Metabolic Response to Fasting in Experimental Intrauterine Growth Retardation Induced by Surgical and Nonsurgical Maternal Stress

Levitsky, Lynne L.; Kimber, Anne; Marchichow, Jo Ann; Uehara, Jane

doi:10.1159/000240981

Cited by 14 publications

(6 citation statements)

References 8 publications

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“…Despite free access to food, maternal exercise during pregnancy had adverse effects on the birth weight of pups. The intra-uterine growth retardation observed in the present study supports previous findings (Terada, 1974;Levitsky et al 1977;Uriu-Hare et al 1989). The competition between maternal exercising muscles and the fetus for substrates may have resulted in a decreased availability of these substrates for normal fetal growth.…”

Section: Discussionsupporting

confidence: 93%

“…Exercise increases energy expenditure and exercise or physical work during pregnancy is thought to be a predisposing factor to premature labour, low-birth-weight babies and increased infant mortality rates (Naeye & Peters, 1982). Adverse effects of maternal exercise during pregnancy and lactation on fetal outcome and postnatal growth in animals have been reported (Terada, 1974;Levitsky et al, 1977;Parizkova, 1979;Jenkins & Ciconne, 1980;Uriu-Hare et al 1989). A preliminary study conducted in our laboratory indicated that the adverse effects of maternal exercise during pregnancy and lactation on fetal and pup growth last beyond the weaning period causing irreversible growth retardation in rats (Pinto & Shetty, 1990).…”

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confidence: 99%

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Influence of exercise-induced maternal stress on fetal outcome in Wistar rats: Inter-generational effects

Pinto

1995

Br J Nutr

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The effects of physical activity during pregnancy and lactation on the fetal outcome and the growth of pups was studied in Wistar rats (n 144). Rats were trained to swim for 2 h every day, 6 d/week through pre-pregnancy, pregnancy and lactation. Maternal exercise during pregnancy, despite the dams having ad lib. access to food, resulted in low-birth-weight pups (5.6 (SD 0.7) g; n 178 in exercised dams v. 6.2 (SD 0.8) g; n 238 in sedentary dams). Maternal exercise continued through lactation exaggerated further the growth retardation of these pups (30.0 (SD 4.7) g; n 78 in exercised dams v. 36.0 (SD 6.9) g; n 126 in sedentary dams). The effects of maternal exercise during pregnancy and lactation studied over two successive generations revealed a reduction in the growth rates of the second generation progeny of both exercised (5.3 (SD 0.9) g; n 125 at birth and 25.1 (SD 6.8) g; n 54 at weaning) and sedentary rats (6.0 (SD 0.2) g; n 110 at birth and 31.3 (SD 4.3) g at weaning) born to first-generation exercised rats. While slower growth in the former indicates a cumulative effect of exercise stress over two generations, that of the latter indicates that the generational effects are manifest even though the dams of the F1 generation were not exposed to exercise stress during pregnancy and lactation. These findings suggest that the adverse effect of maternal exercise during pregnancy and lactation on fetal outcome in one generation is transferred to the subsequent generation.

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 99%

Influence of exercise-induced maternal stress on fetal outcome in Wistar rats: Inter-generational effects

Pinto

1995

Br J Nutr

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“…2). Although this just failed to reach statistical significance it should be noted that sham surgery has been shown to influence growth rate in utero (17) and in some studies is associated with a decrease in birth weight (18). Although in the present study, 24-h weight was not significantly reduced in the sham surgery group, a temporary drop in fetal weight cannot be completely excluded.…”

Section: Discussioncontrasting

confidence: 82%

Increased Elastic Tissue Defect Formation in the Growth Restricted Brown Norway Rat: A Potential Link Between In Utero Condition and Cardiovascular Disease

2008

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Low birth weight for gestational age has been epidemiologically linked to cardiovascular mortality and morbidity in adult life. This study aimed to determine whether in utero growth restriction influences an early feature of atherosclerotic pathology; disruption of the aortic internal elastic lamina (IEL) in the adult Brown Norway (BN) rat. In utero growth restriction was induced by bilateral uterine artery ligation on day 18 of gestation, thereby decreasing newborn BN pup weight by approximately 14%. Restriction surgery significantly increased aortic IEL defect number at 8 wk of age in both sexes compared with no surgery animals (p Ͻ 0.002). At 16 wk of age placental restriction surgery significantly increased the number of defects in males compared with both no surgery and sham surgery control groups (p Ͻ 0.001). The total number of IEL defects was significantly correlated with several postnatal growth rate parameters, including 72-h postpartum weight. Neither blood pressure was significantly different between treatment groups, nor was it correlated with body weight or IEL defect numbers. The findings of this study seem to support the fetal origins of adult disease hypothesis, by demonstrating that a moderate growth restricting insult dramatically increases aortic elastic tissue defect formation via an apparently blood pressure-independent mechanism. (Pediatr Res 64: [125][126][127][128][129][130] 2008)

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“…Fetal weight was unaffected in the normal weight gain group of others (7,32,33). The absence of IUGR in the normal weight expressed as percent change from controls.…”

Section: Discussionmentioning

confidence: 88%

Preserved Fetal Plasma Amino Acid Concentrations in the Presence of Maternal Hypoaminoacidemia

et al. 1986

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ABSTRACT. The effects on the conceptus of persistently decreased maternal plasma amino acid concentrations were studied in pregnant rats by the infusion of glucagon (0.21 mglday) to the mother from day 14 to 20 of gestation with a subcutaneous, osmotically driven minipump. Controls received diluent. The experimental animals either had normal caloric intake and weight gain, or diminished caloric intake with no weight gain. Both experimental groups exhibited a decrease in plasma total amino acid concentration of approximately 50%. Maternal plasma glucose and insulin concentrations were unaffected except for slight decreases in the low weight gain group. At cesarean section on day 20, fetal weight was unaffected in the normal weight gain group, while the low weight gain animals exhibited intrauterine growth retardation. Fetal plasma glucose and insulin concentrations were unaffected. Despite the marked decrease in maternal plasma total amino acid concentration, fetal plasma total amino acid concentration was unaffected. Individual plasma amino acid concentrations in the normal weight gain mothers and fetuses revealed a spectrum of changes. Some maternal amino acids were decreased by more than 60% (a-aminobutyric acid, asparagine, threonine, glutamine, alanine) while others were unaffected (tyrosine, tryptophan, phenylalanine, histidine). In general, amino acids that were decreased in the mother exhibited no change or a lesser decrease in fetal plasma concentration, while those that were unaffected in the mothers showed increased fetal concentrations. Fetuses from the low weight gain mothers had plasma amino acid ~rofiles that were similar to those of the normal weight gain mothers. We speculate that the preserved fetal amino acid concentrations are due to enhanced placental transport of amino acid secondary to maternal substrate decrease. (Pediatr Res 20: 1071-1076,1986 which are specific for each group of nutrients. In the case of amino acids it has been demonstrated that the placenta is capable of concentrating most amino acids intracellularly in order to achieve transport to the fetus against a concentration gradient (1-4). This results in fetal plasma amino acid concentrations which can be more than three times higher than maternal plasma concentrations (1, 5 , 6).Maternal substrate limitation, presumably by limiting nutrient transport to the fetus, can lead to IUGR. This has been demonstrated experimentally in models utilizing starvation (7) or ligation of the uterine artery (8). These manipulations result in nonspecific reduction in the delivery of substrates, including glucose and amino acids, such that the roles of specific substrates remain obscure.The aim of the present study was to develop a model in which maternal plasma amino acid concentrations are selectively reduced without significant changes in the maternal concentrations of other nutrients. In nonpregnant male rats, a persistent increase in glucagon has been shown to be associated with a decrease in total plasma amino acid concentrations (9). Thi...

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Metabolic Response to Fasting in Experimental Intrauterine Growth Retardation Induced by Surgical and Nonsurgical Maternal Stress

Cited by 14 publications

References 8 publications

Influence of exercise-induced maternal stress on fetal outcome in Wistar rats: Inter-generational effects

Influence of exercise-induced maternal stress on fetal outcome in Wistar rats: Inter-generational effects

Increased Elastic Tissue Defect Formation in the Growth Restricted Brown Norway Rat: A Potential Link Between In Utero Condition and Cardiovascular Disease

Preserved Fetal Plasma Amino Acid Concentrations in the Presence of Maternal Hypoaminoacidemia

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