Studies in the Society journals

The following studies, among others, will be published in Endocrine Society journals. Before print, they are edited and posted online in each journal’s Early Release section. You can access the journals at www.endocrine.org.

A Novel Point Mutation of the Human Glucocorticoid Receptor Gene Causes Primary Generalized Glucocorticoid Resistance Through Impaired Interaction with the LXXLL Motif of the p160 Coactivators: Dissociation of the Transactivating and Transreppressive Activities • Nicolas C. Nicolaides, Michael L. Roberts, Tomoshige Kino, Geoffrey Braatvedt, Darrell E. Hurt, Eleni Katsantoni, Amalia Sertedaki, George P. Chrousos, and Evangelia Charmandari • The natural mutant receptor hGRαV575G causes Primary Generalized Glucocorticoid Resistance by affecting multiple steps in the glucocorticoid signaling cascade, including the affinity for the ligand, the time required for nuclear translocation and the interaction with the GRIP1 coactivator.

The HIV Protease Inhibitor Nelfinavir Downregulates RET Signaling and Induces Apoptosis in Medullary Thyroid Cancer Cells • Yevgeniya Kushchayeva, Kirk Jensen, Antony Recupero, John Costello, Aneeta Patel, Joanna Klubo-Gwiezdzinska, Lisa Boyle, Kenneth Burman, and Vasyl Vasko • NFV has a wide spectrum of activity against MTC cells and its cytotoxicity can be augmented by inhibiting autophagy. Expression of NFV molecular targets in metastatic MTC suggests that NFV has a potential to become a thyroid cancer therapeutic agent.

Treadmill Running Reduces Parathyroid Hormone Concentrations During Recovery Compared with a Nonexercising Control Group • Jonathan P. R. Scott, Craig Sale, Julie P. Greeves, Anna Casey, John Dutton, and William D. Fraser • Lower PTH concentrations after acute endurance running compared with a rested control condition suggest a true effect of exercise.

ProgesteroneInduced Migration Inhibition in Male Rat Aortic Smooth Muscle Cells Through the cSrc/ AKT/ERK 2/p38 Pathway-Mediated Up-Regulation of p27 • Hui-Chen Wang and Wen-Sen Lee • The data suggest that P4 increased the levels of p27 in RASMCs through activating the cSrc/ AKT/ERK 2/p38 pathway mediated by nongenomic progesterone receptor. The findings of the present study highlight the molecular mechanisms underlying P4-induced migration inhibition in RASMCs.

Krüppel-Like Factor 9 (KLF9) Deficiency in Uterine Endometrial Cells Promotes Ectopic Lesion Establishment Associated with Activated Notch and Hedgehog Signaling in a Mouse Model of Endometriosis • Melissa E. Heard, Christian D. Simmons, Frank A. Simmen, and Rosalia C.M. Simmen • The results suggest that endometrial KLF9 deficiency promotes endometriotic lesion establishment by the coincident deregulation of Notch, Hedgehog, and steroid receptor-regulated pathways.

Leptin Deficiency in Rats Results in Hyperinsulinemia and Impaired Glucose Homeostasis • Anna M. D’souza, Ali Asadi, James D. Johnson, Scott D. Covey, and Timothy J. Kieffer • Together, these data demonstrate that the absence of leptin in rats recapitulates some of the phenotype previously observed in ob/ob mice including development of hyperinsulinemia, obesity, and insulin resistance.

Chlorinated Persistent Organic Pollutants, Obesity, and Type 2 Diabetes • Duk-Hee Lee, Miquel Porta, David R. Jacobs, and Laura N. Vandenberg • This review examines the relationship between POPs and obesity. There is evidence in animal studies that low dose POP mixtures are obesogenic. However, relationships between POPs and obesity in humans have been inconsistent.

Steroid Receptor Coactivator 1 is an Integrator of Glucose and NAD+/NADH Homeostasis • Massoud Motamed, Kimal I. Rajapakshe, Sean M. Hartig, Cristian Coarfa, Robb E. Moses, David M. Lonard, and Bert W. O’Malley • Knockdown of SRC-1 in glycolytic cancer cells abrogated their ability to grow in the absence of glucose consistent with SRC1’s role in promoting cellular adaptation to reduced glucose availability.

Decreased Genetic Dosage of Hepatic Yin Yang 1 Causes Diabetic-Like Symptoms • Francisco Verdeguer, Sharon M. Blättler, John T. Cunningham, Jessica A. Hall, Helen Chim, and Pere Puigserver • Mechanistically, YY1, through direct recruitment to promoters, functions as a suppressor of genes encoding for metabolic enzymes of the gluconeogenic and lipogenic pathways, and as an activator of genes linked to fatty acid oxidation. These counterregulatory transcriptional activities make targeting hepatic YY1 an attractive approach for treating insulin-resistant diabetes.

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