Growth Hormone During Catch-Up Growth and Failure of Catch-Up Growth in Rats

Mosier, H. David; Jansons, Regina A

doi:10.1210/endo-98-1-214

Cited by 37 publications

(18 citation statements)

References 10 publications

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“…IGF1 serves as both the main mediator of GH action and as a GHindependent growth factor, and is a well-known growth factor for both chondrocytes and osteoblasts. IGF1 concentrations are responsive to changing nutritional status and intake of amino acids and free fatty acids (Mosier & Jansons 1976, Hermanussen et al 1996, and serum IGF1 levels were reduced by RES in all animals studied (Lowe et al 1989, Devlin et al 2010, Pando et al 2012). The reduced serum IGF1 level is likely to contribute to the cortical thinning observed, as a similar phenotype was also observed in liver-specific IGF1 deficient lid/lid mice (Yakar et al 2002).…”

Section: Discussionmentioning

confidence: 90%

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Pando

Masarwi

Shtaif

et al. 2014

Journal of Endocrinology

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Growth stunting constitutes the most common effect of malnutrition. When the primary cause of malnutrition is resolved, catch-up (CU) growth usually occurs. In this study, we have explored the effect of food restriction (RES) and refeeding on bone structure and mechanical properties. Sprague-Dawley male rats aged 24 days were subjected to 10 days of 40% RES, followed by refeeding for 1 (CU) or 26 days long-term CU (LTCU). The rats fed ad libitum served as controls. The growth plates were measured, osteoclasts were identified using tartrate-resistant acid phosphatase staining, and micro-computed tomography (CT) scanning and mechanical testing were used to study structure and mechanical properties. Micro-CT analysis showed that RES led to a significant reduction in trabecular BV/TV and trabecular number (Tb.N), concomitant with an increase in trabecular separation (Tb.Sp). Trabecular BV/TV and Tb.N were significantly greater in the CU group than in the RES in both short-and long-term experiments. Mechanical testing showed that RES led to weaker and less compliant bones; interestingly, bones of the CU group were also more fragile after 1 day of CU. Longer term of refeeding enabled correction of the bone parameters; however, LTCU did not achieve full recovery. These results suggest that RES in young rats attenuated growth and reduced trabecular bone parameters. While nutrition-induced CU growth led to an immediate increase in epiphyseal growth plate height and active bone modeling, it was also associated with a transient reduction in bone quality. This should be taken into consideration when treating children undergoing CU growth.

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Section: Discussionmentioning

confidence: 90%

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Pando

Masarwi

Shtaif

et al. 2014

Journal of Endocrinology

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“…It has been suggested, for example, that increased GH levels might play a role (20,23). Increased GH could also explain the observed increased height of the growth plates.…”

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confidence: 97%

Catch-Up Growth Is Associated with Delayed Senescence of the Growth Plate in Rabbits

et al. 2001

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In mammals, release from growth-inhibiting conditions results in catch-up growth. To explain this phenomenon, we proposed the following model: 1) The normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of replications that growth plate chondrocytes have undergone. 2) Conditions that suppress growth plate chondrocyte proliferation therefore slow senescence. 3) After transient growth inhibition, growth plates are thus less senescent and hence show a greater growth rate than expected for age, resulting in catch-up growth. To test this model, we administered dexamethasone to growing rabbits to suppress linear growth.After stopping dexamethasone, catch-up growth occurred. In distal femoral growth plates of untreated controls, we observed a senescent decline in the growth rate and in the heights of the proliferative zone, hypertrophic zone, and total growth plate. During the period of catch-up growth, in the animals previously treated with dexamethasone, the senescent decline in all these variables was delayed. Prior treatment with dexamethasone also delayed epiphyseal fusion. These findings support our model that linear catch-up growth is caused, at least in part, by a delay in growth plate senescence. More than 35 y ago, Prader, Tanner, and von Harnack observed that children undergo supranormal linear growth after release from growth-inhibiting conditions (1). This phenomenon, termed catch-up growth, was attributed to a CNS mechanism that compares the individual's actual body size with an age-appropriate set-point and then adjusts the growth rate accordingly (2). However, this neuroendocrine hypothesis has not been subjected to a definitive experimental test.More recently, we demonstrated that transient growth inhibition within a single growth plate is followed by local catch-up growth (3). This local catch-up growth cannot be readily explained by a systemic mechanism, which would have affected all the growth plates equally. Instead, it suggests that catch-up growth is due, at least in part, to a mechanism intrinsic to the growth plate.To account for this finding, we speculated that catch-up growth might be caused by a delay in the process of growth plate senescence. The growth plate, a layer of cartilage located between the epiphysis and the metaphysis of mammalian long bones, is composed of three distinct zones: the resting zone, proliferative zone, and hypertrophic zone. With increasing age, the growth plate undergoes a program of structural and functional changes. These senescent changes include a progressive decline in the growth rate accompanied by a decrease in the heights of the proliferative zone (4), the hypertrophic zone (5), and the overall growth plate (6). In some mammals, including humans and rabbits, the senescent growth plates are eventually replaced by bone tissue, a process termed epiphyseal fusion.Specifically, to explain the mechanism underlying local catch-up growth, we hypothesized that growth plate senescence is not a function of age per s...

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“…In both the prenatal and the postnatal animal, there is a complex interplay between overall nutritional status and linear bone growth. There is experimental evidence that GH/IGF-1 concentration is responsive to changing nutritional status (1)(2)(3)(4)(5), and growth responses to food deprivation also have been shown to involve the hormone leptin, which is secreted by adipocytes (6 -8). However, how undernutrition is translated into changing cellular activity during bone elongation has not been studied.…”

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confidence: 99%

Effect of Short-Term Fasting on Bone Elongation Rates: An Analysis of Catch-up Growth in Young Male Rats

Farnum

2003

Pediatric Research

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Bone elongation in the postnatal animal is a result of cellular activity during endochondral ossification. Growth plate chondrocytes undergo a differentiation cascade involving stem cell clonal expansion and cellular enlargement during hypertrophy. Nutritional status has a significant effect on rates of bone growth, and a period of accelerated growth will occur if nutritional stunting of growth in early childhood can be corrected. This study focuses on changes in rates of increase in bone length in a model of catch-up growth in 4-wk-old male rats. Animals fasted for 3 d reached a weight~60% of the control littermates. By 28 d postfasting, fasted animals had regained weight to 95% of control levels. A 3-d fast caused an immediate and profound decrease in rate of growth in the proximal tibial growth plate to only 30% of that of control animals, while stopping growth in the distal tibial growth plate. During the rapid initial rate acceleration of bone elongation, growth rate in both growth plates reached that of the control littermates by 7 d postfasting. The proximal tibial growth plate then maintained rates that were 10 -15% higher than control over the rest of the experimental period. By 10 d postfasting, the previously fasted animals were on the same weight/rate trajectory as the control littermates. Changes in elongation rates were reflected by dramatic changes in growth plate morphology in all cellular zones. This is the first study to directly correlate weight recovery during catch-up with growth rate responses at the level of the growth plate. In both the prenatal and the postnatal animal, there is a complex interplay between overall nutritional status and linear bone growth. There is experimental evidence that GH/IGF-1 concentration is responsive to changing nutritional status (1-5), and growth responses to food deprivation also have been shown to involve the hormone leptin, which is secreted by adipocytes (6 -8). However, how undernutrition is translated into changing cellular activity during bone elongation has not been studied. This is significant for understanding cellular mechanisms behind the complex phenomenon of catch-up growth, which can occur to different extents, and at different rates, depending upon whether nutritional deprivation occurs in utero, during the early neonatal period of nursing, or later in postnatal growth (4 -6, 9 -12). Catch-up growth, as first described by Prader in 1963 (13), is characterized by a period of growth accelerated above normal during recovery from a period of previous deprivation, which allows the child to accelerate toward, and even resume, his/her preillness growth curve (14). A recent definition is "height velocity above the statistical limits of normality for age and/or maturity during a defined period of time, following a transient period of growth inhibition (9)."Multiple rodent models of catch-up growth have been investigated, differing in the timing of, and the nature of, the stimulus for growth retardation. The most common pharmacologically induced models...

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Growth Hormone During Catch-Up Growth and Failure of Catch-Up Growth in Rats

Cited by 37 publications

References 10 publications

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Catch-Up Growth Is Associated with Delayed Senescence of the Growth Plate in Rabbits

Effect of Short-Term Fasting on Bone Elongation Rates: An Analysis of Catch-up Growth in Young Male Rats

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