Gestational diabetes mellitus (GDM) is a common pregnancy complication, in which spontaneous hyperglycemia develops during pregnancy. GDM is usually the result of β-cell dysfunction on a background of chronic insulin resistance during pregnancy. Ace Therapeutics can provide researchers engaged in pathological research of GDM with more efficient function analysis and overall services.

Overview of GDM

GDM is a metabolic disorder that women may have during pregnancy. Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation.

What Causes GDM

Placental prolactin, placental growth hormone, progesterone, cortisol, prolactin, and other hormones may contribute to GDM by interfering with insulin receptor signaling. On the other hand, most patients with GDM have β-cell dysfunction before pregnancy, insufficient islet β-cell adaptation or reserve, unable to meet the needs of insulin secretion in the third trimester. The blood sugar levels will usually return to normal after baby is born.

Simplified Diagram of Insulin Signaling (Jasmine, F. A.; et al. International Journal of Molecular Sciences. 2018)

Complications of GDM

GDM begets important short- and long-term health risks for the mother, developing fetus, and offspring. This includes the high likelihood of subsequent maternal type 2 diabetes, and possible adverse cardiometabolic phenotypes in the offspring.

Offspring Complications: Offspring born to mothers with GDM are at increased risk of multiple immediate complications, including macrosomia, preterm birth, birth injury, shoulder dystocia, neonatal hypoglycemia and respiratory distress.

Maternal Complications: The risks of multiple serious perinatal complications are increased in women with GDM, including gestational hypertension, pre-eclampsia, polyhydramnios, caesarean section, and shoulder dystocia, etc.

Factors Contributing to Maternal Insulin Resistance and Fetal Growth (Jaffar, A. R.; et al. Nature Reviews Endocrinology. 2016)

Pathogenesis of GDM

GDM is usually the result of β-cell dysfunction on a background of chronic insulin resistance during pregnancy and thus both β-cell impairment and insulin resistance represent critical components of the pathophysiology of GDM.

• β-Cell Dysfunction
  When β-cells lose the ability to adequately sense blood glucose concentration, or to release sufficient insulin in response, this is classified as β-cell dysfunction. The majority of susceptibility genes that are associated with GDM are related to β-cell function, including potassium voltage-gated channel KQT-like 1 (Kcnq1) and glucokinase (Gck).
• Chronic Insulin Resistance
  Insulin resistance is usually a failure of insulin signaling, resulting in inadequate plasma membrane translocation of glucose transporter 4 (GLUT4). The rate of insulin-stimulated glucose uptake is reduced by 54% in GDM when compared with normal pregnancy.

Our Services

Ace Therapeutics is able to provide pathological research services related to gestational diabetes and carry out integration and systematic analysis. Our services include but not limited to the followings.

Features of Our Services

Ace Therapeutics offers cost-effect and high-quality research services related to GDM for our clients worldwide. Our assays are developed and processed with the highest standard and the results are delivered on time without compromising quality. Please feel free to contact us.

Reference

1. McIntyre, H. D.; et al. Gestational diabetes mellitus. Nature Reviews Disease Primers. 2019, 5, 47.

• GDM Modeling Service
• GDM Therapy Development Service
• GDM Biomarker Development Service
• GDM Diagnostic Development Services

• Mouse Models
• Assay Kits
• Antibodies
• Cell Lines & Lysates
• Proteins & Peptides
• Inhibitors & Activators