Maternal amino acid supplementation for intrauterine growth restriction

Brown, Laura D.; Green, Alice S.; Limesand, Sean W.; Rozance, Paul J.

doi:10.2741/s162

Cited by 44 publications

(20 citation statements)

References 183 publications

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“…Tau is an essential amino acid for the fetus and neonate and has a variety of physiologic functions (44). Decreased fetal and neonatal concentrations of Tau have been shown in several animal models of IUGR including the one used in the present study (45–47).…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Intrauterine Growth Restriction on the Regional Neurochemical Profile of the Developing Rat Brain

et al. 2015

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Background Intrauterine growth restricted (IUGR) infants are at increased risk for neurodevelopmental deficits that suggest the hippocampus and cerebral cortex may be particularly vulnerable. Objective Evaluate regional neurochemical profiles in IUGR and normally grown (NG) 7-day old rat pups using in vivo 1H magnetic resonance (MR) spectroscopy at 9.4T. Methods IUGR was induced via bilateral uterine artery ligation at gestational day 19 in pregnant Sprague Dawley dams. MR spectra were obtained from the cerebral cortex, hippocampus and striatum at P7 in IUGR (N=12) and NG (N=13) rats. Results In the cortex, IUGR resulted in lower concentrations of phosphocreatine, glutathione, taurine, total choline, total creatine (P<0.01) and [glutamate]/[glutamine] ratio (P <0.05). Lower taurine concentrations were observed in the hippocampus (P<0.01) and striatum (P <0.05). Conclusion IUGR differentially affects the neurochemical profile of the P7 rat brain regions. Persistent neurochemical changes may lead to cortex-based long-term neurodevelopmental deficits in human IUGR infants.

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Section: Discussionmentioning

confidence: 99%

Differential Effects of Intrauterine Growth Restriction on the Regional Neurochemical Profile of the Developing Rat Brain

et al. 2015

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“…Two h post-birth, lambs from Arg ewes had greater concentrations of insulin, isoleucine and leucine whereas IGF-I and metabolite profiles remained unchanged. Arginine and leucine are amino acids that can promote insulin secretion (Brown et al 2011), which in turn can positively affect fetal growth (Fowden 1992). Proline also tended to be increased in lambs born to Arg ewes.…”

Section: Discussionmentioning

confidence: 99%

Parenteral administration of twin-bearing ewes with L-arginine enhances the birth weight and brown fat stores in sheep

et al. 2013

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The objective of this study was to evaluate the effects of parenteral administration of L-arginine (Arg) to well-fed twin-bearing ewes from day (d) 100 of pregnancy to birth on fetal growth, body composition and neonatal behavior. Ewes received an i.v. bolus of either 345 μmol Arg-HCl/kg bodyweight or saline solution (control) 3 times a day. At d 140 of pregnancy, Arg-supplemented and control ewes were euthanized and fetal weight and fetal organ weight recorded, and maternal and fetal plasma concentrations of amino acids, hormones and metabolites analyzed. A subset of ewes was allowed to lamb and birth weight, body dimensions and behavior of the lambs in the first 2 hours(h) following birth recorded and blood samples collected. At d 140 of pregnancy, fetal weight internal organ weights were unaffected by treatment with the exception of brown fat stores which were increased by 16% in fetuses from Arg-supplemented ewes relative to controls (P < 0.05). At birth, there was an interaction (P = 0.06) between treatment and sex for birth weight of the lamb. The ewe lambs from Arg-supplemented ewes were 12% (P < 0.05) heavier at birth compared with controls whereas birth weight of male lambs did not differ. These results indicate that maternal Arg supplementation enhanced brown fat stores in the fetus and countered some effect of fetal growth restriction due to litter size in female lambs. Increasing birth weight of female lambs and enhancing brown fat stores of all lambs may have important implications for lamb survival and postnatal growth.

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“…In the fetus, this results in a situation in which the β-cell acts as a sensor of the fetal nutrient supply from the placenta and can link this supply to appropriate production of fetal growth factors (Brown, et al 2011; Gleason, et al 2007; Newsholme et al 2014). The ability of nutrients to stimulate insulin secretion largely depends on the ability of the β-cell to utilize the nutrient as a fuel source (Malaisse, et al 1979).…”

Section: Pancreatic Developmentmentioning

confidence: 99%

The impact of IUGR on pancreatic islet development and β-cell function

Boehmer

Limesand

Rozance

2017

Journal of Endocrinology

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Placental insufficiency is a primary cause of intrauterine growth restriction (IUGR). IUGR increases the risk of developing type 2 diabetes mellitus (T2DM) throughout life, which indicates that insults from placental insufficiency impair β-cell development during the perinatal period because β-cells have a central role in the regulation of glucose tolerance. The severely IUGR fetal pancreas is characterized by smaller islets, less β-cells, and lower insulin secretion. Because of the important associations among impaired islet growth, β-cell dysfunction, impaired fetal growth, and the propensity for T2DM, significant progress has been made in understanding the pathophysiology of IUGR and programing events in the fetal endocrine pancreas. Animal models of IUGR replicate many of the observations in severe cases of human IUGR and allow us to refine our understanding of the pathophysiology of developmental and functional defects in islet from IUGR fetuses. Almost all models demonstrate a phenotype of progressive loss of β-cell mass and impaired β-cell function. This review will first provide evidence of impaired human islet development and β-cell function associated with IUGR and the impact on glucose homeostasis including the development of glucose intolerance and diabetes in adulthood. We then discuss evidence for the mechanisms regulating β-cell mass and insulin secretion in the IUGR fetus, including the role of hypoxia, catecholamines, nutrients, growth factors, and pancreatic vascularity. We focus on recent evidence from experimental interventions in established models of IUGR to understand better the pathophysiological mechanisms linking placental insufficiency with impaired islet development and β-cell function.

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Maternal amino acid supplementation for intrauterine growth restriction

Cited by 44 publications

References 183 publications

Differential Effects of Intrauterine Growth Restriction on the Regional Neurochemical Profile of the Developing Rat Brain

Differential Effects of Intrauterine Growth Restriction on the Regional Neurochemical Profile of the Developing Rat Brain

Parenteral administration of twin-bearing ewes with L-arginine enhances the birth weight and brown fat stores in sheep

The impact of IUGR on pancreatic islet development and β-cell function

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