Low Intestinal Lactase Activity in Offspring from Ethanol-Treated Mothers

Abstract

Some aspects of small intestine maturation have been studied in the newborns from chronic ethanol-treated pregnant rats (25% ethanol in drinking fluid) immediately after birth (before suckling) and after 30 days of life. Litters delivered by mothers fed ad libitum with a standard diet diluted 50% with cellulose were used as a nutritional control. At birth, pups from ethanol-treated mothers showed significant decreases in total intestinal length and thickness, low total lactase activity and low somatostatin intestinal content. The intestinal alterations of these neonatal parameters are not present in newborns from mothers on fiber-diluted diet. From delivery, pups from different experimental groups were nursed by normal lactating dams. At 30 days of age neither of those parameters differed among the groups. We propose that the low levels of total lactase activity in newborns from alcoholic mothers, that are a consequence of a lower intestinal mucosa content, are a direct effect of ethanol in utero on the fetal gastrointestinal system.

Effect of Prenatal Exposure to Ethanol on Intestinal Development of Rat Fetuses

“…It is notable that prenatal malnutrition has been associated with lower total DNA content than in normal pups (31), due to differences in the intestine of cell proliferation rather than increased cell loss. Our model of malnutrition did not develop those changes in the total DNA or in the total protein content of the fetal intestine, reflecting mild malnutrition during gestation, which is not important for fetal development of the intestine, as we have shown at birth (6).…”

“…This effect could be due, on one hand, to a delay in general maturation, as we have also described for other organs such as the brain (4), or, on the other hand, to a specific alteration of the intestinal mucosal surface caused by ethanol (6), although further structural studies are required (in progress). This could be responsible for altered intestinal somatostatin levels found in the offspring of alcohol‐treated mothers (6). Altered growth hormone secretion and a possible postnatal peripheral resistance to growth‐stimulating hormones (somatomedin, insulin) have been described as resulting from the effects of maternal chronic alcoholism on fetal metabolism (22).…”

“…Moreover, lower brush‐border protein content in fetuses from alcohol‐treated mothers compared to those from control and fiber‐treated mothers (nutritional controls) is especially noticeable on days 20 and 21 of gestation, when intestinal brush‐border development is at its maximum (21). This effect could be due, on one hand, to a delay in general maturation, as we have also described for other organs such as the brain (4), or, on the other hand, to a specific alteration of the intestinal mucosal surface caused by ethanol (6), although further structural studies are required (in progress). This could be responsible for altered intestinal somatostatin levels found in the offspring of alcohol‐treated mothers (6).…”

“…Indeed, in adults ethanol ingestion reduces epithelial cell number and the length of both microvilli and villi, resulting in a lower surface area for absorption (25). Previous observations (6) have shown high neonatal mortality in the offspring of alcohol‐treated mothers and a delay in total lactase activity in the whole intestine. Moreover, the present study shows that lactase‐specific activity, expressed per brush‐border protein content, is indeed lower in fetuses from alcohol‐treated mothers throughout the gestational period studied at onset of this enzyme.…”

“…Previous studies have described some morphological and biochemical alterations in the brain, liver, and small intestine in the offspring of ethanol‐treated pregnant rats (3‐5). In our own studies we mainly emphasized a high neonatal mortality, which takes place immediately after the first suckling, and an impaired postnatal development, which would seem to be related to low intestinal lactase activity and to a general immaturity of small intestine at birth (6).…”