title: Patterns of growth deficiency in rats exposed in utero to undernutrition, ethanol, or the neuroteratogen methylazoxymethanol (MAM).
abstract: Children and experimental animals exposed to ethanol (EtOH) in utero commonly have low birthweights, and many remain small at maturity. Low body weight or small stature in adulthood may reflect an inability to recover from in utero growth retardation, or it may reflect a separate, postnatal growth deficiency. In this study, daily body weights (postnatal days 1 to 60) were compared among the offspring of the following groups of Long Evans rats: dams fed liquid diet containing 35% EtOH-derived calories; their pair-fed and chow-fed controls; and dams exposed to methylazoxymethanol (MAM) in two previous studies, in which offspring exhibited reduced numbers of growth hormone releasing factor (GRF) neurons. All treatments produced a number of offspring with weight deficits beginning after birth and persisting into maturity. Three distinct patterns of growth deficiency were observed: (1) weight loss relative to controls in the first weeks of life, seen in offspring exposed to EtOH, pair feeding, or MAM on gestation day 13 (G13); (2) a delay in the onset of the prepubertal growth spurt, seen in all EtOH-exposed offspring and in G13 MAM-exposed dwarfs; and (3) failure to sustain the prepubertal growth spurt, seen only after exposure to MAM on G14. The results of this study support the view that prenatal EtOH exposure is capable of affecting postnatal growth specifically; moreover, the pattern of growth deficiency seen in EtOH-exposed offspring was distinct from that of the undernourished offspring of pair-fed dams.
authors.affiliation: Department of Obstetrics and Gynecology, University of Rochester, New York 14642.
authors.forename: C E
authors.initials: CE
authors.lastname: Gavin
authors.forename: B
authors.initials: B
authors.lastname: Kates
authors.forename: L A
authors.initials: LA
authors.lastname: Gerken
authors.forename: P M
authors.initials: PM
authors.lastname: Rodier
mesh_terms: D000367:Age Factors; D000818:Animals; D001724:Birth Weight; D001921:Brain / Q000473:pathology; D004249:DNA Damage; D004392:Dwarfism / Q000139:chemically induced / Q000503:physiopathology; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology; D006130:Growth Disorders / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000196:embryology / Q000503:physiopathology; D008297:Male; D008746:Methylazoxymethanol Acetate / Q000031:analogs & derivatives* / Q000633:toxicity; D009419:Nerve Tissue Proteins / Q000032:analysis; D009474:Neurons / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D009748:Nutrition Disorders / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D018019:Receptors, Corticotropin-Releasing Hormone / Q000032:analysis; D012741:Sexual Maturation; D013004:Somatostatin / Q000032:analysis; D015431:Weight Loss
chemical_list: D009419:Nerve Tissue Proteins; D018019:Receptors, Corticotropin-Releasing Hormone; D000431:Ethanol; D013004:Somatostatin; D008746:Methylazoxymethanol Acetate; C030667:methylazoxymethanol