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Journal Article

A longitudinal study of the growth of the black-hooded rat: methods of measurement and rates of growth for skull, limbs, pelvis, nose-rump and tail lengths.

01 Mar 1970-Journal of Anatomy (Wiley-Blackwell)-Vol. 106, pp 349-370
About: This article is published in Journal of Anatomy.The article was published on 1970-03-01 and is currently open access. It has received 122 citations till now. The article focuses on the topics: Rump & Skull.
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Journal ArticleDOI
TL;DR: A line of transgenic mice carrying a chimeric gene composed of human insulin-like growth factor I coding sequences fused to the mouse metallothionein I promoter was generated to study the effects of chronically elevated exposure to IGF-I, resulting in a growth response manifested by a 1.3-fold increase in weight as a result of selective organomegaly without an apparent increase in skeletal growth.
Abstract: A line of transgenic mice carrying a chimeric gene composed of human insulin-like growth factor I (IGF-I) coding sequences fused to the mouse metallothionein I promoter was generated to study the effects of chronically elevated exposure to IGF-I. Mice in this line overexpress IGF-I in most tissues studied and have circulating IGF-I levels 1.5 times the normal value. This results in a growth response manifested by a 1.3-fold increase in weight as a result of selective organomegaly without an apparent increase in skeletal growth. In addition, expression of the endogenous GH and IGF-I genes is inhibited. These results are consistent with IGF-I playing an important role in the control of somatic growth.

456 citations

Journal ArticleDOI
21 Apr 1995-Science
TL;DR: From the combination of knowledge and actions, someone can improve their skill and ability and this will lead them to live and work much better.
Abstract: From the combination of knowledge and actions, someone can improve their skill and ability. It will lead them to live and work much better. This is why, the students, workers, or even employers should have reading habit for books. Any book will give certain knowledge to take all benefits. This is what this patterns of human growth tells you. It will add more knowledge of you to life and work better. Try it and prove it.

327 citations

Journal ArticleDOI
TL;DR: Adult male hooded rats which were offered a mixed, high energy diet for 90 days were hyperphagic and became significantly obese compared to chow‐fed control rats, suggesting that the persisting obesity may not be associated with altered insulin resistance.
Abstract: 1. Adult male hooded rats which were offered a mixed, high energy diet for 90 days were hyperphagic and became significantly obese compared to chow-fed control rats. Fasting plasma insulin and glucose levels were initially elevated in the experimental rats, but later in the 90 day period were similar to control levels. 2. When the high energy foods were withdrawn after 90 days and just chow was available, the obese rats maintained the elevated body weights. The obese rats were initially hypophagic, but chow intakes rapidly reached control levels. Plasma insulin and glucose levels were similar in both groups, suggesting that the persisting obesity may not be associated with altered insulin resistance. 3. Five weeks after withdrawal of the 'fattening' diet, half of the experimental rats were offered restricted access to chow for 27 days to reduce their weights to control levels. When the rats were again given free access to chow, they returned to the previously elevated weight. 4. Eighteen weeks after withdrawal of the 'fattening' diet, the experimental rats had significantly elevated body weights and fat stores. The elevated body weight was not simply due to increased growth because, although the experimental rats had slightly more lean body mass than the control rats, the increase in fat was not related to body size.

177 citations

Journal ArticleDOI
TL;DR: It is proposed that the normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of stem cell divisions, and that glucocorticoid administration, by suppressing stem cell proliferation, delays senescence, resulting in catch-up growth after the growth-inhibiting agent is removed.
Abstract: In humans and other mammals, the release from growth-inhibiting conditions, such as glucocorticoid excess, leads to supranormal linear growth. The prevailing explanation for this catch-up growth involves a central nervous system mechanism that compares actual body size to an age-appropriate set-point and adjusts growth rate accordingly via a circulating factor. Although such a neuroendocrine "sizostat" was hypothesized more than 30 yr ago, its existence has never been confirmed experimentally. Here we show that suppression of growth within a single growth plate by locally administered glucocorticoid is followed by local catch-up growth that is restricted to the affected growth plate. Thus, the catch-up growth cannot be explained by neuroendocrine mechanism but, rather, must arise from a mechanism intrinsic to the growth plate. To explain this finding, we propose that the normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of stem cell divisions, and th...

151 citations

Journal ArticleDOI
TL;DR: It is suggested that a set of growth-regulating imprinted genes is expressed at high levels in multiple tissues in early postnatal life, contributing to rapid somatic growth, but that these genes are subsequently downregulated in multiple organs simultaneously, contributingto coordinate growth deceleration and cessation, thus imposing a fundamental limit on adult body size.
Abstract: In mammals, somatic growth is rapid in early postnatal life but decelerates with age and eventually halts, thus determining the adult body size of the species. This growth deceleration, which reflects declining proliferation, occurs simultaneously in multiple organs yet appears not to be coordinated by a systemic mechanism. We, therefore, hypothesized that growth deceleration results from a growth-limiting genetic program that is common to multiple tissues. Here, we identified a set of 11 imprinted genes that show down-regulation of mRNA expression with age in multiple organs. For these genes, Igf2, H19, Plagl1, Mest, Peg3, Dlk1, Gtl2, Grb10, Ndn, Cdkn1c, and SLC38a4, the declines show a temporal pattern similar to the decline in growth rate. All 11 genes have been implicated in the control of cell proliferation or somatic growth. Thus, our findings suggest that the declining expression of these genes contributes to coordinate growth deceleration in multiple tissues. We next hypothesized that the coordinate decline in expression of these imprinted genes is caused by altered methylation and consequent silencing of the expressed allele. Contrary to this hypothesis, the methylation status of the promoter regions of Mest, Peg3, and Plagl1 did not change with age. Our findings suggest that a set of growth-regulating imprinted genes is expressed at high levels in multiple tissues in early postnatal life, contributing to rapid somatic growth, but that these genes are subsequently downregulated in multiple tissues simultaneously, contributing to coordinate growth deceleration and cessation, thus imposing a fundamental limit on adult body size.

139 citations


Cites background from "A longitudinal study of the growth ..."

  • ...Animals were weighed, and tail lengths were measured before death (15)....

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