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Klf9 null mice exhibited delayed (by 24 h) and attenuated proliferation relative to wild-type (WT) counterparts ( Velarde et al . 2005 ). The decreased numbers of implanting embryos in Klf9 null mutants suggested that the altered pattern of
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, including systemic insulin resistance, has been reported in Pde3b-null mice ( Choi et al . 2006 ). However, because PDE3B is expressed in variety of tissues including adipocytes, liver, pancreatic beta cells and the hypothalamus ( Zhao et al . 2000
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Waseda Research Institute for Science and Engineering, Waseda University, Tokyo, Japan
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
Department of Pediatrics, University of Kansas Medical Center, Kansas City, Kansas, USA
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type (+/+), heterozygous (+/−) and null (−/−) animals. (C) Gross appearance of the scrotal area on postnatal day 21 of wild type (+/+) and Prl3c1 -null (−/−) mice. (D) Gross appearance of adult testis of wild type and Prl3c1 -null mice. (E) Testis
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injected with either vehicle (saline) or 10 μg recombinant FGF23 (gift from Genzyme Corp., Framingham, MA, USA) either i.v. or i.p. The KL -null mice carry the β -galactosidase gene cassette in place of mouse KL exons 2 and 3. Human FGF23 with the R176Q
Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of NJ, Piscataway, New Jersey 08854, USA
Département de Pharmacologie, Faculté de Mèdecine et Institut de Pharmacologie de Sherbrooke, Université de Sherbrooke, Québec, Canada JIH 5N4
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Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of NJ, Piscataway, New Jersey 08854, USA
Département de Pharmacologie, Faculté de Mèdecine et Institut de Pharmacologie de Sherbrooke, Université de Sherbrooke, Québec, Canada JIH 5N4
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Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of NJ, Piscataway, New Jersey 08854, USA
Département de Pharmacologie, Faculté de Mèdecine et Institut de Pharmacologie de Sherbrooke, Université de Sherbrooke, Québec, Canada JIH 5N4
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Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of NJ, Piscataway, New Jersey 08854, USA
Département de Pharmacologie, Faculté de Mèdecine et Institut de Pharmacologie de Sherbrooke, Université de Sherbrooke, Québec, Canada JIH 5N4
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Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of NJ, Piscataway, New Jersey 08854, USA
Département de Pharmacologie, Faculté de Mèdecine et Institut de Pharmacologie de Sherbrooke, Université de Sherbrooke, Québec, Canada JIH 5N4
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Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of NJ, Piscataway, New Jersey 08854, USA
Département de Pharmacologie, Faculté de Mèdecine et Institut de Pharmacologie de Sherbrooke, Université de Sherbrooke, Québec, Canada JIH 5N4
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al. 1998 , Westphal et al. 1999 , Laurent et al. 2002 ). Interestingly, PC2 and 7B2 null mice exhibit exceedingly different phenotypes; PC2 null mice are healthy except for slight hypoglycemia and runting ( Furuta et al. 1997 ), while 7B2
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. 1995 , Venepally et al. 1996 ). However, its physiological function has remained elusive due to the lack of apparent phenotype of Crabp1 -null mice ( de Bruijn et al. 1994 , Gorry et al. 1994 ). Nevertheless, transgenic mice ectopically
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). In a recent paper, Walsh et al. (2003) have shown direct evidence of the lack of S A involvement in the regulation of either basal or salt-related BP in S A -null mice, demonstrating that the absence of differential BP in these animals is not the
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dramatically elevated. Compared with wild-type mice, the amount of mRNA for Tshβ and Cga in Esr α null mice increased by 3.20- and 4.36-fold respectively. Immunostaining using specific antibodies revealed that the number of TSHβ- and CGA-positive cells
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G-protein-coupled bile acid receptor 1 (GPBAR1/TGR5/M-Bar/GPR131) is a cell surface receptor involved in the regulation of bile acid metabolism. We have previously shown that Gpbar1-null mice are resistant to cholesterol gallstone disease when fed a lithogenic diet. Other published studies have suggested that Gpbar1 is involved in both energy homeostasis and glucose homeostasis. Here, we examine the functional role of Gpbar1 in diet-induced obese mice. We found that body weight, food intake, and fasted blood glucose levels were similar between Gpbar1-null mice and their wild-type (WT) littermates when fed a chow or high-fat diet (HFD) for 2 months. However, insulin tolerance tests revealed improved insulin sensitivity in male Gpbar1 −/− mice fed chow, but impaired insulin sensitivity when fed a HFD. In contrast, female Gpbar1 −/− mice exhibited improved insulin sensitivity when fed a HFD compared with their WT littermates. Female Gpbar1 −/− mice had significantly lower plasma cholesterol and triglyceride levels than their WT littermates on both diets. Male Gpbar1 −/− mice on HFD displayed increased hepatic steatosis when compared with Gpbar1 + / + males and Gpbar1 −/− females on HFD. These results suggest a gender-dependent regulation of Gpbar1 function in metabolic disease.
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The possibility that growth hormone (GH) has effects on long bone growth independent of insulin-like growth factor-I (IGF-I) has long been debated. If this is true, then long bone growth should be more profoundly affected by the absence of GH (since both GH and GH-stimulated IGF-I effects are absent) than by the absence of IGF-I alone (since GH is still present and actually elevated). To test this hypothesis, we compared long bone growth in mice with targeted deletions of Igf1 vs growth hormone receptor (Ghr). Tibial linear growth rate was reduced by approximately 35% in Igf1 null mice and by about 65% in Ghr null mice between postnatal days 20 and 40, a time of peak GH effect during normal longitudinal growth. The Igf1 null mouse growth plate demonstrated significant enlargement of the germinal zone; chondrocyte proliferation and numbers were normal but chondrocyte hypertrophy was significantly reduced. In contrast, the Ghr null mouse germinal zone was hypoplastic, chondrocyte proliferation and numbers were significantly reduced, and chondrocyte hypertrophy was also reduced. We have previously demonstrated that IGF-II is highly expressed in growth plate germinal and proliferative zones, so we considered the possibility that GH-stimulated IGF-II production might promote germinal zone expansion and maintain normal proliferation in the Igf1 null mouse growth plate. Supporting this view, IGF-II mRNA was increased in the Igf1 null mouse and decreased in the Ghr null mouse growth plate.Thus, in the complete absence of IGF-I but in the presence of elevated GH in the Igf1 null mouse, reduction in chondrocyte hypertrophy appears to be the major defect in longitudinal bone growth. In the complete absence of a GH effect in the Ghr null mouse, however, both chondrocyte generation and hypertrophy are compromised, leading to a compound deficit in long bone growth. These observations support dual roles for GH in promoting longitudinal bone growth: an IGF-I-independent role in growth plate chondrocyte generation and an IGF-I-dependent role in promoting chondrocyte hypertrophy. The question of whether GH has direct effects on chondrocyte generation is still not settled, however, since it now appears that IGF-II may medicate some of these effects on the growth plate.
