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There is increasing evidence linking bitter taste receptor (BTR) signaling to gut hormone secretion and glucose homeostasis. However, its effect on islet hormone secretion has been poorly characterized. This study investigated the effect of the bitter substance, denatonium benzoate (DB), on hormone secretion from mouse pancreatic islets and INS-1 832/13 cells. DB (0.5-1 mM) augmented insulin secretion at both 2.8 mM and 16.7 mM glucose. This effect was no longer present at 5 mM DB likely due to the greater levels of cellular apoptosis. DB-stimulated insulin secretion involved closure of the KATP channel, activation of T2R signaling in beta-cells, and intraislet glucagon-like peptide-1 (GLP-1) release. DB also enhanced glucagon and somatostatin secretion, but the underlying mechanism was less clear. Together, this study demonstrates that the bitter substance, DB, is a strong potentiator of islet hormone secretion independent of glucose. This observation highlights the potential for widespread off-target effects associated with the clinical use of bitter-tasting substances. [ABSTRACT FROM AUTHOR]

In 2020, the COVID-19 pandemic forced unprecedented disruptions in higher education operations. While the adverse mental health effects experienced by college students due to these changes are well documented, less is known about the impact on their sexual and reproductive health (SRH), and the reciprocal relationships between SRH and mental health among adolescents and emerging adults. This position paper reviews existing literature on the effects of the COVID-19 pandemic on SRH, sexual violence, unintended pregnancy, sexually transmitted illness and human immunodeficiency virus rates and highlights issues specific to college-aged males, females, racial/ethnic and sexual minorities, and individuals with disabilities. The need to conceptualize SRH as an integral component of normal development, overall health, and well-being in the context of COVID-19 is discussed. The need to prioritize the design and implementation of developmentally appropriate, evidence-based SRH interventions specifically targeting college students is identified. Furthermore, an intergenerational approach to SRH that includes parents/caregivers and/or college faculty and staff (e.g., coaches, trainers) could facilitate comprehensive SRH prevention programming that enhances sexual violence prevention training programs currently mandated by many colleges. Policies and programs designed to mitigate adverse pandemic-related exacerbations in negative SRH outcomes are urgently needed and should be included in mainstream clinical psychology, not only focused on preventing unwanted outcomes but also in promoting rewarding interpersonal relationships and overall well-being. Recommendations for clinical psychologists and mental health researchers are made. [ABSTRACT FROM AUTHOR]

Antenatal glucocorticoids accelerate fetal lung maturation and reduce mortality in preterm babies but can trigger adverse effects on the cardiovascular system. The mechanisms underlying off‐target effects of the synthetic glucocorticoids mostly used, Dexamethasone (Dex) and Betamethasone (Beta), are unknown. We investigated effects of Dex and Beta on cardiovascular structure and function, and underlying molecular mechanism using the chicken embryo, an established model system to isolate effects of therapy on the developing heart and vasculature, independent of effects on the mother or placenta. Fertilized eggs were treated with Dex (0.1 mg kg−1), Beta (0.1 mg kg−1), or water vehicle (Control) on embryonic day 14 (E14, term = 21 days). At E19, biometry, cardiovascular function, stereological, and molecular analyses were determined. Both glucocorticoids promoted growth restriction, with Beta being more severe. Beta compared with Dex induced greater cardiac diastolic dysfunction and also impaired systolic function. While Dex triggered cardiomyocyte hypertrophy, Beta promoted a decrease in cardiomyocyte number. Molecular changes of Dex on the developing heart included oxidative stress, activation of p38, and cleaved caspase 3. In contrast, impaired GR downregulation, activation of p53, p16, and MKK3 coupled with CDK2 transcriptional repression linked the effects of Beta on cardiomyocyte senescence. Beta but not Dex impaired NO‐dependent relaxation of peripheral resistance arteries. Beta diminished contractile responses to potassium and phenylephrine, but Dex enhanced peripheral constrictor reactivity to endothelin‐1. We conclude that Dex and Beta have direct differential detrimental effects on the developing cardiovascular system. [ABSTRACT FROM AUTHOR]