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.
Prevalence of Pituitary Dysfunction Following Severe Traumatic Brain Injury in Children and Adolescents: A Large Prospective Study • Claire Personnier, Hélène Crosnier, Philippe Meyer, Mathilde Chevignard, Isabelle Flechtner, Nathalie Boddaert, Sylvain Breton, Caroline Mignot, Yamina Dassa, Jean-Claude Souberbielle, Marie Piketty, Kathleen Laborde, Jean-Philipe Jais, Magali Viaud, Stephanie Puget, Christian Sainte-Rose, and Michel Polak • At one year post-severe TBI, pituitary dysfunction was found in 8% of our study sample. We recommend systematic hormonal assessment in children and adolescents 12 months after severe TBI and prolonged clinical endocrine follow-up.
Development and Characterization of a Differentiated Thyroid Cancer Cell Line Resistant to VEGFR-Targeted Kinase Inhibitors • Crescent R. Isham, Brian C. Netzel, Ayoko R. Bossou, Dragana Milosevic, Kendall W. Cradic, Stefan K. Grebe, and Keith C. Bible • Selection of thyroid cancer cells with clinically utilized therapeutics can lead to acquired drug resistance and altered in vivo xenograft behavior that can recapitulate analogous drug resistance observed in patients. This approach has potential to lead to insights into acquired treatment-related drug resistance in thyroid cancers that can be subjected to subsequent validation in serially collected patient samples — and that has potential to yield preemptive and responsive approaches to dealing with this important clinical problem.
The 51-Deiodinases Are Not Essential for the Fasting-Induced Decrease in Circulating Thyroid Hormone Levels in Male Mice: Possible Roles for the Type 3 Deiodinase and Tissue Sequestration of Hormone • Valerie Anne Galton, Arturo Hernandez, and Donald L. St. Germain • This study shows that the systemic changes in TH economy as a result of acute food deprivation are not dependent on the D1 or D2, but are mediated in part by sequestration of T4 and T3 in tissues and their enhanced metabolism by the D3.
Hyperplasia and Cellularity Changes in IGF-1-Overexpressing Skeletal Muscle of Crucian Carp • Dongliang Li, Qiyong Lou, Gang Zhai, Xuyan Peng, Xiaoxia Cheng, Xiangyan Dai, Zijian Zhuo, Guohui Shang, Xia Jin, Xiaowen Chen, Dong Han, Jiangyan He, and Zhan Yin • The results indicate that the sustained overexpression of IGF-1 in crucian carp skeletal muscle promotes myofiber hyperplasia and cellularity changes, which elicit alterations in the body energy metabolism and skeletal muscle growth.
Circulating Glucagon-Like Peptide-1 (GLP-1) Inhibits Eating in Male Rats by Acting in the Hindbrain and Without Inducing Avoidance • Mukesh Punjabi, Myrtha Arnold, Elisabeth Rüttimann, Mariana Graber, Nori Geary, Gustavo Pacheco-López, and Wolfgang Langhans • The results implicate hindbrain GLP-1R and the AP in the eating-inhibitory effect of circulating GLP-1, but question the physiological relevance of the eating-inhibitory effect of intravenously infused GLP-1 under our conditions.
Treatment with Thyroid Hormone • Bernadette Biondi and Leonard Wartofsky • In this review, we critically discuss the thyroid hormone formulations that are available and approaches to correct replacement therapy with thyroid hormone in primary and central hypothyroidism in different periods of life and in patients with comorbidities.
Growth Hormone, Insulin-Like Growth Factor-1, and the Kidney: Pathophysiological and Clinical Implications • Peter Kamenický, Gherardo Mazziotti, Marc Lombès, Andrea Giustina, and Philippe Chanson • We analyzed how GH and IGF-1 regulate renal development, glomerular functions, and tubular handling of sodium, calcium, phosphate, and glucose.
Thioredoxin-Interacting Protein Stimulates its Own Expression via a Positive Feedback Loop • Junqin Chen, Gu Jing, Guanlan Xu, and Anath Shalev • The results demonstrate for the first time that TXNIP modulates ChREBP activity and thereby uncover a previously unappreciated link between TXNIP signaling and cell metabolism.
FGFR4 Polymorphic Variants Modulate Phenotypic Features of Cushing Disease • Tae Nakano-Tateno, Toru Tateno, Maw Maw Hlaing, Lei Zheng, Katsuhiko Yoshimoto, Shozo Yamada, Sylvia L. Asa, and Shereen Ezzat • FGFR4 transmembrane polymorphic variants can modulate cellular growth and sensitivity to glucocorticoid hormone negative feedback through distinct STAT3 modifications of relevance to the human forms of Cushing disease.