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Growth hormone receptor-deficient pigs resemble the pathophysiology of human Laron syndrome and reveal altered activation of signaling cascades in the liver

Hinrichs, Arne, Kessler, Barbara, Kurome, Mayuko, Blutke, Andreas, Kemter, Elisabeth, Bernau, Maren, Scholz, Armin M., Rathkolb, Birgit, Renner, Simone, Bultmann, Sebastian, Leonhardt, Heinrich, de Angelis, Martin Hrabĕ, Nagashima, Hiroshi, Hoeflich, Andreas, Blum, Werner F., Bidlingmaier, Martin, Wanke, Rüdiger, Dahlhoff, Maik, Wolf, Eckhard·2018·Molecular Metabolism

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  • Elimination of growth hormone receptor gene expression could reduce organ sizes but comes with other undesired biological consequences.

    “Although elimination of growth hormone receptor gene expression could reduce organ sizes2,3, it comes with other undesired biological consequences7.”

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  1. Laron, 1966, Genetic pituitary dwarfism with high serum concentation of growth hormone–a new inborn error of metabolism?, Israel Journal of Medical Sciences, 2, 152
  2. Laron, 2004, Laron syndrome (primary growth hormone resistance or insensitivity): the personal experience 1958–2003, The Journal of Clinical Endocrinology and Metabolism, 89, 1031, 10.1210/jc.2003-031033 · DOI
  3. Laron, 2016, Epilogue: the future of Laron syndrome — the need for changes, Growth Hormone & IGF Research, 28, 79, 10.1016/j.ghir.2015.07.007 · DOI
  4. Guevara-Aguirre, 1993, Growth hormone receptor deficiency in Ecuador: clinical and biochemical phenotype in two populations, The Journal of Clinical Endocrinology and Metabolism, 76, 417
  5. Rosenfeld, 1994, Growth hormone (GH) insensitivity due to primary GH receptor deficiency, Endocrine Reviews, 15, 369, 10.1210/edrv-15-3-369 · DOI
  6. Guevara-Aguirre, 2011, Growth hormone receptor deficiency is associated with a major reduction in pro-aging signaling, cancer, and diabetes in humans, Science Translational Medicine, 3, 10.1126/scitranslmed.3001845 · DOI
  7. Laron, 2017, IGF-I deficiency, longevity and cancer protection of patients with Laron syndrome, Mutation Research Reviews in Mutation Research, 772, 123, 10.1016/j.mrrev.2016.08.002 · DOI
  8. Chernausek, 2007, Long-term treatment with recombinant insulin-like growth factor (IGF)-I in children with severe IGF-I deficiency due to growth hormone insensitivity, The Journal of Clinical Endocrinology and Metabolism, 92, 902, 10.1210/jc.2006-1610 · DOI
  9. Backeljauw, 2013, Adult and near-adult height in patients with severe insulin-like growth factor-I deficiency after long-term therapy with recombinant human insulin-like growth factor-I, Hormone Research in Paediatrics, 80, 47, 10.1159/000351958 · DOI
  10. Cohen, 2014, Managing the child with severe primary insulin-like growth factor-1 deficiency (IGFD): IGFD diagnosis and management, Drugs in R & D, 14, 25, 10.1007/s40268-014-0039-7 · DOI
  11. Shevah, 2007, Patients with congenital deficiency of IGF-I seem protected from the development of malignancies: a preliminary report, Growth Hormone & IGF Research, 17, 54, 10.1016/j.ghir.2006.10.007 · DOI
  12. Steuerman, 2011, Congenital IGF1 deficiency tends to confer protection against post-natal development of malignancies, European Journal of Endocrinology, 164, 485, 10.1530/EJE-10-0859 · DOI
  13. Lapkina-Gendler, 2016, Identification of signaling pathways associated with cancer protection in Laron syndrome, Endocrine-Related Cancer, 23, 399, 10.1530/ERC-16-0054 · DOI
  14. Zhou, 1997, A mammalian model for Laron syndrome produced by targeted disruption of the mouse growth hormone receptor/binding protein gene (the Laron mouse), Proceedings of the National Academy of Sciences of the United States of America, 94, 13215, 10.1073/pnas.94.24.13215 · DOI
  15. List, 2011, Endocrine parameters and phenotypes of the growth hormone receptor gene disrupted (GHR-/-) mouse, Endocrine Reviews, 32, 356, 10.1210/er.2010-0009 · DOI
  16. Duran-Ortiz, 2018, Disruption of the GH receptor gene in adult mice and in insulin sensitive tissues, Growth Hormone & IGF Research, 38, 3, 10.1016/j.ghir.2017.11.003 · DOI
  17. Young, 2016, Deconstructing the growth hormone receptor (GHR): physical and metabolic phenotypes of tissue-specific GHR gene-disrupted mice, Progress in Molecular Biology and Translational Science, 138, 27, 10.1016/bs.pmbts.2015.10.014 · DOI
  18. Rogers, 2016, Genetically engineered livestock for biomedical models, Transgenic Research, 25, 345, 10.1007/s11248-016-9928-6 · DOI
  19. Dahlhoff, 2017, CRISPR-assisted receptor deletion reveals distinct roles for ERBB2 and ERBB3 in skin keratinocytes, FEBS Journal, 284, 3339, 10.1111/febs.14196 · DOI
  20. Umeyama, 2013, Production of diabetic offspring using cryopreserved epididymal sperm by in vitro fertilization and intrafallopian insemination techniques in transgenic pigs, Journal of Reproduction and Development, 59, 599, 10.1262/jrd.2013-069 · DOI
  21. Kurome, 2015, Nuclear transfer and transgenesis in the pig, Methods in Molecular Biology (Clifton, NJ), 1222, 37, 10.1007/978-1-4939-1594-1_4 · DOI
  22. Besenfelder, 1997, Endoscopic embryo collection and embryo transfer into the oviduct and the uterus of pigs, Theriogenology, 47, 1051, 10.1016/S0093-691X(97)00062-9 · DOI
  23. Blum, 1994, Radioimmunoassays for IGFs and IGFBPs, Growth Regulation, 4, 11
  24. Wirthgen, 2016, Quantitative Western ligand blotting reveals common patterns and differential features of IGFBP-fingerprints in domestic ruminant breeds and species, Growth Hormone & IGF Research, 26, 42, 10.1016/j.ghir.2015.11.001 · DOI
  25. Renner, 2010, Glucose intolerance and reduced proliferation of pancreatic beta-cells in transgenic pigs with impaired glucose-dependent insulinotropic polypeptide function, Diabetes, 59, 1228, 10.2337/db09-0519 · DOI
  26. Blutke, 2017, The Munich MIDY Pig Biobank - a unique resource for studying organ crosstalk in diabetes, Molecular Metabolism, 6, 931, 10.1016/j.molmet.2017.06.004 · DOI
  27. Papadopoulos, 2009, Peripartal feeding strategy with different n-6:n-3 ratios in sows: effect on gene expression in backfat white adipose tissue postpartum, British Journal of Nutrition, 101, 197, 10.1017/S0007114508994782 · DOI
  28. Kremer, 2012, In vivo body composition in autochthonous and conventional pig breeding groups by dual-energy X-ray absorptiometry and magnetic resonance imaging under special consideration of Cerdo Iberico, Animal : An International Journal of Animal Bioscience, 6, 2041, 10.1017/S1751731112001267 · DOI
  29. Kremer, 2013, Use of magnetic resonance imaging to predict the body composition of pigs in vivo, Animal : An International Journal of Animal Bioscience, 7, 879, 10.1017/S1751731112002340 · DOI
  30. Albl, 2016, Tissue sampling guides for porcine biomedical models, Toxicologic Pathology, 44, 414, 10.1177/0192623316631023 · DOI
  31. Streckel, 2015, Effects of the glucagon-like peptide-1 receptor agonist liraglutide in juvenile transgenic pigs modeling a pre-diabetic condition, Journal of Translational Medicine, 13, 73, 10.1186/s12967-015-0431-2 · DOI
  32. Dominick, 2015, Regulation of mTOR activity in Snell dwarf and GH receptor gene-disrupted mice, Endocrinology, 156, 565, 10.1210/en.2014-1690 · DOI · Paper page
  33. Rawlings, 2004, The JAK/STAT signaling pathway, Journal of Cell Science, 117, 1281, 10.1242/jcs.00963 · DOI · Paper page
  34. Cui, 2015, Generation of a miniature pig disease model for human Laron syndrome, Scientific Reports, 5, 15603, 10.1038/srep15603 · DOI
  35. Li, 2015, Transgenic Wuzhishan minipigs designed to express a dominant-negative porcine growth hormone receptor display small stature and a perturbed insulin/IGF-1 pathway, Transgenic Research, 24, 1029, 10.1007/s11248-015-9912-6 · DOI
  36. Yakar, 1999, Normal growth and development in the absence of hepatic insulin-like growth factor I, Proceedings of the National Academy of Sciences of the United States of America, 96, 7324, 10.1073/pnas.96.13.7324 · DOI
  37. Wolf, 2005, Functional consequences of IGFBP excess - lessons from transgenic mice, Pediatric Nephrology (Berlin, Germany), 20, 269, 10.1007/s00467-004-1657-z · DOI
  38. Hwa, 1999, The insulin-like growth factor-binding protein (IGFBP) superfamily, Endocrine Reviews, 20, 761
  39. Labarta, 1997, Immunoblot studies of the acid-labile subunit (ALS) in biological fluids, normal human serum and in children with GH deficiency and GH receptor deficiency before and after long-term therapy with GH or IGF-I respectively, Clinical Endocrinology, 47, 657, 10.1046/j.1365-2265.1997.2581078.x · DOI
  40. Laron, 1992, IGF binding protein 3 in patients with Laron type dwarfism: effect of exogenous rIGF-I, Clinical Endocrinology, 36, 301, 10.1111/j.1365-2265.1992.tb01449.x · DOI
  41. Savage, 1993, Clinical features and endocrine status in patients with growth hormone insensitivity (Laron syndrome), The Journal of Clinical Endocrinology and Metabolism, 77, 1465
  42. Hoeflich, 1999, Overexpression of insulin-like growth factor-binding protein-2 in transgenic mice reduces postnatal body weight gain, Endocrinology, 140, 5488, 10.1210/endo.140.12.7169 · DOI
  43. Hoeflich, 2001, Growth inhibition in giant growth hormone transgenic mice by overexpression of insulin-like growth factor-binding protein-2, Endocrinology, 142, 1889, 10.1210/endo.142.5.8149 · DOI
  44. Kaplan, 2007, The somatomedin hypothesis 2007: 50 years later, The Journal of Clinical Endocrinology and Metabolism, 92, 4529, 10.1210/jc.2007-0526 · DOI
  45. Kleinert, 2018, Animal models of obesity and diabetes, Nature Reviews Endocrinology, 14, 140, 10.1038/nrendo.2017.161 · DOI
  46. Laron, 2000, The diagnostic and prognostic importance of neonatal length measurements, The Israel Medical Association Journal : IMAJ, 2, 84
  47. Baker, 1993, Role of insulin-like growth factors in embryonic and postnatal growth, Cell, 75, 73, 10.1016/S0092-8674(05)80085-6 · DOI · Paper page
  48. Hetz, 2015, Growth axis maturation is linked to nutrition, growth and developmental rate, Molecular and Cellular Endocrinology, 411, 38, 10.1016/j.mce.2015.04.009 · DOI
  49. Symonds, 2009, Nutritional programming of the metabolic syndrome, Nature Reviews Endocrinology, 5, 604, 10.1038/nrendo.2009.195 · DOI
  50. Laron, 2006, Body composition in untreated adult patients with Laron syndrome (primary GH insensitivity), Clinical Endocrinology, 65, 114, 10.1111/j.1365-2265.2006.02558.x · DOI
  51. Berryman, 2010, Two-year body composition analyses of long-lived GHR null mice, The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 65, 31, 10.1093/gerona/glp175 · DOI
  52. Arner, 2011, Dynamics of human adipose lipid turnover in health and metabolic disease, Nature, 478, 110, 10.1038/nature10426 · DOI
  53. Vijayakumar, 2010, Biological effects of growth hormone on carbohydrate and lipid metabolism, Growth Hormone & IGF Research, 20, 1, 10.1016/j.ghir.2009.09.002 · DOI
  54. Wang, 2009, Lipoprotein lipase: from gene to obesity, American Journal of Physiology Endocrinology and Metabolism, 297, E271, 10.1152/ajpendo.90920.2008 · DOI · Paper page
  55. Feinberg, 2000, Echocardiographic dimensions and function in adults with primary growth hormone resistance (Laron Syndrome), The American Journal of Cardiology, 85, 209, 10.1016/S0002-9149(99)00642-6 · DOI
  56. Shea, 1987, Growth allometry of the organs in giant transgenic mice, Endocrinology, 121, 1924, 10.1210/endo-121-6-1924 · DOI
  57. Wanke, 1991, Accelerated growth and visceral lesions in transgenic mice expressing foreign genes of the growth hormone family: an overview, Pediatric Nephrology (Berlin, Germany), 5, 513, 10.1007/BF01453693 · DOI
  58. Lombardi, 1997, Effect of growth hormone on cardiac function, Hormone Research, 48, 38, 10.1159/000191311 · DOI
  59. Sjogren, 2000, Disproportional skeletal growth and markedly decreased bone mineral content in growth hormone receptor -/- mice, Biochemical and Biophysical Research Communications, 267, 603, 10.1006/bbrc.1999.1986 · DOI
  60. Guevara-Aguirre, 2015, Obesity, diabetes and cancer: insight into the relationship from a cohort with growth hormone receptor deficiency, Diabetologia, 58, 37, 10.1007/s00125-014-3397-3 · DOI
  61. Laron, 2002, Growth hormone insensitivity (Laron syndrome), Reviews in Endocrine & Metabolic Disorders, 3, 347, 10.1023/A:1020905725012 · DOI
  62. Guevara-Aguirre, 2015, GH receptor deficiency in ecuadorian adults is associated with obesity and enhanced insulin sensitivity, The Journal of Clinical Endocrinology and Metabolism, 100, 2589, 10.1210/jc.2015-1678 · DOI
  63. Renner, 2016, Comparative aspects of rodent and nonrodent animal models for mechanistic and translational diabetes research, Theriogenology, 86, 406, 10.1016/j.theriogenology.2016.04.055 · DOI
  64. Liu, 2004, Disruption of growth hormone receptor gene causes diminished pancreatic islet size and increased insulin sensitivity in mice, American Journal of Physiology Endocrinology and Metabolism, 287, E405, 10.1152/ajpendo.00423.2003 · DOI
  65. Dominici, 2002, Increased insulin sensitivity and upregulation of insulin receptor, insulin receptor substrate (IRS)-1 and IRS-2 in liver of Ames dwarf mice, Journal of Endocrinology, 173, 81, 10.1677/joe.0.1730081 · DOI
  66. Chung, 2015, Measurements of gluconeogenesis and glycogenolysis: a methodological review, Diabetes, 64, 3996, 10.2337/db15-0640 · DOI
  67. Baxmann, 2008, Influence of muscle mass and physical activity on serum and urinary creatinine and serum cystatin C, Clinical Journal of the American Society of Nephrology : CJASN, 3, 348, 10.2215/CJN.02870707 · DOI
  68. Brooks, 2014, Mechanism of activation of protein kinase JAK2 by the growth hormone receptor, Science, 344, 10.1126/science.1249783 · DOI
  69. Waters, 2016, The growth hormone receptor, Growth Hormone & IGF Research, 28, 6, 10.1016/j.ghir.2015.06.001 · DOI
  70. Mukherjee, 2016, Defining human insulin-like growth factor I gene regulation, American Journal of Physiology Endocrinology and Metabolism, 311, E519, 10.1152/ajpendo.00212.2016 · DOI
  71. Rawlings, 2004, The JAK/STAT signaling pathway, Journal of Cell Science, 117, 1281, 10.1242/jcs.00963 · DOI · Paper page
  72. Waters, 2015, JAK2 activation by growth hormone and other cytokines, The Biochemical Journal, 466, 1, 10.1042/BJ20141293 · DOI
  73. Laron, 1998, Serum leptin in obese patients with Laron syndrome before and during IGF-I treatment, Journal of Pediatric Endocrinology & Metabolism : JPEM, 11, 653, 10.1515/JPEM.1998.11.5.653 · DOI
  74. Cohen, 2005, Induction of leptin receptor expression in the liver by leptin and food deprivation, Journal of Biological Chemistry, 280, 10034, 10.1074/jbc.M413684200 · DOI
  75. Ahmadian, 2013, PPARgamma signaling and metabolism: the good, the bad and the future, Nature Medicine, 19, 557, 10.1038/nm.3159 · DOI · Paper page
  76. Coschigano, 2000, Assessment of growth parameters and life span of GHR/BP gene-disrupted mice, Endocrinology, 141, 2608, 10.1210/endo.141.7.7586 · DOI · Paper page
  77. Coschigano, 2003, Deletion, but not antagonism, of the mouse growth hormone receptor results in severely decreased body weights, insulin, and insulin-like growth factor I levels and increased life span, Endocrinology, 144, 3799, 10.1210/en.2003-0374 · DOI · Paper page
  78. Burgstaller, 2017, Aging of cloned animals: a mini-review, Gerontology, 63, 417, 10.1159/000452444 · DOI
  79. Flisikowska, 2012, A porcine model of familial adenomatous polyposis, Gastroenterology, 143, 1173, 10.1053/j.gastro.2012.07.110 · DOI
  80. Renner, 2013, Permanent neonatal diabetes in INS(C94Y) transgenic pigs, Diabetes, 62, 1505, 10.2337/db12-1065 · DOI
  81. Murakami, 2003, Multiplex stress resistance in cells from long-lived dwarf mice, The FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 17, 1565, 10.1096/fj.02-1092fje · DOI · Paper page
  82. Kranzler, 1998, Normal intelligence with severe insulin-like growth factor I deficiency due to growth hormone receptor deficiency: a controlled study in a genetically homogeneous population, The Journal of Clinical Endocrinology and Metabolism, 83, 1953
  83. Nashiro, 2017, Brain structure and function associated with younger adults in growth hormone receptor-deficient humans, The Journal of Neuroscience : The Official Journal of the Society for Neuroscience, 37, 1696
  84. Schuldenzucker, 2017, Behavioral testing of minipigs transgenic for the Huntington gene - A three-year observational study, PLoS One, 12, e0185970, 10.1371/journal.pone.0185970 · DOI
  85. Schlapschy, 2013, PASylation: a biological alternative to PEGylation for extending the plasma half-life of pharmaceutically active proteins, Protein Engineering Design and Selection : PEDS, 26, 489, 10.1093/protein/gzt023 · DOI
  86. Yin, 2014, Genome editing with Cas9 in adult mice corrects a disease mutation and phenotype, Nature Biotechnology, 32, 551, 10.1038/nbt.2884 · DOI · Paper page
  87. Stoller, 2015, Hepatocyte transfection in small pigs after weaning by hydrodynamic intraportal injection of naked DNA/minicircle vectors, Human Gene Therapy Methods, 26, 181, 10.1089/hgtb.2014.140 · DOI

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Metadata

Authors
Hinrichs, A., Kessler, B., Kurome, M., Blutke, A., Kemter, E., Bernau, M., Scholz, A. M., Rathkolb, B., Renner, S., Bultmann, S., Leonhardt, H., de Angelis, M. H., Nagashima, H., Hoeflich, A., Blum, W. F., Bidlingmaier, M., Wanke, R., Dahlhoff, M., & Wolf, E.
Venue
Molecular Metabolism
Publisher
Elsevier BV
Published
2018-05
Volume
11
Pages
113-128
ISSN
2212-8778
Cited by
96
References
6
Language
en

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