Fetal and neonatal exposure to nicotine leads to augmented hepatic and circulating triglycerides in adult male offspring due to increased expression of fatty acid synthase

Ma, Noelle; Nicholson, Catherine J.; Wong, Michael K.; Holloway, Alison C.; Hardy, Daniel B.

doi:10.1016/j.taap.2013.12.010

Cited by 38 publications

(41 citation statements)

References 89 publications

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“…Animal studies have shown that fetal and neonatal exposure to nicotine alone may result in postnatal metabolic alterations [18]. These results suggest that nicotine is the single most important component of cigarette smoke that causes adverse health outcomes in offspring.…”

Section: Discussionmentioning

confidence: 99%

“…According to the specifications of the manufacturer, the delivery periods for the minipumps were 14 (2ML2) and 28 (2ML4) days; therefore, the nicotine delivery continued at birth (2Nicotine) and after birth until postnatal day 14 (4Nicotine), respectively. Because nicotine easily crosses the placenta, entering the fetal blood, and is distributed in breast milk, it was expected that the fetal and neonatal rats would receive nicotine via the placenta and breast milk of the mother [18,19]. Dams were housed in individual cages equipped with access to laboratory food and water ad libitum, kept on a 12-hour light-dark cycle, and allowed to deliver vaginally at term.…”

Section: Methodsmentioning

confidence: 99%

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Maternal Nicotine Exposure Induces Epithelial-Mesenchymal Transition in Rat Offspring Lungs

Chen

Chou²,

Huang

2015

Neonatology

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Background: Maternal nicotine exposure induces lung injuries and fibrosis in rat offspring. Epithelial-mesenchymal transition (EMT) following lung injury is a process in which epithelial cells mediate tissue repair. Objective: To determine the effects of maternal nicotine exposure on EMT in neonatal rat lungs. Methods: Nicotine was administered to pregnant Sprague-Dawley rats using a subcutaneous osmotic minipump that delivered a dose of 6 mg/kg/day on gestational days 7-21 or from gestational day 7 to postnatal day 14. A control group received an equal volume of saline. Results: The percentage of 8-hydroxy-2'-deoxyguanosine-positive cells in nuclear staining was significantly higher, the E-cadherin protein expression was significantly lower, and the N-cadherin protein expression was significantly higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal day 7. These characteristics of EMT were associated with a significant increase in α-smooth muscle actin (SMA) expression on postnatal day 21. Rats born to prenatal and postnatal nicotine-treated dams showed significantly higher α-SMA expression and total collagen than those born to prenatal saline- and nicotine-treated dams on postnatal day 21. The number of cells expressing fibroblast-specific protein 1 and vimentin was higher in rats born to prenatal and postnatal nicotine-treated dams than in those born to prenatal saline- and nicotine-treated dams on postnatal days 7 and 21. Conclusions: Maternal nicotine exposure during gestation and lactation induces EMT and contributes to lung fibrosis in rat offspring.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Maternal Nicotine Exposure Induces Epithelial-Mesenchymal Transition in Rat Offspring Lungs

Chen

Chou²,

Huang

2015

Neonatology

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“…Cigarette smoke contains over 4,000 chemicals, including arsenic, hydrogen cyanide, lead, nicotine, and tar that may be toxic to the fetus (21). However, data from animal studies suggest that fetal and neonatal exposure to nicotine alone may result in postnatal metabolic alterations associated with obesity, type 2 diabetes, hypertension, and hypertriglyceridemia (22). These results suggest that nicotine is the single most important component of cigarette smoke that causes adverse health outcomes in the offspring.…”

Section: Discussionmentioning

confidence: 99%

Maternal nicotine exposure during gestation and lactation induces kidney injury and fibrosis in rat offspring

2014

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“…Our findings are consistent with this evidence, showing short-term oral administration of these substances to significantly increase levels of TG, with fat producing the strongest effect. While circulating TG from Intralipid invariably come from the lipid emulsion itself (Chen, 1984), those from ethanol and nicotine are increased due to de novo synthesis in the liver (Tsukamoto et al, 1984; Ma et al, 2014) or a reduction of basal lipolysis (Ashakumary and Vijayammal, 1997; Szkudelski et al, 2004). There is evidence that lipids can contribute to the stimulation of ENK gene expression, as indicated in studies showing ENK mRNA in the PVN to be increased by acute injection of Intralipid or by the fatty acid linoleic acid and also by the consumption of a fat-rich meal (Oomura et al, 1975; Chang et al, 2004; Chang et al, 2007).…”

Section: 4 Discussionmentioning

confidence: 99%

Common effects of fat, ethanol, and nicotine on enkephalin in discrete areas of the brain

et al. 2014

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Fat, ethanol, and nicotine share a number of properties, including their ability to reinforce behavior and produce overconsumption. To test whether these substances act similarly on the same neuronal populations in specific brain areas mediating these behaviors, we administered the substances short-term, using the same methods and within the same experiment, and measured their effects, in areas of the hypothalamus (HYPO), amygdala (AMYG), and nucleus accumbens (NAc), on mRNA levels of the opioid peptide, enkephalin (ENK), using in situ hybridization and on c-Fos immunoreactivity (ir) to indicate neuronal activity, using immunofluorescence histochemistry. In addition, we examined for comparison another reinforcing substance, sucrose, and also took measurements of stress-related behaviors and circulating corticosterone (CORT) and triglycerides (TG), to determine if they contribute to these substances’ behavioral and physiological effects. Adult Sprague-Dawley rats were gavaged three times daily over five days with 3.5 ml of water, Intralipid (20% v/v), ethanol (12% v/v), nicotine (0.01% w/v) or sucrose (22% w/v) (approximately 7 kcal/dose), and tail vein blood was collected for measurements of circulating CORT and TG. On day five, animals were sacrificed, brains removed, and the HYPO, AMYG, and NAc processed for single- or double-labeling of ENK mRNA and c-Fos-ir. Fat, ethanol, and nicotine, but not sucrose, increased the single- and double-labeling of ENK and c-Fos-ir in precisely the same brain areas, the middle parvocellular but not lateral area of the paraventricular nucleus, central but not basolateral nucleus of the AMYG, and core but not shell of the NAc. While having little effect on stress-related behaviors or CORT levels, fat, ethanol, and nicotine all increased circulating levels of TG. These findings suggest that the overconsumption of these three substances and their potential for abuse are mediated by the same populations of ENK-expressing neurons in specific nuclei of the hypothalamus and limbic system.

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Fetal and neonatal exposure to nicotine leads to augmented hepatic and circulating triglycerides in adult male offspring due to increased expression of fatty acid synthase

Cited by 38 publications

References 89 publications

Maternal Nicotine Exposure Induces Epithelial-Mesenchymal Transition in Rat Offspring Lungs

Maternal Nicotine Exposure Induces Epithelial-Mesenchymal Transition in Rat Offspring Lungs

Maternal nicotine exposure during gestation and lactation induces kidney injury and fibrosis in rat offspring

Common effects of fat, ethanol, and nicotine on enkephalin in discrete areas of the brain

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