Role of ET-1, Physical Activity, and Sedentary Behavior in Microvascular Dysfunction Following GDM

Summary

Women with a history of gestational diabetes mellitus (GDM) are at a 2-fold greater risk for the development of overt cardiovascular disease (CVD) following the effected pregnancy. While subsequent development of type II diabetes elevates this risk, prior GDM is an independent risk factor for CVD morbidity, particularly, within the first decade postpartum. GDM is associated with impaired endothelial function during pregnancy and decrements in macro- and microvascular function persist postpartum, despite the remission of insulin resistance following delivery. Collectively, while the association between GDM and elevated lifetime CVD risk is clear, and available evidence demonstrates a link between GDM and vascular dysfunction in the decade following pregnancy, the mechanisms mediating this persistent dysfunction remain unexamined. The purpose of this investigation is to examine the role of endothelin-1, a potent vasoconstrictor, in aberrant microvascular function in otherwise healthy women with a history of GDM and to identify whether this mechanism is influenced by physical activity and sedentary behavior.

Eligibility

INCLUSION CRITERIA

* history of pregnancy within 5 years of the study visit
* had healthy pregnancy OR had gestational diabetes diagnosed by their obstetrician and confirmed according to the American College of Obstetricians and Gynecologists criteria for gestational diabetes.

EXCLUSION CRITERIA

* skin diseases,
* current tobacco or electronic cigarette/vape pen use,
* diagnosed or suspected hepatic or metabolic disease including diabetes,
* statin or other cholesterol-lowering medication,
* current antihypertensive medication,
* history of preeclampsia or gestational hypertension
* current hypertension,
* current pregnancy,
* body mass index \<18.5 kg/m2,
* allergy to materials used during the experiment.(e.g. latex), known allergies to study drugs.

Conditions4

Interventions1

Locations1 site

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