Conjoint Endocrine Laboratory

Herston, Australia

Conjoint Endocrine Laboratory

Herston, Australia
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Landers K.,Conjoint Endocrine Laboratory | Richard K.,Conjoint Endocrine Laboratory | Richard K.,University of Queensland | Richard K.,Queensland University of Technology
Molecular and Cellular Endocrinology | Year: 2017

Thyroid hormone is essential for normal human fetal growth and brain development. As the fetal thyroid does not secrete thyroid hormones until about 18 weeks gestation, early fetal brain development depends on passage of maternal hormone across the placenta into the fetal circulation. To reach the fetal brain, maternally derived and endogenously produced thyroid hormone has to cross the blood-brain and blood-cerebrospinal fluid barriers. In this review we will discuss the complex biological barriers (involving membrane transporters, enzymes and distributor proteins) that must be overcome to ensure that the developing human brain has adequate exposure to thyroid hormone. © 2017.

PubMed | Conjoint Endocrine Laboratory, Royal Brisbane and Womens Hospital and Queensland University of Technology
Type: | Journal: International journal of endocrinology | Year: 2016

Sex Hormone Binding Globulin (SHBG) is the major serum carrier of sex hormones. However, growing evidence suggests that SHBG is internalised and plays a role in regulating intracellular hormone action. This study was to determine whether SHBG plays a role in testosterone uptake, metabolism, and action in the androgen sensitive LNCaP prostate cancer cell line. Internalisation of SHBG and testosterone, the effects of SHBG on testosterone uptake, metabolism, regulation of androgen responsive genes, and cell growth were assessed. LNCaP cells internalised SHBG by a testosterone independent process. Testosterone was rapidly taken up and effluxed as testosterone-glucuronide; however this effect was reduced by the presence of SHBG. Addition of SHBG, rather than reducing testosterone bioavailability, further increased testosterone-induced expression of prostate specific antigen and enhanced testosterone-induced reduction of androgen receptor mRNA expression. Following 38 hours of testosterone treatment cell morphology changed and growth declined; however, cotreatment with SHBG abrogated these inhibitory effects. These findings clearly demonstrate that internalised SHBG plays an important regulatory and intracellular role in modifying testosterone action and this has important implications for the role of SHBG in health and disease.

Molehin D.,University of Queensland | Dekker Nitert M.,University of Queensland | Richard K.,University of Queensland | Richard K.,Conjoint Endocrine Laboratory | Richard K.,Queensland University of Technology
Journal of Thyroid Research | Year: 2016

Background. Thyroid hormones (THs) are essential for normal human fetal development and play a major role in the regulation of glucose and lipid metabolism. Delivery of TH to target tissues is dependent on processes including TH synthesis, transport, and metabolism. Thyroid hormone endocrine disruptors (TH-EDCs) are chemical substances that interfere with these processes, potentially leading to adverse pregnancy outcomes. Objectives. This review focuses on the effects of prenatal exposures to combinations of TH-EDCs on fetal and neonatal glucose and lipid metabolism and also discusses the various mechanisms by which TH-EDCs interfere with other hormonal pathways. Methods. We conducted a comprehensive narrative review on the effects of TH-EDCs with particular emphasis on exposure during pregnancy. Discussion. TH imbalance has been linked to many metabolic processes and the effects of TH imbalance are particularly pronounced in early fetal development due to fetal dependence on maternal TH for proper growth and development. The pervasive presence of EDCs in the environment results in ubiquitous exposure to either single or mixtures of EDCs with deleterious effects on metabolism. Conclusions. Further evaluation of combined effects of TH-EDCs on fetal metabolic endpoints could improve advice provided to expectant mothers. Copyright © 2016 Deborah Molehin et al.

PubMed | Griffith University, Conjoint Endocrine Laboratory and Queensland University of Technology
Type: | Journal: Placenta | Year: 2016

Pregnancy is a physiological challenge that may require additional nutritional support. Suboptimal micronutrient intakes and micronutrient deficiencies during pregnancy are a global problem, often leading to poor maternal and child outcomes. Micronutrient supplementation is commonly recommended during pregnancy to support and enhance maternal metabolism. Recent studies suggest that the use of multiple micronutrient supplements may be of benefit during a normal pregnancy and may significantly reduce the risk of preeclampsia, preterm delivery, gestational diabetes, and improve pregnancy outcomes. Given the crucial role that the placenta plays in mediating pregnancy outcomes, it is important to consider the impact of micronutrient supplementation on the mechanisms associated with placental function, as well as maternal and fetal homeostasis. This review will consider the role of key micronutrients in supporting pregnancy and the possible mechanisms by which multiple micronutrients influence placental function and modulate placental oxidative stress and inflammation.

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