Volume 13 Issue 1, January 2017

Endocrine-disrupting chemicals (EDCs) can contribute to the development of certain disorders and are known to have a high health-care burden in some countries. A new analysis has revealed the substantial impact of EDCs on health and associated costs in the USA.

The link between mood disorders and hormonal fluctuations has long been known, but the direction of this correlation has been questioned. New research suggests that initiation of hormonal contraception leads to increased risk of first-time diagnosis of or treatment for depression over a short time frame, particularly for adolescents.

Early attempts at the reinduction of ¹³¹I uptake by redifferentiation of ¹³¹I-negative differentiated thyroid cancer (DTC) had limited success. Novel therapies targeting the pathways that restore expression of the sodium iodine symporter now offer new hope of success for redifferentiation therapy in DTCs with the BRAF^V600E mutation.

Sergueï Fetissov discusses the possible involvement of gut bacteria in the host regulation of appetite and proposes an integrative homeostatic model of appetite control that includes the energy needs of both the host and its gut bacteria.

In addition to undergoing adaptive thermogenesis, brown adipose tissue secretes a number of adipokines that can influence systemic metabolism. In this Review, Villarroya and colleagues discuss the current evidence for these so-called 'batokines' and how they might influence whole-body metabolic health.

Peroxisome proliferator-activated receptors (PPARs) are integrators of both inflammatory and metabolic signalling networks. In this Review, the authors provide a comprehensive overview of how PPARs contribute to the development of metabolic disorders and how pharmacologically targeting these pathways can be used to develop new therapeutics for such diseases.

Mericq and colleagues review human data supporting an increased risk of metabolic diseases among children born premature or small for gestational age. The adrenal and pubertal modifications that contribute to this risk and the metabolic changes that occur during adolescence and adulthood are discussed.