Editorial: Molecular Endocrinology Articles in the Spotlight for November 2013 Donald B. DeFranco Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15260

n the November issue of Molecular Endocrinology, the following articles are particularly noteworthy: “Glucose Transporter-8 (GLUT8) Mediates Glucose Intolerance and Dyslipidemia in High-Fructose Diet-Fed Male Mice” by DeBosch et al identifies a potential target that modulates development of diet-induced metabolic syndrome in males. Specifically, this study suggests that hexose delivery across the hepatocyte membrane could have profound effects on whole-body metabolic homeostasis. The article provides evidence that GLUT8 could serve as a “switch” or node that mediates carbohydratefat metabolism in the liver and highlights the long-existing paradigm of sexual dimorphism in this diet-induced model of metabolic syndrome. In “Transgenic Muscle-Specific Nor-1 Expression Regulates Multiple Pathways That Effect Adiposity, Metabolism, and Endurance” (freely available at http:// mend.endojournals.org/), Pearen et al found that transgenic mice overexpressing activated Nor-1 in skeletal muscle have an endurance phenotype and display decreased adiposity and resistance to weight gain. These mice also accumulate hepatic triglyceride on a high-fat diet and exhibit increased glycogen storage. This phenotype is associated with the significant induction of gene expression in pathways associated with glycolysis, TCA


doi: 10.1210/me.2013-1310

cycle, oxidative phosphorylation, fatty acid oxidation, glycogen synthesis, and the malate-aspartate shuttle that maximize ATP production. Furthermore, Nor-1 expression regulated expression of genes encoding several Zdisc and sarcomeric binding proteins (eg, ␣-actinin-3) that modulate fiber type phenotype, oxidative capacity, and endurance in humans. “Smad3 Induces Atrogin-1, Inhibits mTOR and Protein Synthesis, and Promotes Muscle Atrophy In Vivo” by Goodman et al provides the first in vivo evidence establishing that Smad3 is sufficient to directly induce atrophy and inhibit protein synthesis, two characteristics of increased myostatin signaling. Smad3-induced atrophy is associated with the activation of the ubiquitin proteasome E3 ligase atrogin-1 promoter, the inhibition of the PGC1␣ promoter, and activation and inhibition of the fibrosis-related PAI-1 and miR-29 promoters, respectively. Therefore, specific targeting of Smad3 signaling may be a viable approach to inhibit of myostatin, TGF-␤, and/or activatin-induced muscle atrophy and fibrosis. I would like to thank these researchers as well as all the contributors to this issue for their work and research that continue to push the frontiers of science. Donald B. DeFranco, PhD Editor-in-Chief, Molecular Endocrinology

Mol Endocrinol, November 2013, 27(11):1795


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Editorial: Molecular endocrinology articles in the spotlight for November 2013.

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