Smoking related to plasma leptin concentration in pregnant women and their newborn infants

Helland, IB; Reseland, JE; Od, Saugstad; Drevon, C. A.

doi:10.1111/j.1651-2227.2001.tb00305.x

Cited by 25 publications

(6 citation statements)

References 27 publications

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“…Maternal smoking throughout pregnancy may be associated with lower cord blood leptin 77,78 though other studies have not suggested an association. 79,80 Investigations of other possible mediators, including growth hormone and IGF-1, have not been as well studied, 80 and no data exist regarding levels of any of these hormones beyond the newborn period.…”

Section: Discussionmentioning

confidence: 99%

Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis

2007

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Objective: Perform a systematic review of studies reporting on the association between maternal prenatal cigarette smoking and child overweight. Design: Meta-analysis of observational studies. Data sources: Medline search and review of reference lists among studies published through June 2006. Review methods: Included studies reported an association between maternal smoking during pregnancy and risk of overweight among children at least 2 years of age. We did not include in the meta-analysis studies that provided only a continuous measure of adiposity, although those studies are discussed separately. Results: Based on results of 84 563 children reported in 14 observational studies, children whose mothers smoked during pregnancy were at elevated risk for overweight (pooled adjusted odds ratio (OR) 1.50, 95% CI: 1.36, 1.65) at ages 3-33 years, compared with children whose mothers did not smoke during pregnancy. The pooled estimate from unadjusted odds ratios (OR 1.52, 95% CI: 1.36, 1.69) was similar to the adjusted estimate, suggesting that sociodemographic and behavioral differences between smokers and nonsmokers did not explain the observed association. Although we observed evidence for publication bias, simulating a symmetric set of studies yielded a similar estimate (OR 1.40, 95% CI: 1.26, 1.55). Conclusions:Prenatal smoking exposure appears to increase rates of overweight in childhood. In parts of the world undergoing the epidemiologic transition, the continuing increase in smoking among young women could contribute to spiraling increases in rates of obesity-related health outcomes in the 21st century.

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Section: Discussionmentioning

confidence: 99%

Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis

2007

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“…In addition, tobacco smoke constituents may act on various hormonal systems that change metabolic programming 40,41 . There has also been some suggestion that prenatal tobacco smoke exposure may alter infant appetite and leptin concentrations 42–44 …”

Section: Discussionmentioning

confidence: 99%

Prenatal environmental tobacco smoke exposure and early childhood body mass index

Braun

Daniels

Poole

et al. 2010

Paediatric and Perinatal Epidemiology

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Summary Maternal smoking during pregnancy is associated with increased risk of childhood overweight body mass index (BMI). Less is known about the association between prenatal secondhand tobacco smoke (SHS) exposure and childhood BMI. We followed 292 mother-child dyads from early pregnancy to 3 years of age. Prenatal tobacco smoke exposure during pregnancy was quantified using self-report and serum cotinine biomarkers. We used linear mixed models to estimate the association between tobacco smoke exposure and BMI at birth, 4 weeks, and 1, 2, and 3 years. During pregnancy, 15% of women reported SHS exposure and 12% reported active smoking, but 51% of women had cotinine levels consistent with SHS exposure and 10% had cotinine concentrations indicative of active smoking. After adjustment for confounders, children born to active smokers had higher BMI at 2 and 3 years of age (self-report or serum cotinine), compared to unexposed children. Children born to women with prenatal serum cotinine concentrations indicative of SHS exposure had higher BMI at 2 (Mean Difference [MD]:0.3; 95% confidence interval [CI]:−0.1, 0.7) and 3 (MD:0.4; [0, 0.8]) years compared to unexposed children. Using self-reported prenatal exposure resulted in non-differential exposure misclassification of SHS exposures that attenuated the association between SHS exposure and BMI compared to serum cotinine concentrations. These findings suggest active and secondhand prenatal tobacco smoke exposure may be related to an important public health problem in childhood and later life. In addition, accurate quantification of prenatal secondhand tobacco smoke exposures is essential to obtaining valid estimates.

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“…Although inconsistent, there are some reports that smokers have increased blood leptin levels (Eliasson and Smith, 1999;Nicklas et al, 1999) and that chronic nicotine results in higher leptin serum concentrations in adult and prenatal animal models (Arai et al, 2001;Grove et al, 2001), which could be a mechanism for nicotine's anorexic effects. However, others have found no correlation between nicotine consumption, blood leptin levels, and decreased body weight in adult models or in mothers who smoked, questioning the significance of leptin in explaining nicotine's anorexic actions (Helland et al, 2001;Sanigorski et al, 2002).…”

Section: Leptin Does Not Regulate Body Weight In Neonatesmentioning

confidence: 97%

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Huang

Winzer‐Serhan

2007

Developmental Neurobiology

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Maternal smoking results in low birth weight. Using a neonatal gastric intubation model corresponding to the third trimester in humans, nicotine, the major psychoactive ingredient in tobacco, causes growth retardation in rat pups. Here, we wanted to determine the underlying mechanisms of nicotine's anorexic effects. In adults, body weight and energy expenditure are regulated by the adiposity hormone leptin and the orexigenic peptides neuropeptide Y (NPY) and agouti-related peptide (AgRP) and anorexic peptides proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) expressed in the hypothalamic arcuate (Arc) nucleus. Activation of nicotinic acetylcholine receptors (nAChRs) could regulate leptin release and/or peptide expression in the Arc. Neonatal rat pups were treated twice daily with nicotine (0.25, 1.5, and 3 mg/kg) from postnatal day 1 to 8 (P1-8). This resulted in an upregulation of heteromeric nAChR binding sites in the ventromedial nucleus of the hypothalamus and Arc. Nicotine at all three doses significantly reduced body weight gain and increased mRNA expression of NPY, AgRP, and POMC effects, which were blocked by dihydro-beta-erythroidine (DHbetaE), an alpha4beta2* nAChR antagonist, but CART expression was unaffected. In contrast, serum leptin levels were significantly increased only by 3 and 1.5 mg/kg, and the increase was only partially blocked by DHbetaE. These data suggest that in neonates chronic nicotine regulates body weight gain independent from serum leptin levels by a central mechanism involving alpha4beta2* heteromeric nAChRs and stimulated increased expression of the anorexic peptide POMC. Whereas, increased NPY and AgRP expression could be a secondary response to reduction in weight gain.

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Smoking related to plasma leptin concentration in pregnant women and their newborn infants

Cited by 25 publications

References 27 publications

Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis

Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis

Prenatal environmental tobacco smoke exposure and early childhood body mass index

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

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