scholarly journals Dietary Protein Restriction Lowers Plasma Insulin-Like Growth Factor I (IGF-I), Impairs Cortical Bone Formation, and Induces Osteoblastic Resistance to IGF-I in Adult Female Rats1

Endocrinology ◽  
2000 ◽  
Vol 141 (9) ◽  
pp. 3149-3155 ◽  
Author(s):  
S. Bourrin ◽  
P. Ammann ◽  
J. P. Bonjour ◽  
R. Rizzoli
1992 ◽  
Vol 132 (1) ◽  
pp. 141-147 ◽  
Author(s):  
J.-P. Thissen ◽  
L. E. Underwood

ABSTRACT Dietary protein restriction in young rats decreases serum insulin-like growth factor-I (IGF-I) concentrations and the amount of liver IGF-I mRNA, suggesting that regulation for the liver IGF-I gene expression in this model occurs at a pretranslational level. To determine whether there is also translational control, we assessed the association of the liver IGF-I mRNA transcripts with polysomes in livers of normally fed (15% dietary protein) versus protein-restricted (5% dietary protein) rats. One week of dietary protein restriction reduces serum IGF-I concentrations by 54% and the amount of liver IGF-I mRNA by 35%, with the 7·5 kb size-class of IGF-I mRNA being the most affected (−48%). Protein restriction reduces the amount of the polysomal IGF-I mRNAs by 30%, a value in close agreement with the changes in total IGF-I mRNAs. Protein restriction is not associated with changes in the distribution of IGF-I mRNAs between the polysomal and non-polysomal fractions. All major size-classes of IGF-I mRNA transcripts (7·5, 4·7, 1·7, 0·9–1·2 kb) are associated with the polysomes in both dietary groups, suggesting involvement in the initiation phase of the IGF-I translation. We conclude that no untranslatable pool of IGF-I mRNAs is present in the liver of protein-restricted animals. Protein restriction, however, decreases slightly the mean size of polysomes. This decrease in ribosomal number associated with the IGF-I mRNA could decrease translational efficiency. Our data suggest that dietary protein restriction does not impair the initiation of IGF-I mRNA translation. Journal of Endocrinology (1992) 132, 141–147


1999 ◽  
Vol 81 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Myriam Sanchez-Gomez ◽  
Kjell Malmlöf ◽  
Wilson Mejia ◽  
Antonio Bermudez ◽  
Maria Teresa Ochoa ◽  
...  

The aim of the present study was to investigate the influence of dietary protein level on the protein anabolic effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I). Female growing rats were fed on either a high- or a low-protein diet with crude protein contents of 222 and 83 g/kg respectively. The diets contained the same amount of metabolizable energy (15·1 MJ/kg) and were given during a 14 d period. During the same time, three groups of rats (n 8) on each diet received subcutaneous infusions of either saline, recombinant human GH (rhGH) or recombinant human IGF-I (rhIGF-I). rhGH and rhIGF-I were given in doses of 360 and 500 μg/d respectively. The low-protein diet alone reduced significantly (P < 0·05) IGF-I concentrations in serum and in tissue taken from the gastrocnemius muscle as well as IGF-I mRNA from the same muscle. The responses to rhGH and rhIGF-I in terms of muscle IGF-I and its mRNA were variable. However, when rhIGF-I was infused into rats on the high-protein diet, significantly elevated levels of IGF-I in muscle tissues could be observed. This was associated with a significantly (P < 0·05) increased N balance, whereas rhGH significantly (P < 0·05) enhanced the N balance in rats on the low-protein diet. Thus, it can be concluded that the level of dietary protein ingested regulates not only the effect of IGF-I on whole-body N economy but also the regulation of IGF-I gene expression in muscles. The exact mechanism by which GH exerts its protein anabolic effect, however, remains to be elucidated.


Endocrinology ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 429-435 ◽  
Author(s):  
JEAN-PAUL THISSEN ◽  
SANDRINE TRIEST ◽  
BILLIE M. MOATS-STAATS ◽  
LOUIS E. UNDERWOOD ◽  
TEKLA MAUERHOFF ◽  
...  

1998 ◽  
Vol 83 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Tarcisio Bianda ◽  
Yvonne Glatz ◽  
Roger Bouillon ◽  
Ernst Rudolf Froesch ◽  
Christoph Schmid

Administration of insulin-like growth factor-I (IGF-I) or growth hormone (GH) is known to stimulate bone turnover and kidney function. To investigate the effects of IGF-I and GH on markers of bone turnover, eight adult GH-deficient patients (48 ± 14 yr of age) were treated with IGF-I (5 μg/kg/h in a continuous sc infusion) and GH (0.03 IU/kg/daily sc injection at 2000 h) in a randomized cross-over study. We monitored baseline values for three consecutive days before initiating the five-day treatment period, as well as the wash-out period of ten weeks. Serum osteocalcin, carboxyterminal and aminoterminal propeptide of type I procollagen (PICP and PINP, respectively) increased significantly within 2–3 days of both treatments (P &lt; 0.02) and returned to baseline levels within one week after the treatment end. The changes in resorption markers were less marked as compared with formation markers. Total 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) rose significantly, whereas PTH and calcium levels remained unchanged during either treatment. Conclusions: Because the rapid increase in markers of bone formation was not preceded by an increase in resorption markers, IGF-I is likely to stimulate bone formation by a direct effect on osteoblasts. Moreover, because PTH, calcium, and phosphate remained unchanged, IGF-I appears to stimulate renal 1α-hydroxylase activity in vivo.


2003 ◽  
Vol 49 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Sumie NONAKA ◽  
Tsutomu HASHIZUME ◽  
Mami HORIUCHI ◽  
Utako MIKAMI ◽  
Takeshi OSAWA ◽  
...  

1994 ◽  
Vol 267 (1) ◽  
pp. E1-E6 ◽  
Author(s):  
K. Mueller ◽  
R. Cortesi ◽  
D. Modrowski ◽  
P. J. Marie

Although in vitro experiments indicate that insulin-like growth factor I (IGF-I) is an anabolic hormone in bone cell metabolism, the effects of IGF-I in vivo on bone formation are unclear. We thus investigated whether IGF-I is able to stimulate bone formation in adult rats with established osteopenia induced by ovariectomy (OVX). IGF-I was administered at daily doses of 0.05, 0.2, and 0.8 mg/kg for 3 wk. OVX induced a marked osteopenia in femur and tibia. Administration of IGF-I increased trabecular bone mass with a maximal effect at 0.2 mg/kg. The same dose stimulated bone formation, as revealed by an increase in osteoid surface, osteoblast surface, triple tetracycline-labeled surface, and bone formation rate. The mineral apposition rate was equally stimulated at all doses. At the highest dose, IGF-I increased osteoclast surface and osteoclast number. These data indicate that, in the adult OVX rat, IGF-I stimulates bone formation and increases trabecular bone volume at medium doses and enhances the histological indexes of bone resorption at high doses.


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