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2 "Gene-environment interaction"
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Original Article
Metabolic Risk/Epidemiology
Sex Differences in the Effects of CDKAL1 Variants on Glycemic Control in Diabetic Patients: Findings from the Korean Genome and Epidemiology Study
Hye Ah Lee, Hyesook Park, Young Sun Hong
Diabetes Metab J. 2022;46(6):879-889.   Published online February 8, 2022
DOI: https://doi.org/10.4093/dmj.2021.0265
  • 65,535 View
  • 178 Download
  • 1 Web of Science
  • 1 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Using long-term data from the Korean Genome and Epidemiology Study, we defined poor glycemic control and investigated possible risk factors, including variants related to type 2 diabetes mellitus (T2DM). In addition, we evaluated interaction effects among risk factors for poor glycemic control.
Methods
Among 436 subjects with newly diagnosed diabetes, poor glycemic control was defined based on glycosylated hemoglobin trajectory patterns by group-based trajectory modeling. For the variants related to T2DM, genetic risk scores (GRSs) were calculated and divided into quartiles. Risk factors for poor glycemic control were assessed using a logistic regression model.
Results
Of the subjects, 43% were in the poor-glycemic-control group. Body mass index (BMI) and triglyceride (TG) were associated with poor glycemic control. The risk for poor glycemic control increased by 11.0% per 1 kg/m2 increase in BMI and by 3.0% per 10 mg/dL increase in TG. The risk for GRS with poor glycemic control was sex-dependent (Pinteraction=0.07), and a relationship by GRS quartiles was found in females but not in males. Moreover, the interaction effect was found to be significant on both additive and multiplicative scales. The interaction effect was evident in the variants of cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like (CDKAL1).
Conclusion
Females with risk alleles of variants in CDKAL1 associated with T2DM had a higher risk for poor glycemic control than males.

Citations

Citations to this article as recorded by  
  • Hepatic Cdkal1 deletion regulates HDL catabolism and promotes reverse cholesterol transport
    Dan Bi An, Soo-jin Ann, Seungmin Seok, Yura Kang, Sang-Hak Lee
    Atherosclerosis.2023; 375: 21.     CrossRef
Review
Islet Studies and Transplantation
Regulation of Pancreatic β-Cell Mass by Gene-Environment Interaction
Shun-ichiro Asahara, Hiroyuki Inoue, Yoshiaki Kido
Diabetes Metab J. 2022;46(1):38-48.   Published online January 27, 2022
DOI: https://doi.org/10.4093/dmj.2021.0045
  • 4,455 View
  • 197 Download
  • 5 Web of Science
  • 5 Crossref
Graphical AbstractGraphical Abstract AbstractAbstract PDFPubReader   ePub   
The main pathogenic mechanism of diabetes consists of an increase in insulin resistance and a decrease in insulin secretion from pancreatic β-cells. The number of diabetic patients has been increasing dramatically worldwide, especially in Asian people whose capacity for insulin secretion is inherently lower than that of other ethnic populations. Causally, changes of environmental factors in addition to intrinsic genetic factors have been considered to have an influence on the increased prevalence of diabetes. Particular focus has been placed on “gene-environment interactions” in the development of a reduced pancreatic β-cell mass, as well as type 1 and type 2 diabetes mellitus. Changes in the intrauterine environment, such as intrauterine growth restriction, contribute to alterations of gene expression in pancreatic β-cells, ultimately resulting in the development of pancreatic β-cell failure and diabetes. As a molecular mechanism underlying the effect of the intrauterine environment, epigenetic modifications have been widely investigated. The association of diabetes susceptibility genes or dietary habits with gene-environment interactions has been reported. In this review, we provide an overview of the role of gene-environment interactions in pancreatic β-cell failure as revealed by previous reports and data from experiments.

Citations

Citations to this article as recorded by  
  • Increased risk of incident diabetes after therapy with immune checkpoint inhibitor compared with conventional chemotherapy: A longitudinal trajectory analysis using a tertiary care hospital database
    Minyoung Lee, Kyeongseob Jeong, Yu Rang Park, Yumie Rhee
    Metabolism.2023; 138: 155311.     CrossRef
  • The ameliorating effects of mesenchymal stem cells compared to α‐tocopherol on apoptosis and autophagy in streptozotocin‐induced diabetic rats: Implication of PI3K/Akt signaling pathway and entero‐insular axis
    Heba A. Mubarak, Manal M. Kamal, Yossra Mahmoud, Fatma S. Abd‐Elsamea, Eman Abdelbary, Marwa G. Gamea, Reham I. El‐Mahdy
    Journal of Cellular Biochemistry.2023; 124(11): 1705.     CrossRef
  • Leptin Rs7799039 polymorphism is associated with type 2 diabetes mellitus Egyptian patients
    Amal Ahmed Mohamed, Dina M. Abo-Elmatty, Alaa S. Wahba, Omnia Ezzat Esmail, Hadeer Saied Mahmoud Salim, Wafaa Salah Mohammed Hegab, Mona Mostafa Farid Ghanem, Nadia Youssef Riad, Doaa Ghaith, Lamiaa I Daker, Shorouk Issa, Noha Hassan Radwan, Eman Sultan,
    Archives of Physiology and Biochemistry.2023; : 1.     CrossRef
  • Association of Polygenic Variants with Type 2 Diabetes Risk and Their Interaction with Lifestyles in Asians
    Haeng Jeon Hur, Hye Jeong Yang, Min Jung Kim, Kyun-Hee Lee, Myung-Sunny Kim, Sunmin Park
    Nutrients.2022; 14(15): 3222.     CrossRef
  • Chemical Compounds and Ambient Factors Affecting Pancreatic Alpha-Cells Mass and Function: What Evidence?
    Gaia Chiara Mannino, Elettra Mancuso, Stefano Sbrignadello, Micaela Morettini, Francesco Andreozzi, Andrea Tura
    International Journal of Environmental Research and Public Health.2022; 19(24): 16489.     CrossRef

Diabetes Metab J : Diabetes & Metabolism Journal