ABSTRACT
Fetal exposure in adverse environmental factors during intrauterine life can lead to various biological adjustments, affecting not only in utero development of the conceptus, but also its later metabolic and endocrine wellbeing. During human gestation, maternal bone turnover increases, as reflected by molecules involved in bone metabolism, such as vitamin D, osteocalcin, sclerostin, sRANKL, and osteoprotegerin; however, recent studies support their emerging role in endocrine functions and glucose homeostasis regulation. Herein, we sought to systematically review current knowledge on the effects of aforementioned maternal bone biomarkers during pregnancy on fetal intrauterine growth and metabolism, neonatal anthropometric measures at birth, as well as on future endocrine and metabolic wellbeing of the offspring. A growing body of literature converges on the view that maternal bone turnover is likely implicated in fetal growth, and at least to some extent, in neonatal and childhood body composition and metabolic wellbeing. Maternal sclerostin and sRANKL are positively linked with fetal abdominal circumference and subcutaneous fat deposition, contributing to greater birthweights. Vitamin D deficiency correlates with lower birthweights, while research is still needed on intrauterine fetal metabolism, as well as on vitamin D dosing supplementation during pregnancy, to diminish the risks of low birthweight or SGA neonates in high-risk populations.
Subject(s)
Fetal Development , Vitamin D Deficiency , Birth Weight , Child , Female , Humans , Infant, Low Birth Weight , Infant, Newborn , Pregnancy , Vitamin D , VitaminsABSTRACT
Recent studies have shown a rise in precocious puberty, especially in girls. At the same time, childhood obesity due to overnutrition and energy imbalance is rising too. Nutrition and fertility are currently facing major challenges in our societies, and are interconnected. Studies have shown that high-fat and/or high-glycaemic-index diet can cause hypothalamic inflammation and microglial activation. Molecular and animal studies reveal that microglial activation seems to produce and activate prostaglandins, neurotrophic factors activating GnRH (gonadotropin-releasing hormone expressing neurons), thus initiating precocious puberty. GnRH neurons' mechanisms of excitability are not well understood. In this review, we study the phenomenon of the rise of precocious puberty, we examine the physiology of GnRH neurons, and we review the recent literature regarding the pathophysiological mechanisms that connect diet-induced hypothalamic inflammation and diet-induced phoenixin regulation with precocious puberty.
Subject(s)
Diet/adverse effects , Encephalitis/complications , Hypothalamus/metabolism , Peptide Hormones/metabolism , Puberty, Precocious/etiology , Puberty, Precocious/metabolism , Animals , Biomarkers , Disease Susceptibility , Encephalitis/etiology , Encephalitis/pathology , Humans , Hypothalamus/pathologyABSTRACT
Obstetrics/gynecology (OB/GYN) clinicians often manage gender dysphoric patients but frequently lack the necessary training. These individuals comprise a vastly heterogeneous group and gender clinics, staffed by multi-disciplinary teams, should become the standard of care, promoting a holistic approach. All OB/GYN clinicians need to be aware of basic aspects of gender dysphoria.