review · Frontiers in Endocrinology
Gestational diabetes mellitus represents a substantial global health challenge that impacts maternal and fetal health. The condition involves impaired insulin activity and the effects of specific genetic variants, including SLC30A8, CDKAL1, TCF7L2, IRS1, and GCK. These variants alter pancreatic beta-cell function and insulin action across vital tissues, disrupting glucose balance during pregnancy. A related hypothesis suggests that these genetic differences impair zinc transport, which subsequently hinders insulin production and release. In addition, inflammatory pathways involving molecules such as TNF-alpha and IL-6 contribute to disease susceptibility, worsening glucose metabolism dysregulation. The condition also correlates directly with altered cardiometabolic function, elevating risks of atherosclerosis, hypertension, dyslipidaemia, and compromised vascular function in affected women. Resolving these molecular interactions is essential for informing targeted pharmacological and genetic interventions.
Gestational diabetes can cause complications for mothers and infants while elevating long-term risks of cardiovascular disease and hypertension. Understanding the specific genes and inflammatory mechanisms responsible for impaired glucose control provides a foundation for identifying high-risk pregnancies earlier and designing more effective, biologically targeted interventions.
This work points towards future applications in targeted gene therapies, pharmacological treatments, and genetic screening tools for managing gestational diabetes. Potential users include biopharmaceutical developers and clinical geneticists seeking intervention targets. Given that the underlying mechanisms and gene interactions require further fundamental validation, practical applications remain at an early, discovery-stage distance from clinical use.
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Gestational diabetes mellitus (GDM) poses a significant global health concern, impacting both maternal and fetal well-being. Early detection and treatment are imperative to mitigate adverse outcomes during pregnancy. This review delves into the pivotal role of insulin function and the influence of genetic variants, including SLC30A8, CDKAL1, TCF7L2, IRS1, and GCK, in GDM development. These genetic variations affect beta-cell function and insulin activity in crucial tissues, such as muscle, disrupting glucose regulation during pregnancy. We propose a hypothesis that this variation may disrupt zinc transport, consequently impairing insulin production and secretion, thereby contributing to GDM onset. Furthermore, we discussed the involvement of inflammatory pathways, such as TNF-alpha and IL-6, in predisposing individuals to GDM. Genetic modulation of these pathways may exacerbate glucose metabolism dysregulation observed in GDM patients. We also discussed how GDM affects cardiovascular disease (CVD) through a direct correlation between pregnancy and cardiometabolic function, increasing atherosclerosis, decreased vascular function, dyslipidemia, and hypertension in women with GDM history. However, further research is imperative to unravel the intricate interplay between inflammatory pathways, genetics, and GDM. This understanding is pivotal for devising targeted gene therapies and pharmacological interventions to rectify genetic variations in SLC30A8, CDKAL1, TCF7L2, IRS1, GCK, and other pertinent genes. Ultimately, this review offers insights into the pathophysiological mechanisms of GDM, providing a foundation for developing strategies to mitigate its impact.
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DOI: 10.3389/fendo.2024.1399694
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