Short- and long-term effects of maternal nicotine exposure during lactation on body adiposity, lipid profile, and thyroid function of rat offspring

Oliveira, Elaine de; Moura, Egberto Gaspar de; Santos-Silva, Ana Paula; Fagundes, A. T. S.; Rios, André Rangel; Abreu‐Villaça, Yael; Neto, José Firmino Nogueira; Passos, M. C. F.; Lisboa, Patrícia Cristina

doi:10.1677/joe-09-0020

Cited by 80 publications

(103 citation statements)

References 87 publications

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“…This kind of dissociation between fat mass and leptinemia was already reported in other models (Toste et al 2006, Rodrigues et al 2009). Although we cannot draw a direct comparison between the models of nicotine exposure and ETS exposure, Oliveira et al (2009) observed higher adiposity and hyperleptinemia in pups from nicotine-treated dams on lactation, while in the present study, we found lower body fat in S pups, which can be associated with other cigarette components or substances conveyed through the milk, since S offspring had no direct contact with cigarette smoke.…”

Section: Discussioncontrasting

confidence: 81%

“…In the present study, S pups did not display changes of thyroid hormone levels. Previously, we demonstrated that neonate pups from-nicotine treated dams presented primary hypothyroidism (Oliveira et al 2009). It is interesting to note that in the two models, the serum levels of cotinine detected in the progeny, although low, are similar as well as the period of exposure.…”

Section: Discussionmentioning

confidence: 70%

“…In accordance with this suggestion, previous studies show that smoke exposure is associated with reduced oxygen partial pressure in dams signaling a deficient nutritional offer to the mother. Smoke in pregnancy is related to being overweight in childhood (Von Kries et al 2002, Wideroe et al 2003, and higher total body fat mass was described in suckling pups whose mothers were nicotine-treated during lactation (Oliveira et al 2009). However, in the present model, S pups showed no change in BW at weaning, despite higher body protein and lower body fat mass.…”

Section: Discussionmentioning

confidence: 99%

“…At weaning, offspring whose mothers were exposed to nicotine had type 2 diabetes (Bruin et al 2007) and increased adipose tissue weight (Soom et al 2008). When maternal nicotine exposure occurred only during lactation, the 15-day-old pups showed higher adiposity, hyperleptinemia, hypothyroidism, hypercorticosteronemia, and higher adrenal catecholamine content (Oliveira et al 2009.…”

Section: Introductionmentioning

confidence: 97%

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Effects of tobacco smoke exposure during lactation on nutritional and hormonal profiles in mothers and offspring

Santos-Silva

Oliveira²,

Pinheiro³

et al. 2011

Journal of Endocrinology

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Exposure to tobacco smoke is related to changes in energy balance regulation and several endocrine dysfunctions. Previously, we showed that maternal nicotine (the main addictive compound of tobacco) exposure exclusively during lactation affects biochemical profiles in mothers, milk, and pups. As the possible consequences for mothers and offspring of maternal smoking during lactation are still unknown, we evaluated the effects of tobacco smoke exposure on nutritional, biochemical, and hormonal parameters in dams and pups at weaning. After 72 h from birth, lactating rats were divided into two groups: smoke-exposed (S) in a cigarette-smoking machine, 4!1 h per day throughout the lactation period without pups; control (C), rats were treated the same as the experimental group but exposed to filtered air. Dams and pups were killed at weaning (21 days of lactation). Body weight and food intake were evaluated. Milk, blood, visceral fat, adrenal, and carcass were collected. S dams showed hyperprolactinemia (C50%), hypoinsulinemia (K40%), hypoleptinemia (K46%), as well as lower triglycerides (K53%) and very low-density lipoprotein cholesterol (K50%). Milk of S dams had higher lactose (C52%) and triglycerides (C78%). S pups presented higher body protein (C17%), lower total (K24%) and subcutaneous fat contents (K25%), hypoglycemia (K11%), hyperinsulinemia (C28%), hypocorticosteronemia (K40%), lower adrenal catecholamine content (K40%), hypertriglyceridemia (C34%), higher high-density lipoprotein cholesterol (C16%), and lower low-density lipoprotein cholesterol (K45%). In conclusion, tobacco smoke exposure leads to changes in nutritional, biochemical, and hormonal parameters in dams and, passively through the milk, may promote several important metabolic disorders in the progeny.

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Section: Discussioncontrasting

confidence: 81%

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Effects of tobacco smoke exposure during lactation on nutritional and hormonal profiles in mothers and offspring

Santos-Silva

Oliveira²,

Pinheiro³

et al. 2011

Journal of Endocrinology

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“…Rodent studies of tobacco smoke exposure only during lactation demonstrate increased adiposity (9). Furthermore, rodent studies of maternal nicotine, one of the many compounds found in tobacco smoke, demonstrate increased obesity in adult offspring when exposed during gestation or lactation (10)(11)(12). One potential mechanism through which MTS and maternal nicotine may program increased visceral adiposity includes alteration of glucocorticoid action on adipocytes.…”

mentioning

confidence: 99%

Maternal tobacco smoke increased visceral adiposity and serum corticosterone levels in adult male rat offspring

Zinkhan

Lang

et al. 2014

Pediatr Res

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Background: Maternal tobacco smoke (MTS) predisposes human and rat offspring to visceral obesity in early adulthood. Glucocorticoid excess also causes visceral obesity. We hypothesized that in utero MTS would increase visceral adiposity and alter the glucocorticoid pathway in young adult rats. Methods:We developed a novel model of in utero MTS exposure in pregnant rats by exposing them to cigarette smoke from E11.5 to term. Neonatal rats were cross-fostered to control dams and weaned to standard rat chow through young adulthood (postnatal day 60). results: We demonstrated increased visceral adiposity (193%)*, increased visceral adipose 11-β hydroxysteroid dehydrogenase 1 mRNA (204%)*, increased serum corticosterone (147%)*, and no change in glucocorticoid receptor protein in adult male MTS rat offspring. Female rats exposed to MTS in utero demonstrated no change in visceral or subcutaneous adiposity, decreased serum corticosterone (60%)*, and decreased adipose glucocorticoid receptor protein (66%)*. *P < 0.05. conclusion: We conclude that in utero MTS exposure increased visceral adiposity and altered in the glucocorticoid pathway in a sex-specific manner. We speculate that in utero MTS exposure programs adipose dysfunction in adult male rat offspring via alteration in the glucocorticoid pathway.M aternal tobacco smoke (MTS) impacts more than 13% of pregnancies despite aggressive antismoking campaigns (1). In adult human studies, MTS exposure in utero predisposes to the development of metabolic syndrome, including increased visceral adiposity (2). The increased adiposity seen after gestating in an adverse intrauterine environment, such as maternal tobacco or nicotine exposure, is often adipose depot specific, with the visceral adipose tissue (VAT) increasing in excess to the subcutaneous adipose tissue (SAT) (3,4).VAT seems to have a detrimental role in the development of metabolic syndrome (5,6). Even when considering dietary and lifestyle choices, MTS exposure in utero independently increases the risk of developing visceral obesity (7,8). Children whose mothers smoked during pregnancy had decreased birth weights yet an increased obesity and BMI index as early as 9-10 y of age, independent of dietary intake and activity levels (8). Furthermore, the effect of MTS on body weight was stronger when mothers smoked during pregnancy compared with that of isolated smoke exposure in childhood (7). Taken together, these findings suggest that MTS exposure during this developmentally sensitive time period both causes intrauterine growth restriction (IUGR) and adversely programs obesity later in life.Little insight exists on how MTS programs increased visceral adiposity. Rodent studies examining the effect of in utero MTS exposure on the offspring have not examined the etiology of increased visceral adiposity. Rodent studies of tobacco smoke exposure only during lactation demonstrate increased adiposity (9). Furthermore, rodent studies of maternal nicotine, one of the many compounds found in tobacco smoke, demonstrate increa...

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Central dopaminergic circuitry controlling food intake and reward: implications for the regulation of obesity

Vucetic

Reyes

2010

WIREs Mechanisms of Disease

122

108

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Prevalence of obesity in the general population has increased in the past 15 years from 15% to 35%. With increasing obesity, the coincident medical and social consequences are becoming more alarming. Control over food intake is crucial for the maintenance of body weight and represents an important target for the treatment of obesity. Central nervous system mechanisms responsible for control of food intake have evolved to sense the nutrient and energy levels in the organism and to coordinate appropriate responses to adjust energy intake and expenditure. This homeostatic system is crucial for maintenance of stable body weight over long periods of time of uneven energy availability. However, not only the caloric and nutritional value of food but also hedonic and emotional aspects of feeding affect food intake. In modern society, the increased availability of highly palatable and rewarding (fat, sweet) food can significantly affect homeostatic balance, resulting in dysregulated food intake. This review will focus on the role of hypothalamic and mesolimbic/mesocortical dopaminergic (DA) circuitry in coding homeostatic and hedonic signals for the regulation of food intake and maintenance of caloric balance. The interaction of dopamine with peripheral and central indices of nutritional status (e.g., leptin, ghrelin, neuropeptide Y), and the susceptibility of the dopamine system to prenatal insults will be discussed. Additionally, the importance of alterations in dopamine signaling that occur coincidently with obesity will be addressed.

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Short- and long-term effects of maternal nicotine exposure during lactation on body adiposity, lipid profile, and thyroid function of rat offspring

Cited by 80 publications

References 87 publications

Effects of tobacco smoke exposure during lactation on nutritional and hormonal profiles in mothers and offspring

Effects of tobacco smoke exposure during lactation on nutritional and hormonal profiles in mothers and offspring

Maternal tobacco smoke increased visceral adiposity and serum corticosterone levels in adult male rat offspring

Central dopaminergic circuitry controlling food intake and reward: implications for the regulation of obesity

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