Exploring LEPR Gene rs1137100 and rs1137101 Polymorphisms in Gestational Diabetes Mellitus: A Pilot Study From Bangladesh
- 1Bangladesh Medical University (BMU), Shahbag, Dhaka, Bangladesh
- 2Department of Bioprocess and Genetic Engineering, Faculty of Biotechnology and Genetic Engineering, Chattogram Veterinary and Animal Sciences University, Hathazari, Chattogram, Bangladesh
- 3Molecular Biotechnology Division, National Institute of Biotechnology, Ashulia, Bangladesh
Abstract
Introduction: Gestational diabetes mellitus (GDM) is a prevalent pregnancy complication that negatively impacts both the mother and the fetus. Leptin (LEP), a key regulator of glucose metabolism during pregnancy, is influenced by genetic factors. The rs1137101 single-nucleotide polymorphism (SNP) results in a glutamine-to-arginine substitution at position 223 in the LEP receptor, potentially affecting maternal and fetal metabolic outcomes.
Methods: The study investigates the association of rs1137100 and rs1137101 polymorphisms in the LEPR gene with GDM. A total of 38 women with GDM and 72 controls were enrolled based on the WHO 2013 criteria, regardless of gestational age. Fasting insulin and LEP were measured using chemiluminescence immunoassay. Genetic samples were stored in ethylenediaminetetraacetic acid tubes, and genotyping of LEPR rs1137100 and rs1137101 was performed using Sanger sequencing. SNP analysis was done with SNPStats.
Results: Fasting insulin (μIU/L) [GDM: 9.09 (4.18-14) vs normal glucose tolerance: 7.48 (3.06-11.9); P = 0.015] and LEP (ng/ml) [GDM: 170 (57.5-282.5) vs normal glucose tolerance: 118.4 (47.7-189.1); P = 0.031] levels were significantly elevated in GDM cases. Genotype frequencies of rs1137100 and rs1137101 showed no significant differences between GDM and controls (P > 0.05). Multivariate logistic regression under multiple genetic models also revealed no significant association. Linkage disequilibrium analysis indicated that the SNPs are not in linkage disequilibrium (D = −0.066, D’ = 0.651, r2 = 0.106; P < 0.001).
Conclusion: This small pilot study found no statistically significant association of rs1137100 and rs1137101 polymorphisms in the LEPR gene with GDM in this Bangladeshi population cohort.
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BibTeX
@article{tofail2026exploring,
title = {{Exploring LEPR Gene rs1137100 and rs1137101 Polymorphisms in Gestational Diabetes Mellitus: A Pilot Study From Bangladesh}},
author = {Tania Tofail and Siratul Kubra Shifat and Farhana Sayeed and Mashfiqul Hasan and U.S. Mahzabin Amin and Muhammad Abul Hasanat},
journal = {AACE Endocrinology and Diabetes},
year = {2026},
month = jul,
doi = {10.1016/j.aed.2026.07.008},
url = {https://doi.org/10.1016/j.aed.2026.07.008},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Exploring LEPR Gene rs1137100 and rs1137101 Polymorphisms in Gestational Diabetes Mellitus: A Pilot Study From Bangladesh
AU - Tania Tofail
AU - Siratul Kubra Shifat
AU - Farhana Sayeed
AU - Mashfiqul Hasan
AU - U.S. Mahzabin Amin
AU - Muhammad Abul Hasanat
PY - 2026
DA - 2026/07/24
JO - AACE Endocrinology and Diabetes
DO - 10.1016/j.aed.2026.07.008
UR - https://doi.org/10.1016/j.aed.2026.07.008
AB - Introduction: Gestational diabetes mellitus (GDM) is a prevalent pregnancy complication that negatively impacts both the mother and the fetus. Leptin (LEP), a key regulator of glucose metabolism during pregnancy, is influenced by genetic factors. The rs1137101 single-nucleotide polymorphism (SNP) results in a glutamine-to-arginine substitution at position 223 in the LEP receptor, potentially affecting maternal and fetal metabolic outcomes. Methods: The study investigates the association of rs1137100 and rs1137101 polymorphisms in the LEPR gene with GDM. A total of 38 women with GDM and 72 controls were enrolled based on the WHO 2013 criteria, regardless of gestational age. Fasting insulin and LEP were measured using chemiluminescence immunoassay. Genetic samples were stored in ethylenediaminetetraacetic acid tubes, and genotyping of LEPR rs1137100 and rs1137101 was performed using Sanger sequencing. SNP analysis was done with SNPStats. Results: Fasting insulin (μIU/L) [GDM: 9.09 (4.18-14) vs normal glucose tolerance: 7.48 (3.06-11.9); P = 0.015] and LEP (ng/ml) [GDM: 170 (57.5-282.5) vs normal glucose tolerance: 118.4 (47.7-189.1); P = 0.031] levels were significantly elevated in GDM cases. Genotype frequencies of rs1137100 and rs1137101 showed no significant differences between GDM and controls (P > 0.05). Multivariate logistic regression under multiple genetic models also revealed no significant association. Linkage disequilibrium analysis indicated that the SNPs are not in linkage disequilibrium (D = −0.066, D’ = 0.651, r2 = 0.106; P < 0.001). Conclusion: This small pilot study found no statistically significant association of rs1137100 and rs1137101 polymorphisms in the LEPR gene with GDM in this Bangladeshi population cohort.
SN - 3050-9157
ER -