 Days and 12 Hours

Abstract

BACKGROUND

Gestational diabetes mellitus (GDM) is a metabolic disorder causing hyperglycemia during pregnancy. Insulin resistance and decreased insulin secretion are linked to altered lipid metabolism that leads to progression of GDM. CD36 is a membrane glycoprotein involved in lipid metabolism and insulin sensitivity. Studies indicate that the CD36 gene is substantially linked to type 2 diabetes mellitus (T2DM) and could also influence GDM susceptibility. Insulin resistance and decreased insulin secretion are the hallmarks of T2DM, which is thought to have a similar genetic pathophysiology in GDM.

AIM

To investigate the impact of CD36 gene polymorphisms [rs1761667 (G/A) and rs75326924 (C/T)] and mRNA expression in GDM women.

METHODS

The case-control study involved a total of 400 pregnant women, (200 healthy controls and 200 GDM cases). The study of CD36 gene polymorphisms G/A (rs1761667) and C/T (rs75326924)) were determined by polymerase chain reaction-restriction fragment length polymorphism. The mRNA expression study of CD36 gene was analyzed by quantitative polymerase chain reaction/quantitative real-time polymerase chain reaction followed by statistical analysis done using GraphPad Prism8 software (ver. 8.0).

RESULTS

The study revealed statistically significant association (P < 0.05) in anthropometric/biochemical parameters (age, gestational age, body mass index, fasting prandial glucose, post-prandial glucose, triglyceride, low-density lipoprotein) between GDM cases and healthy controls. CD36 G/A(rs1761667) and CD36 C/T (rs75326924) polymorphisms were significantly associated with GDM cases. The heterozygous genotypes (GA and CT) of both variants showed significant association (P = 0.0001 and P = 0.0025, odds ratio = 2.683 and 2.022 respectively). Allele frequency of ‘T’ allele in CD36 C/T (rs75326924) polymorphism was also found to be significant (P = 0.0046). CD36 gene was upregulated in individuals with GDM as compared to healthy controls (P = 0.0001). However, the upregulation of gene expression was not significantly associated with the genotypes of CD36 G/A (rs1761667) and CD36 C/T (rs75326924) polymorphisms.

CONCLUSION

Heterozygous genotypes GA and CT of CD36 gene variants and expression are linked to GDM, potentially serving as predictive biomarkers for GDM susceptibility; further exploration needed in diverse ethnic communities.

Keywords: Association; Cluster of differentiation; Gene expression; Gene variants; Gestational diabetes mellitus; Polymerase chain reaction-restriction fragment length polymorphism

Core Tip: Gestational diabetes mellitus (GDM) is a metabolic disorder causing hyperglycemia during pregnancy. GDM is associated with adverse feto-maternal outcomes, type-2-diabetes mellitus (T2DM), GDM-recurrence, future obesity. Insulin-resistance is a physiological trait associated with progressing pregnancy that provides an adequate nutritional supply for the mother and fetus. Disruptions in this mechanism might facilitate onset of GDM. CD36-transmembrane glycoprotein receptor, contributes to fatty-acid absorption. Genetic alterations in CD36 gene can modulate expression of genes along these pathways to mitigate the diabetic effect during pregnancy. The integration of genotyping-expression studies will be crucial for advancing investigation in GDM treatment.