Cardiovascular dysfunctions complicate 10-20% of pregnancies, increasing the risk for postpartum mortality. Various gestational insults, including preeclampsia are reported to be associated with adverse maternal cardiovascular outcomes. One such insult, gestational hyperandrogenism increases the risk for preeclampsia and other gestational morbidities but its impact on postpartum maternal health is not well known. We hypothesize that gestational hyperandrogenism such as testosterone (T) excess will adversely impact the maternal heart in the postpartum period. Pregnant ewes were injected with T propionate from to of gestation (term 147 days). Three months postpartum, echocardiograms, plasma cytokine profiles, cardiac morphometric, and molecular analysis were conducted [control (C) = 6, T-treated (T) = 7 number of animals]. Data were analyzed by two-tailed Student's test and Cohen's effect size () analysis. There was a nonsignificant large magnitude decrease in cardiac output (7.64 ± 1.27 L/min vs. 10.19 ± 1.40, = 0.22, = 0.81) and fractional shortening in the T ewes compared with C (35.83 ± 2.33% vs. 41.50 ± 2.84, = 0.15, = 0.89). T treatment significantly increased ) left ventricle (LV) weight-to-body weight ratio (2.82 ± 0.14 g/kg vs. 2.46 ± 0.08) and LV thickness (14.56 ± 0.52 mm vs. 12.50 ± 0.75), ) proinflammatory marker [tumor necrosis factor-alpha (TNF-α)] in LV (1.66 ± 0.35 vs. 1.06 ± 0.18), ) LV collagen (Masson's Trichrome stain: 3.38 ± 0.35 vs. 1.49 ± 0.15 and Picrosirius red stain: 5.50 ± 0.32 vs. 3.01 ± 0.23), ) markers of LV apoptosis, including TUNEL (8.3 ± 1.1 vs. 0.9 ± 0.18), bcl-2-associated X protein (Bax)+-to-b-cell lymphoma 2 (Bcl2)+ ratio (0.68 ± 0.30 vs. 0.13 ± 0.02), and cleaved caspase 3 (15.4 ± 1.7 vs. 4.4 ± 0.38). These findings suggest that gestational testosterone excess adversely programs the maternal LV, leading to adverse structural and functional consequences in the postpartum period. Using a sheep model of human translational relevance, this study provides evidence that excess gestational testosterone exposure such as that seen in hyperandrogenic disorders adversely impacts postpartum maternal hearts.
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http://dx.doi.org/10.1152/ajpheart.00763.2023 | DOI Listing |
Cureus
December 2024
Internal Medicine and Family Medicine, Larkin Community Hospital Palm Springs Campus, Miami, USA.
The purpose of this review is to explore the relationship between weight loss (WL), specifically reductions in body mass index (BMI), and increases in testosterone levels. Obesity and excess body fat are linked to reduced testosterone levels, which can lead to metabolic dysfunctions, reduced libido, and diminished muscle mass. To attain this purpose, this review will summarize current evidence on how weight reduction interventions, including dietary changes, exercise, and bariatric surgery, affect testosterone production in overweight and obese individuals.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Harbin 150030, China. Electronic address:
Bisphenol A (BPA) is a common endocrine disruptor chemical that is widely used in the production of food plastic packaging, and it has been shown to potentially harm the reproductive system. However, the specific mechanism by which BPA induces apoptosis of Leydig cells (LCs) and inhibits testosterone synthesis in these cells is unclear. In the present study, TM3 cells were used as an experimental model in combination with a reactive oxygen species (ROS) scavenger (N-acetylcysteine), Caspase-3 inhibitor (Ac-DEVD-CHO), autophagy activator (Torin2), and autophagy inhibitor (Chloroquine) to investigate the potential mechanisms by which BPA causes TM3 cell damage in vitro.
View Article and Find Full Text PDFF S Rep
December 2024
Departments of Neurology, Division of Sleep Medicine, and Obstetrics & Gynecology, Michigan Medicine, Ann Arbor, Michigan.
Objective: Incorporate sleep into a novel lifestyle intervention strategy in adolescents with Emerging symptoms of polycystic ovary syndrome (E-PCOS).
Design: A single-center cohort study.
Setting: University hospital-based clinic for adolescents with PCOS.
J Endocr Soc
November 2024
Division of Endocrinology, Metabolism and Diabetes, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA.
"Pseudo-endocrine disorders" refer to proposed conditions that have never been scientifically proven to exist but, due to widespread misinformation available on the internet and other media, are relatively commonly diagnosed and treated with equally unproven and sometimes dangerous treatments. Adrenal fatigue is a nonexistent condition that supposedly results from adrenal exhaustion and atrophy due to chronic stress and has been promoted as a potential explanation for a variety of symptoms. Testing consists of nonvalidated online surveys and salivary cortisol profiles while treatment is not evidence-based at best and can be dangerous.
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