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2006 ). Scarb1 -null mice show high HDL-associated cholesterol (HDL-C) levels due to impaired selective uptake of cholesterol by the liver ( Rigotti et al . 1997 ). Also, Scarb1 -null male mice exhibit lack of SR-BI-mediated cholesterol uptake from
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1997 ). pttg -null male mice develop hyperglycemia secondary to hypoinsulinemia starting at 6 months of age ( Wang et al. 2003 ). By 1 year, >80% of male pttg −/− mice are diabetic with hypoinsulinemia secondary to reduced post-natal β
Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Monash Medical Centre, Clayton, Victoria, Australia
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Department of Molecular and Translational Research, Monash University, Melbourne, Victoria, Australia
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mice. Tissue compartment Cre driver Phenotype Cell-specific effects Reference Complete null None (all cells) Early postnatal death from sodium and fluid loss Elevated renin, high aldosterone ENaC and Na/K-ATPase normal
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times through regulated expression of PAPP-A and its associated proteolytic activity ( Pintar et al. 1998 ). Recently, we generated PAPP-A-null mice which, similar to IGF-II-null mice, were born as proportional dwarfs ( Conover et al. 2004 ). The
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The latent transforming growth factor (TGF)-beta binding proteins (LTBP)-1, -3 and -4 bind the latent form of the multipotent cytokine TGF-beta. To examine the function of the LTBPs, we made a null mutation of Ltbp-3 by gene targeting. The homozygous mutant animals developed cranio-facial malformations by 12 days. By three months, there was a pronounced rounding of the cranial vault, extension of the mandible beyond the maxilla, and kyphosis. The mutant animals developed osteosclerosis of the long bones and vertebrae as well as osteoarthritis between 6 and 9 months of age. These latter phenotypic changes were similar to those described for mice that have impaired TGF-beta signaling. Thus, we suggest that Ltbp-3 plays an important role in regulating TGF-beta bioavailability as the phenotype of the Ltbp-3 null mouse appears to result from decreased TGF-beta signaling. Histological examination of the skulls from null animals revealed no effects on calvarial suture closure. However, the synchondroses in the skull base were obliterated within 2 weeks of birth. This is in contrast to the wild-type synchondroses, which remain unossified throughout the life of the animal and enable growth of the skull base through endochondral ossification. Histological changes in mutant basooccipital-basosphenoid synchondrosis were observed 1.5 days after birth. Compared with wild-type or heterozygous littermates, the basooccipital-basosphenoid synchondrosis of Ltbp-3 null mice contained increased numbers of hypertrophic chondrocytes. The expression of bone sialoprotein-1 (a marker for osteoblasts) was observed in cells surrounding the synchondrosis at postnatal day 1.5 indicating ectopic ossification. The expression of Indian hedgehog (Ihh) (a marker for chondrocytes committed to hypertrophic differentiation) was found through the basooccipital-basosphenoid synchondrosis, whereas the expression of parathyroid hormone related protein (PTHrP), which inhibits chondrocyte differentiation, appeared to be diminished in Ltbp-3 null mice. This suggests that Ltbp-3 may control chondrocyte differentiation by regulating TGF-beta availability. TGF-beta may regulate PTHrP expression either downstream of Ihh or independently of Ihh signaling.
Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Departments of Clinical Biochemistry and Medicine, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK
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Improved lipid and lipoprotein profile, hepatic insulin sensitivity, and glucose tolerance in 11β-hydroxysteroid dehydrogenase type 1 null mice. Journal of Biological Chemistry 276 41293 –41300. Morton NM , Paterson JM
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developmental period in the somatotrope Lepr exon 1 -null mouse and evaluate possible paracrine effects of the deletion. This report also details normal anterior pituitary hormone levels throughout development in normal mice, providing a valuable roadmap for
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Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, USA
Department of Child Health, University of Missouri, Columbia, Missouri, USA
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al. 1996 ), and mice null for UCP1 are more susceptible to western diet (WD)-induced insulin resistance ( Winn et al. 2017 b ). In considering that E 2 has protective actions in adipose tissue, which may contribute to the metabolic protection
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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-type (+/+), heterozygous (+/−), and null (−/−) females. Lactation performance was also compared among dams heterozygous for both IRS-1 and IRS-2. Mice carrying germline mutations in the Irs1 or Irs2 genes were previously described ( Araki et al. 1994 , Kubota
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onset of the disorder and because of the effects of allelic heterogeneity and environmental factors that cannot be readily controlled ( Nadeau 2005 ). However, these variables can be controlled in studies of inbred laboratory mice, which may also develop
