Failure of Compensatory (Catch-up) Growth in the Rat

Mosier, H. David

doi:10.1203/00006450-197102000-00002

Cited by 29 publications

(10 citation statements)

References 4 publications

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“…Therefore, when examining the magnitude of the response in the present study, it is important that comparisons be made with other investigations in which the age, sex, species (and even strain) of the animals, and duration of the fast, are comparable. The percent weight loss that we recorded after a 3-dfast (29.8%, starting with male rats weighing~100 g) was comparable to that seen in several previous similarly designed studies: 25% loss, starting at weights of~120 g (26); 42.8% loss, starting at weights of~70 g (17); and 28% loss, starting at weights of~125 g (16). Thus, this model is one of acute and severe nutritional deprivation, in which we have demonstrated that changes in bone growth rates are even more dramatic than changes in rates of weight gain/ loss.…”

supporting

confidence: 61%

“…The most common pharmacologically induced models to rapidly slow growth use either the anti-thyroid agent PTU (15)(16)(17) or dexamethasone (5,14,(17)(18)(19). Models in which manipulation of nutrition is the primary variable include 1) food restriction to the mother during gestation and/or lactation (20,21); 2) bilateral uterine artery ligation during late gestation (22,23); 3) manipulation of litter size during weaning, contrasting litters of four pups to litters of 16 or more pups (11,18,24); and 4) short periods of fasting to the postweaning animal (3,5,17,(25)(26)(27)(28)(29). These experiments have demonstrated that the timing and the duration of the stimulus are critical, with differing outcomes in prenatal/postnatal and preweaning/postweaning experiments (27).…”

mentioning

confidence: 99%

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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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supporting

confidence: 61%

mentioning

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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“…Full catch-up after early malnutrition in rats was demonstrated (32) when measurements were continued until growth ceased at about 32 weeks of age. Less prolonged studies showed failure of rats to compensate for cortisone-induced growth retardation (20). The long-term deleterious effect on growth in children arises from the disproportionate effect of corticosteroids on velocity oi' linear growth and skeletal maturation.…”

Section: Discussionmentioning

confidence: 99%

Catch-up Growth in Cortisone–Treated Rats: Effects of Calcium and Vitamin D

1978

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SummaryThe aim of the study was to develop an animal model of steroid stunting and catch-up growth and to investigate the possibility that calcium supplements, with or without vitamin D supplements, might mitigate the effects of corticosteroids on linear growth.In the first experiment, newly weaned Wistar rats were allocated to four groups and weight and tail length measured weekly. In three groups cortisone was injected daily for 28 days. Two of the cortisone-treated groups were given calfium supplekents daily in different dosage schedules. During cortisone treatment (Table I), animals given cortisone gained less weight than the controls ( P < 0.01). After cortisone was stopped the groups previously given cortisone showed greater weight gain than the controls ( P < 0.01). Changes in tail length (Fig. 2), representing changes in linear growth, showed that groups receiving cortisone grew less than the controls during cortisone treatment. After cortisone was stopped the control group grew less than the three groups that had previously received cortisone. There was no beneficial effect of supplemental calcium on either the degree of growth retardation or of catch-up growth (Tables 1 and 2).A second experiment was performed to test the reproducibility of the method and to study the effects of calcium and vitamin D supplements on growth. Newly weaned rats were allocated to four groups. Three groups received cortisone for 42 days. Two of the cortisone-treated groups received vitamin D once a week and one of these groups received calcium supplements. Weight and tail length velocities (Figs. 5 and 6) show less velocity than that of the cortisone-treated groups during cortisone treatment, and after cortisone was stopped the control group had lesser velocity. During cortisone treatment (Table 3), the control groups gained more weight than the three groups given cortisone ( P < 0.001). After cortisone was stopped the groups previously receiving cortisone gained more weight than the control group ( P < 0.01 for cortisone alone and P < 0.001 for cortisone and vitamin D). Changes in mean tail lengths (Table 4) show that during cortisone treatment the three groups given cortisone alone, cortisone and vitamin D, and cortisone, vitamin D, and calcium, all gained less than the controls ( P < 0.001). After cortisone was stopped the groups previously treated with cortisone had a greater increase in tail length than the control groups (P < 0.001). The group given vitamin D supplements grew more than the group given cortisone without such supplements (P < 0.01). The food consumed by the animals (g/100 g body wt/day) was measured ( Fig. 7), and at no time did the control group eat more than the cortisone-treated groups. Reduced calorie intake was not the explanation for retardation of growth, and the increased food intake after cortisone was presumably necessary for catch-up. The serum calcium and total body calcium at the end of the experiment (Table 5) did not suggest that cortisone had depleted the skeleton of calcium.The experimen...

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“…Mosier (21) proposed that incomplete compensatory growth in rats given cortisone as weanlings might be attributable to alterations in chondrocytes. Laron et al (20) described morphologic changes in the epiphyseal cartilage of rats given large dose corticosteroids (6-methylprednisolone.…”

Section: Discussionmentioning

confidence: 99%

Effects of Neonatal Stunting on the Development of Rats: Early and Late Effects of Neonatal Cortisone on Physical Growth and Skeletal Maturation

Sobel

1978

Pediatr Res

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SummaryCortisone acetate, 1.25 mg, was given im to each pup of eight eight-pup litters; saline was given to each pup of eight litters. At 21 days body weight, stem length, and length of long bones was less in the treated animals ( P < 0.001). The number of ossification centers was greater in the treated animals ( P < 0.05). Brain weight was less in the treated animals ( P < 0.001). For 84-day-old animals body weight ( P < 0.02) and length of most long bones ( P < 0.05) were less in the treated females. Body weight ( P < 0.01), stem length ( P < 0.01) and some bones ( P < 0.02) were smaller in the treated males. There was no difference in the number of epiphyseal fusions. The brains of the treated males weighed less than those of the controls ( P < 0.01).The effect on linear growth is in conformity with observations in children but the accelerated skeletal maturation was unexpected. The effect on skeletal maturation was less persistent than that on bone length. SpeculationThe unexpected acceleration of skeletal maturation found at weaning in rats given corticosteroid treatment in the neonatal period offers at least a partial explanation of persistent stunting because the expected depression of physical growth was found.The experiments to be reported were conducted as part of a research program designed to examine the long term effects of neonatal stunting on the later physical growth and behavioral development of rats. Growth retardation as a result of adverse conditions during fetal or neonatal life may have permanent effects on weight (15, 27). length (8,25), and on the growth of several organs, including the brain (9, 15).Cortisone given during the neonatal period has been shown to affect certain aspects of growth in the rat. Winick and Coscia (28) reported that rats given I mg cortisone acetate were stunted in body weight and in the weight or composition of several soft tissues. Sawano er al. (23) noted growth retardation by 1 week of age (body weight) in rats given 1 mg cortisol or of cortisone acetate on the first postnatal day, as did Schapiro (24). Cotterrell el al. (4) reported no effect on body weight, although brain weight was reduced; they used ip cortisol acetate, which is not absorbed well. Ioachim (14) used various doses of cortisone in rats from 1-4 days of age; even those animals given 1.25 mg cortisone acetate on day 4 gained very poorly until age 31 days, and a deficit in body weight and cellular growth was still present at 120 days. Howard induced growth retardation in mice by implanting pellets of corticosterone on the second day of life. She reports reduced weight gain (12) and changes in chemical composition of the brain (I I) comparable to those induced by food restriction.This study was undertaken to assess the early and long range effects of neonatal cortisone treatment on the growth and skeletal maturation of rats. MATERIALS A N D METHODSAll rats used were offspring of Cesarian-derived Sprague-Dawley descendents purchased from the Charles River Laboratories as young adults of proven fer...

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Failure of Compensatory (Catch-up) Growth in the Rat

Cited by 29 publications

References 4 publications

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

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

Catch-up Growth in Cortisone–Treated Rats: Effects of Calcium and Vitamin D

Effects of Neonatal Stunting on the Development of Rats: Early and Late Effects of Neonatal Cortisone on Physical Growth and Skeletal Maturation

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