Long-Term Effects of Gestational Protein Malnutrition on Postnatal Growth, Insulin-Like Growth Factor (IGF)-I, and IGF-Binding Proteins in Rat Progeny

Muaku, Séverin M; Beauloye, Véronique; Thissen, Jean‐Paul; Underwood, Louis E.; Fossion, Chantal; Guy, Gérard; Ketelslegers, Jean‐Marie; Maiter, Dominique

doi:10.1203/00006450-199604000-00015

Cited by 30 publications

(15 citation statements)

References 36 publications

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“…However, in our study this would seem unlikely as there was no reduction in plasma IGF-I concentrations as a result of programming or hypercaloric nutrition. This fits with work by ourselves (Woodall et al 1996) and others showing that postnatal alterations in GH secretion and IGF-I concentrations as a result of prenatal events are normalised at a young age (Muaku et al 1996).…”

Section: Discussionsupporting

confidence: 92%

Adult growth hormone treatment reduces hypertension and obesity induced by an adverse prenatal environment

Vickers

Ikenasio²,

Breier³

2002

Journal of Endocrinology

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The discovery of a link between an adverse in utero environment and the propensity to develop metabolic and cardiovascular disease in adult life is one of the most important advances in epidemiological research of recent years. Increasing experimental evidence suggests that alterations in the fetal environment may have long-term consequences for the development of metabolic disorders in adult life. This process has been termed 'fetal programming' and we have shown that undernutrition of the mother during gestation leads to development of the metabolic syndrome X during adult life. Striking metabolic similarities exist between syndrome X and untreated GH deficiency (GHD). In the present study we have investigated the effects of GH treatment on blood pressure and metabolic parameters. Virgin Wistar rats (age 75 5 days, n=20 per group) were time-mated and randomly assigned to receive food either ad libitum (AD) or 30% of AD intake (UN) throughout pregnancy. At weaning, male offspring were assigned to one of two diets (control or hypercaloric (30% fat)). Systolic blood pressure was measured at day 100 and following twice daily treatment with recombinant bovine GH for 21 days. GH treatment increased body weights in all treated animals but significantly reduced retroperitoneal and gonadal fat pad weights. Following GH treatment, systolic blood pressure was markedly decreased in all UN offspring. Salinetreated animals showed no change in systolic blood pressure over the treatment period. GH treatment increased heart-to-body weight ratio in all GH-treated animals. Our data demonstrated that GH treatment reduces hypertension and improves cardiovascular function in animals exposed to adverse environmental conditions during fetal or postnatal life.

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Section: Discussionsupporting

confidence: 92%

Adult growth hormone treatment reduces hypertension and obesity induced by an adverse prenatal environment

Vickers

Ikenasio²,

Breier³

2002

Journal of Endocrinology

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show abstract

“…However, in our model, the litter size of SGA pups was kept at a maximum of 6 pups per lactating mother whereas 12–14 pups is a normal litter size in this strain of rats. Sufficient food intake in SGA pups is also confirmed by previous studies [16]. Therefore, the nutritional statuses of SGA rats and AGA control rats were comparable.…”

Section: Discussionsupporting

confidence: 86%

Impaired Growth Hormone Receptor Signaling during Non-Catch-Up Growth in Rats Born Small for Gestational Age

Huang

Du²,

Zhuang³

et al. 2010

Horm Res Paediatr

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Background/Aims: Non-catch-up growth (NCG) in children born small for gestational age (SGA) is associated with growth hormone (GH) resistance, although the mechanisms of this association are unknown. Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling is involved in GH signal transduction. This study examined the role of JAK/STAT signaling in GH resistance of SGA rats. Methods: NCG-SGA was induced by uterine artery ligation in pregnant rats. NCG-SGA rats were treated with GH for 7 days and rats appropriate for gestational age (AGA) served as controls. Phosphorylation of JAK2/STAT5 and expression of GH receptor, suppressor of cytokine signaling 2 (SOCS-2) and cytokine-inducible SH2-containing protein (CIS) in the liver were determined by Western blotting. The expression of insulin-like growth factor 1 (IGF-1) mRNA was examined by the reverse transcription-polymerase chain reaction. Results: GH treatment significantly increased body weight and length growth rate in AGA but not in NCG-SGA rats. The increase in serum IGF-1 level and expression of IGF-1 mRNA in response to GH treatment in NCG-SGA rats was significantly less than in AGA rats. GH-induced increase in phosphorylation of JAK2/STAT5 in response to acute GH stimulation was significantly lower in NCG-SGA rats compared to AGA controls. SOCS-2 and CIS expressions significantly increased in NCG-SGA rats following GH treatment. Conclusion: GH resistance in NCG-SGA rats is associated with impaired JAK/STAT signaling and upregulated SOCS-2 and CIS expression.

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“…Interestingly, at weaning and adult age, pancreas weight recovered proportionally to body weight in this animal group whereas liver and kidney weight, which were already more affected at birth, were still reduced. These latter results were not observed at adult age in off-spring born to food-restricted [17] or proteinrestricted [20] mothers. In this rat model, a more dramatic pattern was observed in the offspring when maternal undernutrition was maintained postnatally.…”

Section: Discussionmentioning

confidence: 59%

Postnatal Somatic Growth and Insulin Contents in Moderate or Severe Intrauterine Growth Retardation in the Rat

1998

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A rat model of perinatal malnutrition was designed to study the role of nutrition in postnatal somatic growth and insulin stores until adulthood. Maternal food restriction (50%) from day 15 of pregnancy resulted in intrauterine growth retardation (IUGR) in the offspring. The outcome of moderate or severe IUGR was investigated. Neonates with moderate IUGR normally nourished postnatally showed normal body and organ weights and normal insulin contents in adulthood. Offspring with severe IUGR normally nourished postnatally also rapidly recovered normal body and pancreatic weights, but liver and kidney weights were significantly reduced at adult age. Malnutrition until weaning in offspring with severe IUGR induced marked growth retardation (50%) in body and organ weights at weaning. Although pancreatic weight recovered at adult age, body, liver and kidney weights were irreversibly affected, despite several months of normal nutrition. Furthermore, severe IUGR at birth resulted in decreased insulin content at adult age, irrespective of postnatal nutrition. In conclusion, this animal model demonstrates that normalization of adult size can be dissociated from organ growth and also that altered insulin stores in adulthood are more dependent on the severity of IUGR at birth than on postnatal catch-up in organ growth.

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Long-Term Effects of Gestational Protein Malnutrition on Postnatal Growth, Insulin-Like Growth Factor (IGF)-I, and IGF-Binding Proteins in Rat Progeny

Cited by 30 publications

References 36 publications

Adult growth hormone treatment reduces hypertension and obesity induced by an adverse prenatal environment

Adult growth hormone treatment reduces hypertension and obesity induced by an adverse prenatal environment

Impaired Growth Hormone Receptor Signaling during Non-Catch-Up Growth in Rats Born Small for Gestational Age

Postnatal Somatic Growth and Insulin Contents in Moderate or Severe Intrauterine Growth Retardation in the Rat

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