Department of Neurological Surgery, Oregon Health & Science University, Portland, Oregon, USA
Pituitary Center, Oregon Health & Science University, Portland, Oregon, USA
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Department of Neurological Surgery, Oregon Health & Science University, Portland, Oregon, USA
Pituitary Center, Oregon Health & Science University, Portland, Oregon, USA
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Department of Neurological Surgery, Oregon Health & Science University, Portland, Oregon, USA
Pituitary Center, Oregon Health & Science University, Portland, Oregon, USA
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comorbidities related to the tumor itself (e.g. headache, oculomotor never palsy or hypopituitarism) or to GH and insulin-like growth factor-1 (IGF-1) excess (arthralgia, morphologic changes, or obstructive sleep apnea (OSA), cardiovascular disease, and
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Introduction Growth hormone (GH) is a significant regulator of growth and metabolism ( 1 ). In the liver, GH stimulates the synthesis and secretion of insulin-like growth factor 1 (IGF-1) ( 2 ). The GH/IGF-1 axis can regulate hepatic glucose
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functions in normal tissues and tumors, plays an important role in the pathophysiology of GEP NETs (2) . The IGF system consists of different IGF-related genes: two ligands (IGF1 and IGF2), two IGF receptors (IGF1R and IGF2R), two insulin receptors (IR
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Introduction GH regulates β-cell function (βCF) and insulin sensitivity (IS) both directly and via complex interactions with its principal mediator, insulin-like growth factor 1 (IGF1) (1) . While GH reduces IS, IGF1 increases it. The hyperglycemic
Department of Anatomy and UMIB (Unit for Multidisciplinary Biomedical Research) of ICBAS, Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Department of Endocrinology, University of Porto, Porto, 4050-313, Portugal
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Department of Anatomy and UMIB (Unit for Multidisciplinary Biomedical Research) of ICBAS, Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Department of Endocrinology, University of Porto, Porto, 4050-313, Portugal
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proliferation (Ki-67), and cell adhesion (E-cadherin and β-catenin), and the growth factor IGF2 and its receptor IGF1R. Subjects and methods Patients and tumors Paraffin-embedded adrenal samples from a total of 43 patients were used. These included ACA samples
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Department of Health & Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
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Department of Health & Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
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). Mouse gene PCR primer sets (RT 2 ) for VDR, IGF1, IGF2, FGF1, FGF2, MSTN and FST were obtained from SABiosciences. The Power SYBR green PCR Master Mix (Applied Biosystems) was used with Step-One-Plus real-time PCR System (Applied Biosystems). The
PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France
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PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France
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CIC INSERM 1411, Hôpital Gui de Chauliac, CHU Montpellier, Montpellier Cedex 5, France
Institut de Génomique Fonctionnelle, CNRS UMR 5203/INSERM U661/Université Montpellier, Montpellier, France
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CIC INSERM 1411, Hôpital Gui de Chauliac, CHU Montpellier, Montpellier Cedex 5, France
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Département de Biochimie, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
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Département d’Urgence et Post-Urgence Psychiatrique, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
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Département d’Urgence et Post-Urgence Psychiatrique, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
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Département Endocrinologie, Nutrition, Diabète, Equipe Nutrition, Diabète, CHU Montpellier, Montpellier, France
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these bone characteristics may explain the increased fracture risk observed in this population ( 7 ). Various endocrine and metabolic disturbances, including hypothyroidism ( 8 ), hypogonadism ( 1 , 9 , 10 ), hypercortisolism ( 2 , 11 ) and IGF-1
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Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität München, Munich, Germany
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.95 35.05 n.a. n.a. n.a. n.a. n.a. White blood cell count (×10 9 /L) 108 7 6.24 1.35 n.a. n.a. n.a. n.a. n.a. IGF-1-SDS (ng/mL) 100 15 136.75 72.99 n.a. n.a. n.a. n.a. n.a. GHD, growth
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are conflicting concerning leptin levels (5, 17, 18, 19) but elevated levels have been observed in prepubertal SGA children with catch-up growth (19) . IGF-binding protein-1 (IGFBP1) modulates the effect of IGF1 at target tissue. IGFBP1 levels are
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and HESX1 ) that could cause FSS and multiple pituitary hormone deficiency ( 14 , 15 ). Insensitivity to GH (IGF deficiency and IGF resistance) may also be inherited in an AD manner (e.g., IGF1R , GHR and STAT5B genes) ( 2 , 16 ). Despite the