Maternal nutrient restriction in early pregnancy programs hepatic mRNA expression of growth-related genes and liver size in adult male sheep.
Melanie A. Hyatt,G. S. Gopalakrishnan,J. Bispham,Sheridan Gentili,Isabella Caroline McMillen,Stewart M. Rhind,M. T. Rae,Carol Kyle,A. N. Brooks,C Jones,Helen Budge,David Walker,Terence Stephenson,Michael E. Symonds +13 more
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Maternal nutrient restriction in early gestation results in adult offspring with smaller livers, which may be mediated by alterations in both hepatic mitogenic and apoptotic factors.Abstract:
The liver is a major metabolic and endocrine organ of critical importance in the regulation of growth and metabolism. Its function is determined by a complex interaction of nutritionally regulated counter-regulatory hormones. The extent to which hepatic endocrine sensitivity can be programed in utero and whether the resultant adaptations persist into adulthood is unknown and was therefore the subject of this study. Young adult male sheep born to mothers that were fed either a control diet (i.e.100% of total live weight-maintenance requirements) throughout gestation or 50% of that intake (i.e. nutrient restricted (NR)) from 0 to 95 days gestation and thereafter 100% of requirements (taking into account increasing fetal mass) were entered into the study. All mothers gave birth normally at term, the singleton offspring were weaned at 16 weeks, and then reared at pasture until 3 years of age when their livers were sampled. NR offspring were of similar birth and body weights at 3 years of age when they had disproportionately smaller livers than controls. The abundance of mRNA for GH, prolactin, and IGF-II receptors, plus hepatocyte growth factor and suppressor of cytokine signaling-3 were all lower in livers of NR offspring. In contrast, the abundance of the mitochondrial protein voltage-dependent anion channel and the pro-apoptotic factor Bax were up regulated relative to controls. In conclusion, maternal nutrient restriction in early gestation results in adult offspring with smaller livers. This may be mediated by alterations in both hepatic mitogenic and apoptotic factors.read more
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Adverse effects of nutritional programming during prenatal and early postnatal life, some aspects of regulation and potential prevention and treatments.
TL;DR: Early infancy may provide an opportunity for intervention aimed at reducing later disease risk and the development of new, rational, and effective preventive and/ or therapeutic options before and/or after birth are suggested.
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A review of fundamental principles for animal models of DOHaD research: An Australian perspective
Hayley Dickinson,Timothy J. M. Moss,Kathryn L. Gatford,Karen M. Moritz,Lisa K. Akison,Tod Fullston,Deanne H. Hryciw,Christopher A. Maloney,Margaret J. Morris,Amy L. Wooldridge,John E. Schjenken,Sarah A. Robertson,Brendan J. Waddell,Peter J. Mark,Caitlin S. Wyrwoll,Stacey J. Ellery,Kent L. Thornburg,Beverly S. Muhlhausler,Janna L. Morrison +18 more
TL;DR: This review summarizes the contributions of animal research to the understanding of DOHaD, and makes recommendations for the design and conduct of animal experiments to maximize relevance, reproducibility and translation of knowledge into improving health and well-being.
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Maternal undernutrition and the ovine acute phase response to vaccination
Peter David Eckersall,Fraser P Lawson,Carol Kyle,Mary Waterston,Laura Bence,Michael J. Stear,Stewart M. Rhind +6 more
TL;DR: Decreased SAA concentrations, post-vaccination, in lambs born to ewes on the HL diet shows that maternal undernutrition prior to parturition affects the innate immune system of the offspring.
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Nutrient intake in the bovine during early and mid-gestation causes sex-specific changes in progeny plasma IGF-I, liveweight, height and carcass traits
TL;DR: Heifer nutrient intake during the first and second trimesters causes persistent and sex-specific programming of progeny plasma IGF-I, postnatal liveweight and carcass weight.
Journal ArticleDOI
Hypertension and impaired renal function accompany juvenile obesity: the effect of prenatal diet.
P.J. Williams,Lesia O. Kurlak,Alan C. Perkins,Helen Budge,T Stephenson,Duane H. Keisler,Michael E. Symonds,David S. Gardner +7 more
TL;DR: In this paper, the effects of prenatal nutrient restriction and juvenile obesity in sheep were examined and it was found that juvenile obesity led to chronic hyperleptinemia and reduced renal function as assessed by nuclear scintigraphy.
References
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Maternal Undernutrition from Early- to Mid-Gestation Leads to Growth Retardation, Cardiac Ventricular Hypertrophy, and Increased Liver Weight in the Fetal Sheep
Kimberly A. Vonnahme,Bret W. Hess,Thomas R. Hansen,Richard J. McCormick,Daniel C. Rule,Gary E. Moss,William J. Murdoch,Mark J. Nijland,Donal C. Skinner,Peter W. Nathanielsz,Stephen P. Ford +10 more
TL;DR: Altered alterations in fetal/placental development may be beneficial to early fetal survival in the face of a nutrient restriction, but their effects later in gestation as well as in postnatal life need further investigation.
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In vivo response of hepatocytes to growth factors requires an initial priming stimulus
TL;DR: The results suggest that a small functional deficit in the liver that by itself causes little DNA synthesis “primes” hepatocytes for replication and that the loss of liver mass and growth factor infusions complement each other by providing essential stimuli needed for DNA synthesis.
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Adult glucose and lipid metabolism may be programmed during fetal life
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Liver regeneration in recipients and donors after transplantation
Seiji Kawasaki,Masatoshi Makuuchi,Shinpachi Ishizone,Hidetoshi Matsunami,Masaru Terada,Hideo Kawarazaki +5 more
TL;DR: In each recipient, the size of the transplanted liver tended to converge to the standard liverVolume with time, regardless of whether initial liver-graft volume was smaller or larger than standard liver volume, suggesting that regeneration is regulated mainly by factors other than the hepatocytes themselves.
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Ethanol feeding of micropigs alters methionine metabolism and increases hepatocellular apoptosis and proliferation.
Charles H. Halsted,Jesus A. Villanueva,Carol J. Chandler,Sally P. Stabler,R. H. Allen,Levan Muskhelishvili,S. J. James,L. Poirier +7 more
TL;DR: It is suggested that chronic ethanol feeding perturbs methamphetamineionine metabolism by impairment of methionine synthase activity, resulting in deoxynucleoside triphosphate (dNTP) imbalance, increased apoptosis, and regenerative proliferation, which may provide a promoting environment for carcinogenesis during long‐term ethanol exposure.