Regulation of testicular insulin-like growth factor-I in pubertal growth hormone-deficient male rats

1991 ◽  
Vol 131 (2) ◽  
pp. 279-285 ◽  
Author(s):  
J. Spiteri-Grech ◽  
J. M. S. Bartlett ◽  
E. Nieschlag
Keyword(s):  
Growth Factor ◽  
Male Rats ◽  
Testicular Development ◽  
Insulin Like Growth Factor ◽  
Deficient Mutant ◽  
Factor I ◽  
Pubertal Growth ◽  
Body Weights ◽  
Igf I ◽  
Growth Factor I

ABSTRACT GH plays a major role in pubertal growth, effects mainly mediated by stimulation of insulin-like growth factor-I (IGF-I) production by the liver. However, the role of GH in the regulation of pubertal onset, spermatogenesis and fertility is still under debate. GH and FSH have, in addition, been implicated in the regulation of IGF-I production by Sertoli cells in a number of studies, although conflicting results have been reported. The interpretation of studies using GH-deficient mutant mice has been complicated by the presence of additional defects in the hypothalamic-pituitary-gonadal axis of these animals. We have therefore used GH-deficient mutant male rats with no other documented hormonal deficiencies to study the effect of GH administration on somatic and testicular development, circulating and testicular IGF-I concentrations and testicular histology. Body weights in GH-deficient rats substituted with GH were not significantly different from untreated or GH-treated normal rats and were significantly higher than body weights in untreated dwarf rats. Similarly, circulating IGF-I concentrations in GH-treated GH-deficient rats were not significantly different from those in untreated or GH-treated normal rats but were significantly higher than circulating IGF-I concentrations in untreated dwarf rats. No differences in testicular IGF-I concentrations were observed in any of the groups studied. Testicular weights remained low in both untreated and GH-treated GH-deficient animals compared with control animals but spermatogenesis was qualitatively and quantitatively normal in all groups at the end of the observation period. We conclude that GH does not play a major role in the regulation of testicular IGF-I production at puberty although we cannot exclude the possibility that the low but detectable levels of GH in the blood of mutant rats is sufficient to augment testicular responsiveness to gonadotrophins and therefore result in normal gonadal development. Journal of Endocrinology (1991) 131, 279–285

Interactions of insulin-like growth factor I with dexamethasone on trabecular bone density and mineral metabolism in rats

1994 ◽  
Vol 130 (4) ◽  
pp. 387-393 ◽  
Author(s):  
Katharina Binz ◽  
Christoph Schmid ◽  
Roger Bouillon ◽  
E Rudolf Froesch ◽  
Kay Jürgensen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Bone Density ◽  
Trabecular Bone ◽  
Mineral Metabolism ◽  
Male Rats ◽  
Insulin Like Growth Factor ◽  
Trabecular Bone Density ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Binz K, Schmid C, Bouillon R, Froesch ER, Jürgensen K, Hunziker EB. Interactions of insulin-like growth factor I with dexamethasone on trabecular bone density and mineral metabolism in rats. Eur J Endocrinol 1994;130:387–93. ISSN 0804–4643 Glucocorticoid treatment causes osteoporosis and growth retardation in humans. Insulin-like growth factor I (IGF-I) stimulates differentiation and replication of cultured osteoblast-like cells and induces longitudinal bone growth in IGF-I-deficient rats. We investigated the influence of subcutaneously infused IGF-I on bone and mineral metabolism of male rats treated with a high dose of dexamethasone. Dexamethasone was added to the drinking water in a concentration of 1 mg/l. After 30 days of dexamethasone treatment, recombinant human IGF-I (300 μg/day) or solvent was infused sc by osmotic minipumps for 21 days while dexamethasone was continued. Age-matched untreated male rats served as healthy controls. Dexamethasone-treated rats lost weight. Their IGF-I levels were decreased to 36% of healthy controls. Infusion of IGF-I resulted in an increase in IGF-I serum levels (582% compared to healthy controls) and allowed some weight gain. Osteocalcin and calcitriol levels were markedly decreased in dexamethasone-treated rats and were not influenced significantly by IGF-I infusion. In contrast, IGF-I treatment restored the free calcitriol concentration (molar ratio of calcitriol to vitamin D-binding protein) towards normal. Furthermore, infusion of IGF-I partially corrected the dexamethasone-induced hyperinsulinemia. Histomorphometric analysis revealed no difference in vertebral trabecular bone density (i.e. growth-independent bone remodeling) between the three groups. In contrast, mean trabecular bone density in tibial metaphyses was increased markedly by dexamethasone, presumably due to osteoclast inhibition. Insulin-like growth factor I infusion did not significantly influence these structural metaphyseal bone parameters. We conclude that IGF I-infusion in male rats treated with high doses of dexamethasone reduces insulin resistance and restores calcitriol production but not osteoblast function or responsiveness to calcitriol. K Binz, Division de Diabétologie, Hôpital Cantonal Universitaire, 1211 Geneva, Switzerland

Role of testosterone in regulating the growth of mice from lines selected for low vs high plasma insulin-like growth factor-I concentrations

1989 ◽  
Vol 121 (5) ◽  
pp. 686-690 ◽  
Author(s):  
Rafat A. Siddiqui ◽  
Stuart N. McCutcheon ◽  
Duncan D. S. Mackenzie ◽  
Hugh T. Blair ◽  
J. Eldon Ormsby ◽  
...  
Keyword(s):  
Body Weight ◽  
Growth Factor ◽  
High Plasma ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Pubertal Growth ◽  
Igf I ◽  
Growth Factor I ◽  
Circulating Levels

Abstract. A study was undertaken to investigate the role of testosterone in regulating growth and circulating levels of insulin-like growth factor-I in male mice from lines divergently selected on the basis of plasma IGF-I. Controls of each lines were sham-operated at 10 days of age and treated with peanut oil from day 14 to day 70. A second group, which was castrated at 10 days and treated with testosterone enanthate (0.5 μg · (g body weight) −1 · day−1) from day 14 to 70, did not differ from controls in body weight but had higher plasma IGF-I concentrations. Delaying testosterone therapy until day 42 in a third group retarded growth, with body weights being significantly lower than those of other two groups from days 35 to 56. However, plasma IGF-I levels in this group were not different from those of controls. Effects of line and treatment were additive. It is concluded that the greater pubertal growth of high-line compared to low-line males is not due to greater stimulation of circulating IGF-I by testosterone. Furthermore, testosterone does not appear to influence pubertal growth by acting on circulating levels of IGF-I.

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