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decreased Zn accumulation in islets ( Lemaire et al . 2009 , Nicolson et al . 2009 , Pound et al . 2009 ). ZnT8 null mice also exhibited decreased GSIS and altered glucose homeostasis ( Pound et al . 2009 ). However, ZnT8 null mice exhibited altered
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Department of Medicine (AH), Walter and Eliza Hall Institute of Medical Research, Harry Perkins Institute of Medical Research, The School of Medical Sciences Edith Cowan University, Austin Hospital, University of Melbourne, Level 7, Lance Townsend Building, Studley Road, Heidelberg, Victoria 3084, Australia
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secretion ( Seghers et al . 2000 , Nakazaki et al . 2002 , Shiota et al . 2002 ). Furthermore, the response of the SUR1 null mice to non-glucose stimuli such as carbachol, TPA, amino acids, acetylcholine and IBMX was comparable with the control mice
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hypogonadism of kiss1r −/− and kiss1 −/− null mice ( de Roux et al . 2003 , Seminara et al . 2003 , d'Anglemont de Tassigny et al . 2007 ). These mice have normal levels of hypothalamic GnRH. As expected, kisspeptin administration to Kiss1 −/− mice
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coactivators in regulating energy metabolism ( Dasgupta et al. 2014 ). Whole body knockout of SRC-1 in mice causes an increased risk of obesity due to decreased energy expenditure. SRC-1 null mice also display hypoglycemia due to impaired hepatic
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CIBER Fisiopatologia de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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phenotypic characteristics. For example, while loss of the MAGE -family gene, Necdin has no effect on growth or adiposity ( Cattanach et al. 1992 , Muscatelli et al. 2000 ) Necdin -null mice display enhanced differentiation and/or proliferation of
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Physiology of bone loss . Radiologic Clinics of North America 48 483 – 495 . doi:10.1016/j.rcl.2010.02.014 . Couse JF Korach KS 1999 Estrogen receptor null mice: what have we learned and where will they lead us? Endocrine Reviews 20 358
Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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Department of Biomedical Sciences and
RCMI DNA Molecular Core, Charles R Drew University of Medicine and Science, Los Angeles, California 90059, USA
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine of Keck School of Medicine at University of Southern California, Los Angeles, California 90017, USA
Section of Endocrinology, Diabetes, and Nutrition, Boston Medical Center, Boston, Massachusetts 02118, USA
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(−/−), mice, provided kindly by Dr S J Lee, were bred in our vivarium (BalbC/Mst (−/−); McPherron et al. 1997). As reported previously by Dr Lee’s group, these Mst null mice show greater muscularity and lower fat mass than age-matched wild-type (WT) controls
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has so far been studied almost exclusively in male rodents and it is not known how ANXA1 varies with the estrous cycle of the rat and the female sex estrogen status. Our recent findings demonstrate that ANXA1 null mice exhibit sexual dimorphisms in HPA
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
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Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
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Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
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Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
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Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
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Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
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( Artenstein & Opal 2011 ). In the reproductive system, PCs participate in follicle and embryo development. Male Pcsk4 -null mice exhibited severely impaired fertility and female Pcsk4 -null mice exhibited delayed folliculogenesis in the ovaries ( Mbikay et
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Institute of Dental Research, The Research Center for Bone and Stem Cells, Department of Medicine, Stomatological College
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mandibles. Materials and Methods 1α(OH)ase and PTH null mice and genotyping The generation of 1α(OH)ase −/− and PTH −/− mice and mouse genotyping were described previously ( Panda et al . 2001 , Xue et al . 2005 ). The mice were fed autoclaved rodent