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In the currently overwhelming era of polypharmacy, the balance of the dynamic and delicate endocrine system can easily be disturbed by interfering pharmaceutical agents like medications. Drugs can cause endocrine abnormalities via different mechanisms, including direct alteration of hormone production, changes in the regulation of the feedback axis, on hormonal transport, binding and signaling, as well as similar changes to counter-regulatory hormone systems. Furthermore, drugs can interfere with the hormonal assays, leading to erroneous laboratory results that disorientate clinicians from the right diagnosis. The purpose of this review is to cover a contemporary topic, the drug-induced endocrinopathies, which was presented in the monothematic annual Combo Endo Course 2018. This challenging part of endocrinology is constantly expanding particularly during the last decade, with the new oncological therapeutic agents, targeting novel molecular pathways in the process of malignancies. In this new context of drug-induced endocrine disease, clinicians should be aware that drugs can cause endocrine abnormalities via different mechanisms and mimic a variety of clinical scenarios. Therefore, it is extremely important for clinicians not only to promptly recognize druginduced hormonal and metabolic abnormalities, but also to address the therapeutic issues for timely intervention. [ABSTRACT FROM AUTHOR]

The so-called 'endocrine disruption hypothesis' suggests that exposures to endocrine disruption (EDs) during fetal, neonatal and adult life may interfere with the development of reproductive organs and alter semen quality and reproductive hormone production. Even though animal studies provide substantial evidence of adverse effects of EDs on male reproductive system, epidemiological studies in humans arrive at conflicting results. The aim of the present study was to systematically review the literature to locate methodological characteristics of the studies that struggle the formation of an association between EDs and human male reproduction. Such characteristics include: (i) definition of the exposed and the non-exposed population, (ii) age, (iii) insufficient control for confounders, (iv) ED assay and threshold, (v) time parameters of ED exposure, and (vi) study outcomes. Additional issues are: (i) the late effect of an early exposure, (ii) the multiple exposure effect, and (iii) the fact the same ED may exhibit different modes of action. Unfortunately, the nature of the field precludes the conduction of randomized-controlled trials, which could result to etiological associations between EDs and human male reproduction. Consequently, there is a great need to conduct well-designed studies of case-control or cohort type to evaluate EDs effects on human male reproductive health, and apply possible measures that could limit dangerous exposures. [ABSTRACT FROM AUTHOR]

Glucococorticoids play a critical role in the developmental programing and fetal growth. Key molecules mediating and regulating tissue-specific glucocorticoid actions are 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 and 2 isozymes, both of which are expressed in the placenta and the fetal membranes. 11beta-HSD1 is implicated in the pathogenesis of metabolic syndrome and its dysregulation has been observed in pregnancy-related complications (pre-eclampsia, intrauterine growth restriction). Interestingly, preliminary clinical data have associated certain 11beta-HSD1 gene polymorphisms with hypertensive disorders in pregnancy, suggesting, if confirmed by further targeted studies, it’s potential as a putative prognostic marker. Animal studies and observations in humans have confirmed that 11beta-HSD2 insufficiency is related with pregnancy adversity (pre-eclampsia, intrauterine growth restriction, preterm birth). Importantly, down-regulation or deficiency of placental 11beta-HSD2 is associated with significant restriction in fetal growth and low-birth weight, and unfavorable cardio-metabolic profile in adulthood. The potential association of 11beta-HSD1 tissue-specific dysregulation with gestational diabetes, as well as the plausible utility of 11beta-HSD2, as a biomarker of pregnancy adversity and later life morbidity, are emerging areas of intense scientific interest and future investigation. [ABSTRACT FROM PUBLISHER]

Endocrine disruptors are chemical substances (natural or synthetic) that interfere with endogenous hormone function in humans and animals. The use of these chemicals is widespread and the sources of human exposure are multiple, including food, water, air and soil. Maternal-child exposure (through the placenta or breast milk) is an additional source. More than one hundred natural or synthetic compounds affecting thyroid function by multiple mechanisms have been identified. Endocrine disruptors may inhibit thyroidal iodine uptake (perchlorate, thiocyanate and nitrate ions), or thyroperoxidase activity (isoflavones), act directly on the thyroid hormone receptor (polychlorinated biphenyls, polybrominated biphenyls, bisphenol-A and triclosan), or affect the transport and metabolism of thyroid hormones (polychlorinated biphenyls, polybrominated biphenyls, genistein, dioxins and others). Exposure to endocrine disruptors is an important health issue for the general population, but humans are more vulnerable during gestation and childhood, as endocrine disruptors may affect development at several stages. In certain cases there is a significant time lag between exposure to endocrine disruptors and clinical presentation of the effects, which makes their study particularly difficult. Some thyroid disruptors have been studied exclusively in vitro or in experimental animals, and their effects in humans are still under investigation. In this review, thyroid disruptors are classified and presented according to their mode of action, including their potential role in thyroid tumorigenesis. Additional epidemiological studies are needed to further elucidate their action. Preventive strategies are becoming necessary to avoid public exposure to these substances. [ABSTRACT FROM AUTHOR]

The aim of the study was to examine the frequency and relationship of peroxisome proliferator-activated receptor (PPAR)-γ and PPAR-δ gene polymorphisms to polycystic ovary syndrome (PCOS) characteristics. We conducted a case-control study protocol, which included 183 PCOS women and 148 healthy volunteers. Genetic, clinical, hormonal, and metabolic characteristics of PCOS patients and controls were estimated and compared. Genotype and allele frequencies did not differ significantly. The Pro12Ala polymorphism in exon 2 of the PPAR-γ gene was found in low frequency. Regarding the polymorphism in exon 6, the T-allele carrier PCOS women had significantly lower total testosterone levels. Regarding the +294T/C polymorphism in the exon 4 of the PPAR-δ gene, the C-allele carrier PCOS women had significantly higher fasting glucose levels. In conclusion, the PPAR-γ gene polymorphisms do not appear to affect the risk for PCOS, except for the reduced testosterone levels. The +294T/C polymorphism in the exon 4 of the PPAR-δ gene seems to cause an increase in fasting glucose levels. [ABSTRACT FROM AUTHOR]

During pregnancy, important changes take place in maternal metabolism because of the growing fetus and placental formation. The increase in insulin resistance during pregnancy is paralleled by the progressive increase of maternal adipose tissue deposition. This review examines the topography of fat mass deposition during pregnancy in relation to factors such as parity and maternal age that might affect this deposition. We also examine adipose tissue markers, such as pregravid weight and weight gain during pregnancy, and their effect on fetal growth and pregnancy outcomes. In addition, this review studies the possible effects of cytokines that are produced by adipose tissue and the placenta on maternal metabolism and its complications. Finally, we also consider the possible role of maternal adipocytokines and fetal adipocytokines on fetal growth. [ABSTRACT FROM AUTHOR]

Gestational hypertension complicates approximately 5%-7% of pregnancies and it may be deleterious to both maternal and fetal health. Gestational hypertension is a multisystem disorder which always resolves itself after delivery; its primary pathology still remains incompletely clarified. The renin-aldosterone system is a major determinant of sodium balance in pregnancy. To evaluate the changes in renin and aldosterone levels during normal and hypertensive pregnancy we undertook this study. Plasma renin activity and aldosterone levels were measured in 71 pregnant (43 normotensive, 28 hypertensive) and 24 non-pregnant (12 normotensive, 12 hypertensive) women, aged 19-43 years (mean +/- SD 28 +/- 2.8). Women were allocated into the following five groups: Groups 1 and 2 consisted of 12 normotensive and 12 hypertensive non-pregnant women, respectively; group 3 consisted of 20 women (14 normotensive and 6 hypertensive) at 11-19 weeks of gestation; group 4 consisted of 24 women (14 normotensive and 10 hypertensive) at 20-29 weeks of gestation, and group 5 consisted of 27 women (15 normotensive and 12 hypertensive) at 30-37 weeks of gestation. Both plasma renin activity and aldosterone levels progressively increased during normotensive pregnancy and were higher compared to normotensive non-pregnant women. Among hypertensive pregnant women, plasma renin activity levels remained unchanged during the three trimesters of pregnancy and were higher compared to hypertensive non-pregnant women. Only during the third trimester did aldosterone levels significantly increase in hypertensive pregnant women, compared to hypertensive non-pregnant women. Despite stable renin levels, aldosterone levels increased significantly during the third trimester of hypertensive pregnancy. Thus, we conclude that aldosterone biology seems to be directly or indirectly involved in the etiology of gestational hypertension independently of renin levels. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of acute resistance exercise on adipose tissue triacylglycerol lipase activity (TGLA) in lean and obese men.Research Design and Methods: Nine lean and eight obese men performed 30 min of circuit resistance exercise. Adipose tissue and blood were sampled during exercise for TGLA, metabolite, and hormone determinations. Respiratory exchange ratio (RER) was measured throughout exercise.Results: Energy expenditure of exercise relative to body mass was higher in the lean and RER was higher in the obese men, suggesting lower fat oxidation. TGLA increased 18-fold at 5 min of exercise in the lean men and 16-fold at 10 min of exercise in the obese men. The delayed lipolytic activation in the obese men was reflected in serum nonesterified fatty acid and glycerol concentrations. Plasma insulin increased in the obese but did not change in the lean men.Conclusions: Resistance exercise upregulated adipose tissue lipolysis and enhanced energy expenditure in lean and obese men, with a delayed lipolytic activation in the obese men. [ABSTRACT FROM AUTHOR]

Objective . To investigate the possible link between insulin resistance and preeclampsia. Methods . The study included 30 primigravidas between 28 and 34 weeks of gestation. The study subjects were divided into two groups: Group A consisted of 15 normotensive women of a mean gestational age of 31.6 weeks and group B consisted of 15 preeclamptic women of a mean gestational age of 29.9 weeks. Glucose and insulin levels were measured at 0, 1 and 2 h of an OGTT (after 75 g oral glucose administration). Insulin resistance and sensitivity were evaluated with the use of IR HOMA, QUICKI and IS OGTT. Results . Glucose and insulin levels at 0, 1 and 2 h of the OGTT as well as IR HOMA, QUICKI and IS OGTT were comparable between preeclamptic and normotensive pregnant women. Conclusions . Our results indicate that preeclampsia is not associated with hyperinsulinaemia and/or insulin resistance, in either the fasting or the postprandial state. [ABSTRACT FROM AUTHOR]

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