An imbalance in the methionine content of the maternal diet reduces postnatal growth in the rat

Rees, William D.; Hay, Susan M.; Cruickshank, Morven

doi:10.1016/j.metabol.2006.01.012

Cited by 36 publications

(30 citation statements)

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“…The plasma Thr levels in the LP group were reduced to 69% and 23% of controls at days 14 and 18 of pregnancy, respectively. This is consistent with reports by others (70)(71)(72). The remarkable decrease of Thr is coincident with a 2-to 3-fold increase in Gly levels and a 1.8-2.1-fold increase in Ser in the LP group at days 14, 18 and 21 of pregnancy (Table 3).…”

Section: Discussionsupporting

confidence: 93%

Maternal protein restriction regulates IGF2 system in placental labyrinth

Yallampalli¹

2012

Front Biosci

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This study was to test the hypothesis that altered IGF2 system in the placental labyrinth zone (LZ) impairs feto-placental growth in response to maternal protein restriction. Rats were fed a 20% protein diet and an isocaloric 6% protein diet (LP) from day 1 to days 14, 18, or 21 of pregnancy. The effects of diet, gender of placenta and fetus, and day of pregnancy on placental weight, fetal weight, and expression of the IGF2 axis in the placental LZ and amino acids in maternal plasma were analyzed. Growth restriction occurred in both female and male fetuses by LP, coincident with impaired LZ growth and efficiency. The expression of Igf2, Igf2P0, Igf1r, Igf2r, Insr, Igfbp1, and Igfbp2 in placental LZ were affected by diet, gender and/or day of pregnancy. Concentrations of total essential amino acids and total nonessential amino acids were reduced and increased, respectively, in maternal plasma of LP-fed rats. These results indicate that adaptation of the IGF2 system in rat LZ occurs in a sex-and time-dependent manner in response to maternal protein restriction; however, these adaptations cannot prevent the growth restriction of both male and female fetuses during late pregnancy. KeywordsProtein Restriction; Pregnancy; Fetal Growth; IGF2; IGF2P0; IGFBP; Gene Expression; Placenta; Labyrinth Zone INTRODUCTIONInsulin-like growth factor 2 (IGF2), as well as IGF1, plays a critical role in the feto-placental development and growth in mammalian species. They have metabolic, mitogenic, and differentiative actions in a wide range of fetal tissues, including the placenta. However, IGF1 and IGF2 have distinct actions on maternal adaptation to pregnancy and feto-placental growth according to hormone sources, bioavailability, and actions (1-3). Most direct evidence from knockout and overexpression of IGF axis genes support the notion that IGF2 acts as a direct regulator of feto-placental development (4-6). Fetal growth depends mostly on nutrients, including oxygen, obtained from the mother through the placenta. Not being a passive receiver, fetal demand for growth drives placental transport of nutrients partly by regulating expression of imprinted genes in both the fetus and the placenta (7,8). Among Send correspondence to: Chandra Yallampalli, 301 University Boulevard, Galveston, TX 77555-1062, Tel: 409-772-7593, Fax: 409-747-0475, chyallam@utmb.edu. NIH Public Access Author ManuscriptFront Biosci (Elite Ed). Author manuscript; available in PMC 2013 July 16. Published in final edited form as:Front Biosci (Elite Ed). ; 4: 1434-1450. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript these imprinted genes, IGF2 together with IGF2P0, a placental-specific IGF2, regulates both placental development and nutrient transport (4-6, 9-11).In rodents, labyrinth zone (LZ), the zone near the chorionic plate, represents the main area of the placenta for maternal-fetal hemotrophic exchange (12). Therefore, LZ is of great importance in fetal survival and development. Maternal blood flows through irregularly ...

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Section: Discussionsupporting

confidence: 93%

Maternal protein restriction regulates IGF2 system in placental labyrinth

Yallampalli¹

2012

Front Biosci

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“…In the study of Burdge et al (2008), where the Southampton low protein diet was used, the protein-restricted diet with additional folic acid caused reduced weight gain, but no effect on adiposity was reported. In the present study, as in the studies of Rees et al (2006b), there was no effect of protein content in the maternal diet on fat accretion in the offspring. On the contrary, in female offspring of dams fed during gestation with the protein-restricted Hope Farm diet, a lower weight of endometrial fat pads was observed (Rees et al 2006c).…”

Section: Discussionsupporting

confidence: 85%

“…Different variants of a maternal diet may evoke different long-term effects, and methionine content and sulfur amino acid balance in the maternal diet has been identified as one of the most important programming factors (Langley-Evans 2000; Rees et al 2006a, b, c). Sulfur amino acids are involved not only in methylation processes, but are also regulators of lipid metabolism (Oda 2006).…”

Section: Introductionmentioning

confidence: 99%

Protein and folic acid content in the maternal diet determine lipid metabolism and response to high-fat feeding in rat progeny in an age-dependent manner

et al. 2011

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Maternal diet during gestation can exert a long-term effect on the progeny’s health by programming their developmental scheme and metabolism. The aim of this study is to analyze the influence of maternal diet on lipid metabolism in 10- and 16-week-old rats. Pregnant dams were fed one of four diets: a normal protein and normal folic acid diet (NP-NF), a protein-restricted and normal folic acid diet (PR-NF), a protein-restricted and folic-acid-supplemented diet (PR-FS), or a normal protein and folic-acid-supplemented diet (NP-FS). We also tested whether prenatal nutrition determines the reaction of an organism to a postweaning high-fat diet. Blood biochemistry and biometrical parameters were evaluated. The expression patterns of PPARα, PPARγ, and LXRα in the liver and adipose tissue were examined by real-time PCR. In the 10-week-old, rats folic acid supplementation of the maternal diet was associated with reduced circulating glucose and total cholesterol concentrations (P < 0.01 and P < 0.001, respectively). Neither prenatal diets nor postnatal feeding affected blood insulin concentrations. In the 16-week-old rats, body weight, abdominal fat mass and central adiposity were reduced in the progeny of the folic acid–supplemented dams (P < 0.01, P < 0.001 and P < 0.01, respectively). Maternal protein restriction had no effect on biometry or blood biochemical parameters. Folic acid supplementation of the maternal diet was associated with reduced expression of PPARα, PPARγ, and LXRα in the liver (P < 0.001). Reduced protein content in the maternal diet was associated with increased PPARα mRNA level in the liver (P < 0.001) and reduced LXRα in adipose tissue (P < 0.01). PPARα and PPARγ transcription in the liver, as well as LXRα transcription in adipose tissue, was also dependent on interaction effects between prenatal and postnatal diet compositions. PPARγ transcription in the liver was correlated with the abdominal fat mass, body weight, and calorie intake, while PPARγ transcription in adipose tissue was correlated with reduced body weight and calorie intake. Total serum cholesterol concentration was correlated with LXRα transcription in the liver. Folic acid supplementation of the maternal diet may have favorable effects for lipid metabolism in the progeny, but these effects are modified by the postnatal diet and age. Furthermore, the expression of LXRα, PPARα, and PPARγ in the liver and adipose tissue largely depends on the protein and folic acid content in the maternal diet during gestation. However, the altered transcription profile of these key regulators of lipid metabolism does not straightforwardly explain the observed phenotype.

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“…However, MLP diets of differing composition used in different laboratories have yielded inconsistent data on the relationship between maternal protein intake and offspring blood pressure [66] . A critical role of methionine content in the MLP model was highlighted in work by Langley-Evans et al [66] and Rees et al [138,139] whereby different levels of methionine resulted in the MLP diets leading to different phenotypic outcomes. Several maternal dietary co-factors have also been shown to prevent the development of hypertension in offspring of MLP dams although the mechanisms are not well established.…”

Section: Critical Windows Of Development and Avenues For Interventionmentioning

confidence: 99%

Developmental programming of the metabolic syndrome - critical windows for intervention

Vickers

2011

WJG

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Metabolic disease results from a complex interaction of many factors, including genetic, physiological, behavioral and environmental influences. The recent rate at which these diseases have increased suggests that environmental and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity and the metabolic syndrome. Although the mechanisms are yet to be fully elucidated, this programming was generally considered an irreversible change in developmental trajectory. Recent work in animal models suggests that developmental programming of metabolic disorders is potentially reversible by nutritional or targeted therapeutic interventions during the period of developmental plasticity. This review will discuss critical windows of developmental plasticity and possible avenues to ameliorate the development of postnatal metabolic disorders following an adverse early life environment.

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An imbalance in the methionine content of the maternal diet reduces postnatal growth in the rat

Cited by 36 publications

References 34 publications

Maternal protein restriction regulates IGF2 system in placental labyrinth

Maternal protein restriction regulates IGF2 system in placental labyrinth

Protein and folic acid content in the maternal diet determine lipid metabolism and response to high-fat feeding in rat progeny in an age-dependent manner

Developmental programming of the metabolic syndrome - critical windows for intervention

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