Maternal Endocrine Adaptation throughout Pregnancy to Nutritional Manipulation: Consequences for Maternal Plasma Leptin and Cortisol and the Programming of Fetal Adipose Tissue Development

Bispham, J; Gopalakrishnan, G.; Dandrea, J; Wilson, Victoria; Budge, Helen; Keisler, D.H.; Pipkin, F. Broughton; Stephenson, Terence; Symonds, Michael

doi:10.1210/en.2003-0320

Cited by 218 publications

(209 citation statements)

References 48 publications

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“…The observed decreases in circulating total IGF-I level and IGF-I:IGFBP-3 ratio for both mother and fetus in the presence of moderate maternal NR are consistent with other mammalian studies. In response to 60% global diet restriction in sheep pregnancy, Bispham et al [17] observed lower maternal total and free IGF-I levels and normal maternal glucose, consistent with our findings in the baboon. IGFBPs stabilize the IGF-I level across the 24-h period.…”

Section: Effects Of Maternal Nr On the Maternal And Fetal Igf-igfbp Asupporting

confidence: 91%

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The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

Li¹,

Levitz²,

Hubbard³

et al. 2007

Placenta

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Information on the influence of poor maternal nutrition on the regulation of responses to pregnancy, placental and fetal growth and development is critical to a better understanding of pregnancy physiology and pathophysiology. We determined normal changes and effects of controlled and monitored moderate nutrient restriction (NR) (global nutrient intake reduced to 70% of food consumed by mothers feeding ad libitum from 0.16 to 0.5 of gestation) in the baboon, on important hematological, biochemical, and hormonal indices of fetal growth and placental function. Serum IGF-I:IGFBP-3 ratio was lower in pregnant than control non-pregnant baboons feeding ad libitum. Serum concentrations of total and free IGF-I were decreased in NR mothers compared with controls (p < 0.05). The decrease in fetal IGF-I did not reach significance (p = 0.057). Serum IGF-I: IGFBP-3 ratio was decreased by NR in both mothers and fetuses. Maternal serum IGF-II was unchanged by NR. Placental IGF-I mRNA and protein abundance were similarly reduced whereas IGF-II mRNA increased in placental tissue of NR compared to control mothers. Systemic (maternal) and local (placental) IGFBP-1 and IGFBP-3 mRNA and protein abundance were unchanged by NR. Type 1 IGF receptor protein in the syncytiotrophoblast increased in NR. Type 2 IGF receptor protein was present in the stem villi core, and decreased after NR. We conclude that moderate NR in this important non-human primate model significantly disrupts the maternal and placental IGF-IGFBP axis and influences placental expression of this key system at the gene and protein level. Changes observed appear to be directed toward preserving placental growth.

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Section: Effects Of Maternal Nr On the Maternal And Fetal Igf-igfbp Asupporting

confidence: 91%

“…[7]). Global NR during pregnancy at levels similar to that in our study [17,18], and even more extreme restriction [19], has been extensively studied in sheep, pigs, and rats [17][18][19][20]. The IGF system within the placenta and several fetal organs has been shown to respond to both global and other forms of NR during pregnancy.…”

Section: Discussionsupporting

confidence: 66%

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

Li¹,

Levitz²,

Hubbard³

et al. 2007

Placenta

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“…43,44 In sheep, maternal nutrient restriction over the period of rapid placental growth followed by restoration of maternal nutrition over the second half of gestation enhances the adipose tissue development at the end of gestation, which was thought to increase the risk of obesity in later life. 45 However, this does not lead to significant increase in adipose and fat mass at adulthood. 46 Bilateral uterine artery ligation performed on day 19 of gestation in rat leads to intrauterine growth retardation (IUGR).…”

Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

Programming of obesity and cardiovascular disease

2004

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BACKGROUND: There is evidence that malnutrition in early life induces a growth retardation leading, in adult life, to manifest components of the metabolic syndrome. However, the impact on obesity seems less clearly established. OBJECTIVE: To review the effects of foetal and postnatal malnutrition on the programming of obesity in the context of the metabolic syndrome, as well as the link between central obesity and cardiovascular diseases. METHODS: Included in the review were recent papers exploring the mechanisms linking maternal nutrition with impaired foetal growth and later obesity, cardiovascular disease, hypertension and diabetes in humans and animals. RESULTS: The programming of obesity during foetal and early postnatal life depends of the timing of maternal malnutrition as well as the postnatal environment. Obesity arises principally in offspring submitted to malnutrition during early stages of gestation and which presented early catch-up growth. The programming may involve the dysregulation of appetite control or the hormonal environment leading to a context favourable to obesity development (hypersecretion of corticosteroids, hyperinsulinaemia and hyperleptinaemia and anomalies in the IGF axis). Adipose tissue secretes actively several factors implicated in inflammation, blood pressure, coagulation and fibrinolysis. The programmed development of intra-abdominal obesity after early growth restriction may thus favour higher prevalence of hypertension and cardiovascular diseases. CONCLUSIONS: Abdominal obesity appears in malnourished offspring and is aggravated by early catch-up growth. Higher rates of intra-abdominal obesity observed after growth restriction may participate to hypertension and create atherothrombotic conditions leading to the development of cardiovascular diseases.

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“…Du et al (2010) proposed that the fetal stage offers the greatest chance to improve the ability of livestock to deposit intramuscular fat due to a greater abundance of non-committed pluripotent cells. Studies utilizing sheep have reported adipose tissue in the fetus can be manipulated by maternal nutrition (Bispham et al, 2003;Ford et al, 2007). Research in sheep also indicates that maternal nutrition during gestation influences gene expression necessary for intramuscular adipocyte development (Tong et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The influence of maternal nutrition on expression of genes responsible for adipogenesis and myogenesis in the bovine fetus

Jennings

Gonda

Underwood

et al. 2016

Animal

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The objective of this study was to determine whether altered maternal energy supply during mid-gestation results in differences in muscle histology or genes regulating fetal adipose and muscle development. In total, 22 Angus cross-bred heifers (BW = 527.73 ± 8.3 kg) were assigned randomly to the three dietary treatments providing 146% (HIGH; n = 7), 87% (INT; n = 7) or 72% (LOW; n = 8) of the energy requirements for heifers from day 85 to day 180 of gestation. Fetuses were removed via cesarean section at day 180 of gestation and longissimus muscle (LM) and subcutaneous fat were collected and prepared for analysis of gene expression. Samples from the LM and semitendinosus (ST) were evaluated for muscle fiber diameter, area and number. The right hind limb was dissected and analyzed to determine compositional analysis. Fetal growth and muscle histology characteristics of the LM and ST were similar among treatments. Preadipocyte factor-1 expression was up-regulated in fetal LM ( P < 0.05) of HIGH fetuses as compared with INT, whereas LOW fetuses showed increased CCAAT/enhancer-binding protein-β (C/EBP-β) expression in LM as compared with INT ( P < 0.05). Peroxisome proliferator-activated receptor γand C/EBP-α did not differ as a result of dietary treatment in LM or subcutaneous fat samples. There was a tendency for increased expression of fatty acid synthase in LM of LOW fetuses as compared with INT ( P < 0.10). Myogenin was more highly expressed ( P < 0.05) in LM of the LOW fetuses, whereas μ-calpain expression was increased in the HIGH treatment compared with INT. A tendency for increased expression of IGF-II was observed for both LOW and HIGH fetuses compared with INT ( P < 0.10). Expression of stearoyl-CoA desaturase, myoblast determination protein 1, myogenic factor 5, myogenic regulatory factor-4, m-calpain, calpastatin, IGF-I and myostatin was similar between treatments. Collectively, these results suggest that fetal growth characteristics are not affected by the level of maternal nutritional manipulation imposed in this study during mid-gestation. However, differences in expression of fetal genes regulating adipose and muscle tissue growth and development could lead to differences in postnatal composition and warrants further investigation.

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Maternal Endocrine Adaptation throughout Pregnancy to Nutritional Manipulation: Consequences for Maternal Plasma Leptin and Cortisol and the Programming of Fetal Adipose Tissue Development

Cited by 218 publications

References 48 publications

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

The IGF Axis in Baboon Pregnancy: Placental and Systemic Responses to Feeding 70% Global Ad Libitum Diet

Programming of obesity and cardiovascular disease

The influence of maternal nutrition on expression of genes responsible for adipogenesis and myogenesis in the bovine fetus

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