Intrauterine growth retardation induced by thiamine deficiency and pyrithiamine during pregnancy in the rat

Roecklein, Bryan A.; Levin, Sondra W.; Comly, Marcella E.; Mukherjee, Anil B.

doi:10.1016/0002-9378(85)90269-8

Cited by 30 publications

(29 citation statements)

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“…Therefore, the thiamine antagonist pyrithiamine, which alone has been shown not to affect pregnancy outcome , has previously been used in conjunction with dietary thiamine deprivation for investigation of the mechanisms by which nutritional factors may contribute to the intrauterine growth retardation characteristic of FAS Roecklein et al 1985). In the present study, this animal model was used to explore the possible role of thiamine deficiency in more subtle fetal alcohol effects.…”

Section: Discussionmentioning

confidence: 96%

“…It is believed that thiamine deficiency alters intermediary metabolism and thereby contributes to the toxicity of ethanol in various organ systems (Martin et al 1986). For example, thiamine deficiency has been implicated as a possible contributing factor in intrauterine growth retardation, a prominent characteristic of FAS in which neural development is compromised Roecklein et al 1985). Thiamine insufficiency during gestation may have significant fetal CNS effects because the midline periventricular structures of the brainstem and diencephalon are among the most vulnerable to the pathologic effects of this avitaminosis in the adult (Victor et al 1971 ;Hakim and Pappius 1983).…”

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confidence: 98%

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Thiamine deficiency in utero alters response to ethanol in adulthood

et al. 1989

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To determine whether prenatal thiamine deficiency, a frequent concomitant of alcoholism, reduces the response to ethanol during adulthood in the rat as does ethanol exposure in utero (Abel et al. 1981), pregnant Sprague-Dawley rats received either control or thiamine deficient diets together with daily injections of the thiamine antagonist pyrithiamine. At 7 months of age, male offspring were exposed to precisely regulated ethanol vapor concentrations in an inhalation chamber for 24 h and blood ethanol concentrations (BECs) and ethanol-induced intoxication were determined. Prenatally thiamine deficient rats and controls were indistinguishable in terms of appearance, body and liver weights, and the ratios of liver to body weight and brain to liver weight. However, total body water was significantly greater, and BECs and behavioral impairment were decreased, in the experimental rats. These findings indicate that prenatal thiamine deprivation is associated with reduced pharmacologic effect of ethanol as a result of increases in its volume of distribution and rate of metabolism.

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Section: Discussionmentioning

confidence: 96%

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confidence: 98%

Thiamine deficiency in utero alters response to ethanol in adulthood

et al. 1989

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“…In Group 2, the experimental dams began to lose weight during the gestational period within 8-10 days on deficient diet (Fig. 2) as would be expected for animals which were being made thiamine-deficient [13]. On Day 15 of biotinthiamine-deficient diet experimental dams were reconstituted with thiamine, and a subsequent weight gain ensued within 24 h.…”

Section: Maternal Parametersmentioning

confidence: 97%

“…Previous work from our laboratory has implicated thiamine deficiency as one possible cause of this growth retardation [13]. It is well known that chronic alcohol consumption can deplete the body of water-soluble vitamins, such as thiamine.…”

Section: Introductionmentioning

confidence: 98%

Intrauterine growth retardation caused by dietary biotin and thiamine deficiency in the rat

1985

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The effects on fetal development of maternal biotin deficiency, alone and in conjunction with thiamine deficiency, were investigated in rats. Fetuses from dams given biotin-deficient diet throughout gestation demonstrated only some characteristics of intrauterine growth retardation (IUGR) including abnormal liver weight and a higher brain/liver ratio. However, fetuses from dams given biotin-thiamine-deficient diet and daily pyrithiamine (a thiamine antagonist used to insure thiamine deficiency) injections demonstrated severe IUGR along all of the fetal parameters investigated. We conclude that biotin and thiamine deficiency during intrauterine growth of the fetus may be partially responsible for the development of IUGR, a frequent concomitant of fetal alcohol syndrome.

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“…Vitamin B1 is an essential vitamin for vertebrates. Our reasons for testing TPK1 as a candidate gene for birth weight control was: i) TPK1 harbours a number of common variants in Caucasians; ii) TPK1 is implicated in thiamine metabolism, and maternal thiamine deficiency causes intra-uterine growth retardation in rats (Butterworth, 1993b;Roecklein et al 1985), and children born to mothers suffering from hyperemesis gravidarum, a disease often accompanied by thiamine deficiency, are known to have a decreased birth weight (Dornhorst & Girling, 1995;Langer et al 1989).…”

Section: Introductionmentioning

confidence: 99%

Three Common Intronic Variants in the Maternal and Fetal Thiamine Pyrophosphokinase Gene (TPK1) are Associated with Birth Weight

Fradin

Bougnères

2007

Annals of Human Genetics

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SummaryExtreme variations in birth weight increase immediate postnatal mortality and morbidity, and are also associated with the predisposition to metabolic diseases in late adulthood. Birth weight in humans is influenced by yet unknown genetic factors. Since the 7q34-q35 region showed linkage with birth weight in a recent human genome scan (p = 8.10− 5 ), this study investigated the TPK1 (thiamine pyrophosphokinase) gene locus, located in 7q34-36. Having found no coding variants in the TPK1 gene, we genotyped 43 non coding SNPs spanning a region of 420kb, and used the QTDT method to test their association with birth weight in 964 individuals from 220 families of European ancestry. Family-based tests detected association of 8 SNPs with birth weight (p<0.008), but after correction for multiple tests only rs228581 C/T (p = 0.03), rs228582 A/G (p = 0.04) and rs228584 C/T (p = 0.03) were still associated with birth weight, as well as their T-A-T haplotype (p = 0.03). In addition, we found an association between maternal rs228584 genotype and offspring birth weight (p = 0.027).These observations suggest that genomic variations in the fetal and maternal TPK1 gene could contribute to the variability of birth weight in normal humans.

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Intrauterine growth retardation induced by thiamine deficiency and pyrithiamine during pregnancy in the rat

Cited by 30 publications

References 9 publications

Thiamine deficiency in utero alters response to ethanol in adulthood

Thiamine deficiency in utero alters response to ethanol in adulthood

Intrauterine growth retardation caused by dietary biotin and thiamine deficiency in the rat

Three Common Intronic Variants in the Maternal and Fetal Thiamine Pyrophosphokinase Gene (TPK1) are Associated with Birth Weight

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