During peripuberty, normal male rats grow at a maximal speed that cannot be further increased by exogenous GH treatment, whereas age-matched female rats or older males grow at a slower rate than peripubertal males. Thus, exogenous rhGH administration is capable of enhancing growth velocity.
Twelve female rats weighing 150 g received in the submaxillary gland a pellet capable of releasing 3·5 µg GHRH/h for 60 days. Another eight sex-and weightmatched animals received placebo pellets in the same place. After two months the animals were killed, heart blood was collected and pituitary and submaxillary glands were carefully dissected. Pituitary GH content in both placebo-and GHRH-treated animals showed similar values, but plasma GH and IGF-I levels were significantly lower in the animals carrying GHRH pellets (P<0·03); these animals also had a significantly higher GH content in the submaxillary gland (19·2 8 ng/mg protein) compared with the placebo-treated group (1·1 0·3 ng/mg protein). GH mRNA was present only in the submaxillary gland of GHRH-treated rats as determined by PCRSouthern blot and by in situ hybridization methods. It is concluded that high local GHRH levels are capable of inducing transdifferentiation in submaxillary gland cells to synthesize GH.
Rats lacking progesterone action due to RU486 treatment have been reported to show numerous endocrine and morphological similarities with respect to human polycystic ovary syndrome (PCO). Nevertheless, abnormalities on insulin or insulin-like growth factor I (IGF-I) production, a frequent finding in the polycystic disease, have not been studied in such rats yet. The aim of these experiments was to evaluate the serum concentrations of IGF-I in rats treated with 4 mg of the antiprogestagen RU486 over 4 or 8 consecutive days starting on estrus (day 1) and decapitated on the morning of day 5 and 9. Serum levels of growth hormone (GH), luteinizing hormone (LH), testosterone (T) and 17 beta estradiol (E2) were determined and correlated with those of IGF-I. Controls were rats injected with oil and killed in the morning of metestrus, diestrus, proestrus and estrus. Rats treated with RU486 had increased serum concentrations of IGF-I, LH, T and E2 with respect to control rats on estrus, while no differences were found in the serum concentrations of GH. Parallel estrous cycle related changes were observed in the serum concentrations of IGF-I, T and E2 with the highest values at proestrus. However, changes on serum concentrations of GH were not associated with those of IGF-I in control rats through the estrous cycle. The present results are consistent with the idea that beside on GH, serum concentrations of IGF-I in the rat depend also on LH or LH-dependent ovarian steroid production. Moreover, the results indicate that IGF-I production increased in RU486-treated rats, which may have a role in the ovarian abnormalities induced by RU486 treatment in the rat.
To monitor growth, a novel noninvasive leg length measurement technique, called microknemometry, which allows daily observation of tibial growth rate, was used. The rat exhibits a striking sex-related difference in postpubertal growth. Exogenous GH administration results in a sexually dimorphic response, affecting growth in normal young female rats but not in males. Here we investigated how chronic GH deficiency affects male and female rat growth patterns. The degree of growth rate recovery was investigated after exogenous GH administration to chronically deficient males and females. The deficiency was induced by neonatal monosodium glutamate (MSG) treatment. Since the neonatal gonadal environment plays an important role in the dimorphic growth pattern, neonatal androgenization of female rats with testosterone or neonatal feminization of male rats by castration was performed and the growth pattern monitored. MSG treatment decreased pituitary GH content and plasma IGF I levels in both sexes, but caused a less marked reduction of female rat tibial growth and body weight gain than in males. Additionally, only MSG-treated males showed decreased pituitary LH content, so that the dimorphic action of MSG on the gonadal axis may contribute to the observed differences in growth rate. GH administration was able to increase leg length in all MSG-treated rats but was more effective in females, despite a similar restoration of plasma IGF I levels in both sexes. Although neonatal castration of male rats resulted in a reduction of tibial growth rate and body weight, and neonatal testosterone administration to female rats caused a slight increase in body weight, a complete modification of the gender-dependent growth pattern was not achieved, indicating that appropriate steroid environment is also needed in puberty and adulthood.
Microknemometry, a novel non-invasive technique, allows the accurate measurements of the lower leg length in the conscious rat, not only daily but even in periods smaller than 24 hours. Its use revealed the presence of nonlinear growth increments (mini-growth spurts) with periods between 4 and 5 days, that presented a gradual decline in amplitude when the animals were getting older, and a maximal growth rate between 0600h and 0900h. A sexual dimorphic growth pattern could be established with females growing less and presenting spurts of lower amplitude and smaller duration than males. High doses of recombinant human Growth Hormone (rhGH) stimulated growth velocity in female rates, but did not show any effect on males. Neonatal Monosodium Glutamate (MSG) treatment reduced growth both in males and females. Growth hormone (GH) replacement therapy in MSG treated animals was capable of increasing growth velocity, from day 30 onwards. The recovery was partial in males and complete in females. In intact male rats growth blockade induced by fasting was not followed by a catch up effect after refeeding, although growth velocity tended to increase and a clear catch up effect on weight was detected. Male rats seemed to grow at a maximal speed over at least the first 60 days of life, that cannot be accelerated with GH treatment, whereas female rats did respond to exogenous GH.
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