), suggesting that gender may affect the bone response to other hormones. To determine whether the response of mouse bone to PTH differed according to gender, we determined the bone response to PTH at the tissue level, cellular level and molecular level
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Yongmei Wang, Takeshi Sakata, Hashem Z Elalieh, Scott J Munson, Andrew Burghardt, Sharmila Majumdar, Bernard P Halloran, and Daniel D Bikle
M S Mondal, H Yamaguchi, Y Date, K Toshinai, T Kawagoe, T Tsuruta, H Kageyama, Y Kawamura, S Shioda, Y Shimomura, M Mori, and M Nakazato
rats, including the stomach and intestine ( Fuji et al. 2002 ). NPW mRNA is expressed in the stomach, but a cellular source has yet to be identified ( Tanaka et al. 2003 ). In this study, we investigated the cellular source of NPW in the rat, mouse
W. G. BEAMER and EVA M. EICHER
SUMMARY
The new mouse mutation little (lit) in the homozygous state causes a pituitary deficiency involving at least growth hormone (GH) and prolactin. The resultant growth failure of lit/lit mice was shown to be reversed by experimental conditions that enhanced levels of GH or GH and prolactin in the circulation. Two measures of growth, actual weight gain and bone dimension, were significantly improved by the physiological processes of pregnancy and pseudopregnancy, by extra-sellar graft of a normal mouse pituitary, and by treatment with GH but not prolactin. These data confirmed pituitary dysfunction as the basic defect caused by the mutation lit and showed that the GH deficiency is responsible for growth failure. However, the biological site of gene action, the pituitary or hypothalamus, has not been established.
Little mice exhibit a number of characteristics similar to those of human genetic ateleotic dwarfism Type 1, namely genetic inheritance, time of onset of growth retardation, proportionate skeletal size reduction, and pituitary GH deficiency.
Shaodong Guo
Foxo knockout mice using the Cre-LoxP genetic approaches Tissue-specific Irs or Foxo null mouse genotype Phenotype Cre-mice References Hypothalamic and β-cell Irs2 −/− Obesity; hyperglycemia; insulin resistance RIP-cre Lin et al . (2004
Ashley Gray, William J Aronson, R James Barnard, Hemal Mehta, Junxiang Wan, Jonathan Said, Pinchas Cohen, and Colette Galet
results were reproduced in a transgenic mouse model of prostate cancer in which 7-month c-Myc transgenic mice fed an isocaloric low-fat diet displayed elevated IGFBP1 levels compared with c-Myc mice fed a high-fat diet. Using an ex vivo assay, LNCaP and
Liselotte Fransson, Stephanie Franzén, Victoria Rosengren, Petra Wolbert, Åke Sjöholm, and Henrik Ortsäter
mouse models have been used. Implantation of corticosterone pellets subcutaneously into Sprague–Dawley rats in combination with a high-fat diet gave rise to glucose intolerance and elevated triglyceride levels in serum, thus mimicking some aspects of the
J Manolopoulou, M Bielohuby, S J Caton, C E Gomez-Sanchez, I Renner-Mueller, E Wolf, U D Lichtenauer, F Beuschlein, A Hoeflich, and M Bidlingmaier
. 2001 , Vinson 2003 , 2004 ). However, genetically altered animal models which are of increasing importance for intervention studies and to establish a genotype–phenotype relationship are restricted to the mouse ( Peters et al . 1999 , 2007
Zhenping Liu, Per Bendix Jeppesen, Søren Gregersen, Lotte Bach Larsen, and Kjeld Hermansen
incubation, mouse islets were incubated in RPMI 1640 with 11.1 mM glucose in the presence of 1, 5, and 10 mM leucine, respectively, the normal RPMI 1640 containing 0.38 mM leucine as control (all the following experiments take 0.38 mM leucine as control
Ying Chen, Kelsey Breen, and Melissa E Pepling
Introduction Formation of functional gametes is essential for reproduction. In the mouse, primordial germ cells (PGCs) migrate to the gonad during embryonic development ( Bendel-Stenzel et al . 1998 ). In the female, after the PGCs arrive at the
T Yoshida, K Yamanaka, S Atsumi, H Tsumura, R Sasaki, K Tomita, E Ishikawa, H Ozawa, K Watanabe, and T Totsuka
Abstract
This paper describes a novel mutant mouse that has been spontaneously derived from the Snell's dwarf (DW/J) mouse. It was named the 'growth-retarded mouse' because of a characteristic growth pause followed by the delayed onset of pubertal growth. The onset of the increase in pituitary GH content that normally occurs concomitant with pubertal growth was also delayed in the growth-retarded mice. The serum concentration of thyroxine was very low in these mice from the neonatal period through adulthood, and a supplement of tri-iodothyronine was effective in shortening the growth pause and commencing the suppressed pubertal growth. Histological and immunohistochemical studies revealed that the anterior pituitary gland of the growth-retarded mouse contains clustered unusual chromophobic cells which are not reactive to various antisera against anterior pituitary hormones and the gland becomes enlarged with age. Breeding data indicated that these characteristics of the mice show an autosomal recessive inheritance and the gene responsible was designated as 'grm'. Partial linkage analysis utilizing microsatellite polymorphism demonstrated that the grm gene does not identify with the lit or hyt genes. Based on comparison of the hormonal status and growth pattern between growth-retarded, dwarf and normal mice, we have suggested the existence of a mutual interaction, possibly positive feedback regulation, between the pituitary and thyroid glands, that develops or matures the hormonal network which is responsible for rapid somatic growth and metabolic changes at puberty in mice.
Journal of Endocrinology (1994) 142, 435–446
