article · Egyptian Journal of Medical Human Genetics
Gestational diabetes mellitus represents a major contributor to the worldwide rise in diabetes cases. An examination of biological drivers identifies eighty-three candidate genes associated with the condition, with TCF7L2, MTNR1B, CDKAL1, IRS1, and KCNQ1 occurring most frequently. Variations within these genes can promote beta-cell dysfunction, insulin resistance, adiposity, and obesity. Additionally, environmental factors including diet, environmental pollutants, and microbes can prompt epigenetic modifications that disrupt glucose metabolism and normal insulin function. Without timely detection and adequate clinical management, the condition can progress to maternal type 2 diabetes and predispose offspring to future obesity and diabetes. In rare instances, the condition also associates with type 1 diabetes and maturity-onset diabetes of the young. Addressing these genetic targets offers a pathway to curb disease incidence.
Gestational diabetes is increasingly common and creates substantial health risks for both mothers and their children. Uncovering the genetic and environmental influences behind the condition clarifies why early screening is vital. Prompt intervention can resolve the condition following delivery, preventing the onset of lifelong metabolic diseases and curbing the expanding global burden of diabetes.
The identified candidate genes provide potential targets for developing diagnostic screening tests and targeted drug therapies for use by medical practitioners treating gestational diabetes. Because the underlying research synthesises candidate genes and their biological mechanisms through a review, any translation into practical diagnostics or clinical treatments remains at an early stage of development.
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Abstract Background Many studies have been conducted on the genetic and epigenetic etiology of gestational diabetes mellitus (GDM) in the last two decades because of the disease’s increasing prevalence and role in global diabetes mellitus (DM) explosion. An update on the genetic and epigenetic etiology of GDM then becomes imperative to better understand and stem the rising incidence of the disease. This review, therefore, articulated GDM candidate genes and their pathophysiology for the awareness of stakeholders. Main body (genetic and epigenetic etiology, GDM) The search discovered 83 GDM candidate genes, of which TCF7L2 , MTNR1B , CDKAL1 , IRS1 , and KCNQ1 are the most prevalent. Certain polymorphisms of these genes can modulate beta-cell dysfunction, adiposity, obesity, and insulin resistance through several mechanisms. Environmental triggers such as diets, pollutants, and microbes may also cause epigenetic changes in these genes, resulting in a loss of insulin-boosting and glucose metabolism functions. Early detection and adequate management may resolve the condition after delivery; otherwise, it will progress to maternal type 2 diabetes mellitus (T2DM) and fetal configuration to future obesity and DM. This shows that GDM is a strong risk factor for T2DM and, in rare cases, type 1 diabetes mellitus (T1DM) and maturity-onset diabetes of the young (MODY). This further shows that GDM significantly contributes to the rising incidence and burden of DM worldwide and its prevention may reverse the trend. Conclusion Mutations and epigenetic changes in certain genes are strong risk factors for GDM. For affected individuals with such etiologies, medical practitioners should formulate drugs and treatment procedures that target these genes and their pathophysiology.
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DOI: 10.1186/s43042-020-00054-8
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