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J M Hanson Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 8, PO Box 80.154, NL-3508 TD Utrecht, The Netherlands

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H S Kooistra Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 8, PO Box 80.154, NL-3508 TD Utrecht, The Netherlands

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J A Mol Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 8, PO Box 80.154, NL-3508 TD Utrecht, The Netherlands

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E Teske Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 8, PO Box 80.154, NL-3508 TD Utrecht, The Netherlands

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B P Meij Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 8, PO Box 80.154, NL-3508 TD Utrecht, The Netherlands

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The 6-h plasma profiles of adrenocorticotropic hormone (ACTH), cortisol, α-melanocyte-stimulating hormone (α-MSH), and GH were studied in 17 dogs with pituitary-dependent hyperadrenocorticism (PDH) before and after hypophysectomy. The aim of the study was to investigate the relation between the hormone profile characteristics and recurrence of PDH after surgery.

The hormones were secreted in a pulsatile fashion. The basal plasma cortisol concentration and area under the curve (AUC) for cortisol were significantly higher in the PDH cases than in eight controls. The characteristics of the plasma profiles of ACTH and α-MSH were not significantly different between the PDH cases and the controls. In the PDH cases, less GH was secreted in pulses than in the controls, but the difference was not significant. The basal plasma cortisol concentration, the AUC for ACTH and cortisol, and the pulse frequency of ACTH and cortisol decreased significantly after hypophysectomy for the group of PDH cases. The basal plasma concentrations of ACTH and α-MSH, the AUC for α-MSH, and the characteristics of the plasma GH profiles of the PDH cases remained unchanged after hypophysectomy. No pulses of α-MSH were observed after hypophysectomy. The co-occurrence between the ACTH and cortisol pulses decreased significantly with hypophysectomy. The postoperative pulse frequency of ACTH was the only characteristic with predictive value for the recurrence of PDH after hypophysectomy.

The results of this study demonstrate that ACTH, cortisol, α-MSH, and GH are secreted in a pulsatile fashion in dogs with PDH. Hypophysectomy effectively reduces the secretion of ACTH and cortisol. The presence of ACTH pulses after hypophysectomy is a risk factor for the recurrence of hyperadrenocorticism.

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Sjoerd D Joustra Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands
Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Onno C Meijer Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Charlotte A Heinen Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands
Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Isabel M Mol Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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El Houari Laghmani Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Rozemarijn M A Sengers Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Gabriela Carreno Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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A S Paul van Trotsenburg Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Nienke R Biermasz Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Daniel J Bernard Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Jan M Wit Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Wilma Oostdijk Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Ans M M van Pelt Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Geert Hamer Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Gerry T M Wagenaar Department of Pediatrics, Department of Medicine, Department of Pediatric Endocrinology, Endocrinology and Metabolism, Developmental Biology and Cancer Programme, Department of Pharmacology and Therapeutics, Center for Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Loss-of-function mutations in the immunoglobulin superfamily member 1 (IGSF1) gene cause an X-linked syndrome of central hypothyroidism, macroorchidism, variable prolactin and GH deficiency, delayed pubertal testosterone rise, and obesity. To understand the pathophysiology of this syndrome, knowledge on IGSF1's place in normal development is imperative. Therefore, we investigated spatial and temporal protein and mRNA expression of IGSF1 in rats using immunohistochemistry, real-time quantitative PCR (qPCR), and in situ hybridization. We observed high levels of IGSF1 expression in the brain, specifically the embryonic and adult choroid plexus and hypothalamus (principally in glial cells), and in the pituitary gland (PIT1-lineage of GH, TSH, and PRL-producing cells). IGSF1 is also expressed in the embryonic and adult zona glomerulosa of the adrenal gland, islets of Langerhans of the pancreas, and costameres of the heart and skeletal muscle. IGSF1 is highly expressed in fetal liver, but is absent shortly after birth. In the adult testis, IGSF1 is present in Sertoli cells (epithelial stages XIII–VI), and elongating spermatids (stages X–XII). Specificity of protein expression was corroborated with Igsf1 mRNA expression in all tissues. The expression patterns of IGSF1 in the pituitary gland and testis are consistent with the pituitary hormone deficiencies and macroorchidism observed in patients with IGSF1 deficiency. The expression in the brain, adrenal gland, pancreas, liver, and muscle suggest IGSF1's function in endocrine physiology might be more extensive than previously considered.

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