Editorial:Molecular EndocrinologyArticles in the Spotlight for March 2013

Abstract

Welcome to the March issue of Molecular Endocrinology. We think you will find these articles to be interesting and enlightening: In their article, “Impaired Fertility and FSH Synthesis in Gonadotrope-Specific Foxl2 Knockout Mice,” Tran et al describe the first gonadotrope-specific knockout model with a selective impairment in FSH synthesis and secretion. Their work establishes forkhead protein L2 (FOXL2) as the first cell-restricted transcription factor required for FSH -subunit (FSHb) expression in vivo. This important study advances our understanding of mechanisms of differential regulation of the gonadotropins. “The Endocrine Disrupting Chemical Tolylfluanid Alters Adipocyte Metabolism via Glucocorticoid Receptor Activation” by Neel et al finds that despite lacking structural similarity to known glucocorticoids, the fungicide tolylfluanid activates glucocorticoid signaling and alters insulin signal transduction through enhanced glucocorticoid receptor (GR) binding to a specific response element in the insulin receptor substrate-1 (IRS-1) gene. This effect mimics the action of low-dose corticosterone. Furthermore, tolylfluanid and corticosterone result in duration-dependent effects on insulin signaling. Therefore, tolylfluanid, an endocrine-disrupting chemical found on fruit crops in Europe that acts on GR may play a heretofore-unrecognized role in metabolic disorders. List et al’s “The Role of GH in Adipose Tissue: Lessons From Adipose-Specific GH Receptor Gene-Disrupted Mice” (freely available at http://mend.endojournals.org/) uses healthy obese mice in which the GH receptor (GHR) gene is disrupted to study the in vivo effects of GH directly on adipose tissue. Surprisingly, the adipose-specific GH receptor knockout shares few metabolic characteristics of a global GHR knockout. For example, the adipose-specific GHR knockout mice are obese with increased total body fat and increased adipocyte size, but resistin and adiponectin levels as well as glucose metabolism are not altered. Therefore, increased circulating adipokines in GHR global knockout mice are likely due to altered GH signaling in nonadipose tissue. Our thanks and congratulations go out to these and all of the authors of this issue’s excellent research. Donald B. DeFranco, PhD. Editor-in-Chief, Molecular Endocrinology