Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT₁R, AT₂R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response(P<0.05versus SD) in intact (e+) but not in endothelium-free (e−) vessels. Losartan reduced GDM but not SD e− vasoconstriction(P<0.01versus SD). AT₁R, AT₂R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels(P<0.05versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT₂vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations.

To study whether hypercaloric diet–induced obesity deteriorates vascular contractility of rat aorta through functional changes in α₁ adrenergic and/or AT1 Angiotensin II receptors. Angiotensin II- or phenylephrine-induced contraction was tested on isolated aorta rings with and without endothelium from female Wistar rats fed for 7 weeks with hypercaloric diet or standard diet. Vascular expression of Angiotensin II Receptor type 1 (AT1R), Angiotensin II Receptor type 2 (AT2R), Cyclooxygenase-1 (COX-1), Cyclooxygenase-2 (COX-2), inducible Nitric Oxide Synthase (iNOS) and endothelial Nitric Oxide Synthase (eNOS), as well as blood pressure, glucose, insulin and angiotensin II blood levels were measured. Diet-induced obesity did not significantly change agonist-induced contractions (Emax and pD₂ hypercaloric diet vs standard diet n.s.d.) of both intact (e+) or endothelium free (e−) vessels but significantly decrease both phenylephrine and angiotensin II contraction (Emax p < 0.01 hypercaloric diet vs standard diet) in the presence of both prazosin and losartan but only in endothelium-intact vessels. Diet-induced obesity did not change angiotensin II AT1, AT2 receptor proteins expression but reduced COX-1 and NOS2 (p < 0.05 vs standard diet). Seven-week hypercaloric diet–induced obesity produces alterations in vascular adrenergic and angiotensin II receptor dynamics that suggest an endothelium-dependent adrenergic/angiotensin II crosstalk. These changes reflect early-stage vascular responses to obesity.

Obesity is a complex metabolic disorder resulting from interactions among genetic, environmental, and dietary factors. Traditional clinical markers may provide limited insight into the biochemical mechanisms that link nutrition and metabolic dysfunction; in this context, the epigenetic mechanisms through which nutrients modulate gene expression are central to understanding metabolic homeostasis. This review summarizes the published evidence on nutrient-driven epigenetic processes in obesity, focusing on DNA methyl donors, such as folate, vitamin B12, choline, betaine, serine, and methionine, and their effects on methylation and DNA methyltransferase activity. Metabolites such as acetyl-CoA, NAD⁺, and short-chain fatty acids (SCFAs) can also influence histone modifications, while diet-responsive microRNAs can regulate networks involved in adipogenesis, lipid metabolism, inflammation, and insulin signaling. Recent studies have identified epigenetic signatures associated with adiposity and metabolic traits, many of which are linked to the risk of cardiometabolic disease. This review is structured around the concept that nutrient-sensitive epigenetic mechanisms act as candidate biomarkers, linking dietary exposure to metabolic dysfunction. Recent evidence supports the idea that nutrient–epigenetic variation could complement traditional metabolic evaluations by offering mechanistic insight and translational direction. These findings suggest that nutrient-sensitive epigenetic mechanisms are biologically plausible candidate biomarker layers; however, their clinical implementation is currently limited by issues including tissue specificity, reproducibility, and the need for prospective validation.

Pregnancy is the human reproductive process that begins with the implantation of the conceptus into the endometrium and concludes with birth. During this stage, the maternal organism undergoes a series of physiological adaptations aimed at ensuring the success of the mother–child dyad. In this context, free radicals play a crucial role in the development of pregnancy, as their participation in both embryo implantation and subsequent development has been well-demonstrated. Oxidative stress arises from an increase in free radicals, specifically reactive oxygen species (ROS), or a decrease in antioxidant defense mechanisms. During a healthy pregnancy, a certain amount of ROS is required for the progression of normal cellular functions; however, excessive ROS production can overwhelm the body’s natural antioxidant defense system. This creates an environment unsuitable for normal female physiological reactions, leading to pregnancy complications such as spontaneous abortion, recurrent pregnancy loss, preeclampsia, and intrauterine growth restriction. This chapter will address the role of free radicals during the development of a healthy pregnancy, further describing how their imbalance impacts the pathogenesis of the primary conditions affecting pregnancy.