12 research outputs found

    Nucleotide sequence analysis of a cDNA encoding human ubiquitin reveals that ubiquitin is synthesized as a precursor

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    Isolement d'un cDNA humain codant 95% de la molécule d'ubiquitine, une séquence précurseur carboxyterminale et une queue polyA. L'existence de précurseur ubiquitine peut jouer un rôle dans la compartimentation de la protéine et de ses précurseurs. L'analyse des mRNA révèle l'existence de trois mRNA codant pour l'ubiquitine chez l'homme et de quatre mRNA chez le rat

    Postnatal catch-up growth induced by growth hormone and insulin-like growth factor-I in rats with intrauterine growth retardation caused by maternal protein malnutrition

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    In this study, we examined the effects of exogenous IGF-I and GH on postnatal growth of rat pups with intrauterine growth retardation due to gestational protein restriction. From birth until weaning (d 23), pups born from dams fed ad libitum a low (5% casein; P5 pups) or a normal protein diet (20% casein; P20 controls) were cross-fostered to well nourished lactating dams. On d 2, the litters (n = 6/dietary group) were reduced in size to 6 pups, and littermates received, through postnatal d 23, two daily s.c. injections of bovine GH (2.5 microg/g of body weight (BW)/day), human IGF-I (1.8 microg/g of BW/day), or saline. At birth, BW and tail length (TL) of P5 pups were markedly decreased (to 72 and 70% of controls, respectively; p < 0.001). Despite food rehabilitation, stunting of body growth was still apparent on d 23 in the saline-injected P5 rats (BW and TL: 76 and 83% of age-matched saline-injected controls; p < 0.01). Serum IGF-I (-51%; p < 0.001) and weight of liver, heart, kidney, brain, and thymus (-13 to -35%; p < 0.01) were also reduced. Administration of GH in P5 rats raised their serum IGF-I (1-fold) to levels observed in saline-injected controls, and restored normal BW and TL (94 and 98% of controls, respectively), and organ weight (91-107% of those of controls). Injections of IGF-I in P5 rats increased after 1 h their serum IGF-I to levels 3 times greater than in saline-injected controls, and resulted in normalization of BW and TL (94 and 96% of controls), and organ weight (92-111% of controls). In P20 controls, 3-wk GH and IGF-I injections significantly increased serum IGF-I (0.6- and 2-fold increases, respectively), BW (14 and 11%), TL (12 and 11%), and organ weight (+10 to 30%) compared with saline-injected rats (p < 0.01). We conclude that under conditions of adequate nutrition, both GH and IGF-I may equally promote postnatal catch-up growth in rats with intrauterine growth retardation caused by gestational protein malnutrition

    Long-term effects of gestational protein malnutrition on postnatal growth, insulin-like growth factor (IGF)-I, and IGF-binding proteins in rat progeny.

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    We examined the long-term effects of dietary protein restriction during rat pregnancy on serum IGF-I, serum IGF binding proteins, and liver IGF-I gene expression during postnatal development. Pregnant Wistar rats were fed ad libitum throughout gestation a normal (20% casein diet; P20 controls) or a low (5% casein; P5) protein diet. At birth, the pups from both P20 and P5 dams were cross-fostered to well nourished lactating dams, and litters (n = 5/dietary group) were reduced in size to 6 pups. After weaning (d 22), the pups were fed the control diet ad libitum. The pups were killed at 8, 22, and 63 d of age. Gestational protein restriction caused significant growth retardation and mortality in newborn pups. Despite food rehabilitation during the suckling period (d 0-22), body weight, tail length, and the weight of liver, heart, kidney, and brain in the P5 pups remained significantly reduced at 8 and 22 d (-17 to -35%) compared with control pups. At the same time, serum and liver IGF-I concentrations in the P5 pups (on d 8: 100 +/- 9 ng/mL and 11 +/- 1 ng/g, respectively; on d 22: 340 +/- 20 ng/mL and 42 +/- 3 ng/g) were lower than in age-matched controls (on d 8: 170 +/- 12 ng/mL and 26 +/- 2 ng/g; on d 22: 470 +/- 30 ng/mL and 73 +/- 5 ng/g), although liver IGF-I mRNA abundance was not affected. After long-term food rehabilitation (d 63), tail length and organ weight recovered, and serum and liver IGF-I concentrations were normalized. However, although the P5 rats had resumed a normal growth rate, their body weight remained lower than in the controls. There were no differences in serum IGF binding proteins 1-4, insulin, and GH concentrations between the groups at any age studied. These results suggest that reduction in serum IGF-I may contribute to the reduced somatic and organ growth observed in rats after gestational protein malnutrition, and further support a role for IGF-I in the control of catch-up growth
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