Effects of cigarette smoking and its cessation on body weight and plasma leptin levels

Nicklas, Barbara J.; Tomoyasu, Naomi; Muir, J.; Goldberg, Andrew P.

doi:10.1016/s0026-0495(99)90183-x

Cited by 89 publications

(77 citation statements)

References 24 publications

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“…[13][14][15] We did not measure leptin in premature fore-and hindmilk because leptin levels did not differ in these. 18 Maternal factors [21][22][23][24][25][26] and neonatal factors 21,27 in part influence infant serum leptin variability. In our study sample, there was no effect of infant gender on breast milk leptin concentrations.…”

Section: Discussionmentioning

confidence: 99%

Leptin Levels in Preterm Human Breast Milk and Infant Formula

et al. 2001

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ABSTRACT. Objective. Leptin, a hormone present in breast milk, is involved in energy regulation and metabolism. The purpose of this investigation was to determine whether leptin is present in either preterm breast milk (PBM) or preterm formula (PF). The effects of delivery methods and pasteurization on leptin levels also were evaluated.Methods. PBM samples were obtained from 29 mothers who delivered infants at between 23 and 34 weeks' gestation. Leptin levels were measured in PBM and PF with the use of a radioimmunoassay specific for human and bovine leptin, respectively. Milk samples were pasteurized by fast-and slow-heating methods. PBM and PF spiked with human leptin were delivered through catheters by bolus and continuous administration to determine the effects of delivery method on recoverable leptin levels.Results. Median PBM leptin concentration was 5.28 ng/mL (intraquartile range: 24.79). Birth gestational age, birth weight, and gender of the infant did not significantly influence PBM leptin levels. Neither bolus nor continuous feeding practices affected leptin levels in PBM or spiked PF. However, pasteurization significantly reduced the amount of detectable leptin in PBM.Conclusions. PBM leptin levels were highly variable and similar to levels reported for term breast milk. There was no effect of postnatal age on PBM leptin concentrations. Sterilization decreased detectable leptin levels, whereas feeding practices had no adverse effect on the quantity of leptin delivered. Although no infant formula contained leptin, leptin could be added to formula and delivered through various feeding methods without loss. Pediatrics 2001;108(1). URL: http://www.pediatrics.org/ cgi/content/full/108/1/e15; delivery method, infant formula, leptin, pasteurization, preterm breast milk.ABBREVIATIONS. PBM, preterm breast milk; PF, preterm formula; RIA, radioimmunoassay. L eptin can no longer be viewed as solely an antiobesity hormone. Although leptin plays an important role in modulating adaptation to energy regulation and utilization in the fasting state, 1 it also affects angiogenesis, 2 wound healing, 3 hematopoiesis, 4,5 bone metabolism systems, 6 and the neuroendocrine 7 and immune systems. 8 In utero, the fetus is exposed to leptin derived primarily from the placenta 9,10 and from its own tissues. 11 Premature delivery separates the infant from its principal source of leptin before the late-gestation rise in leptin levels. 9 Premature infants have significantly lower serum leptin levels than full-term infants. 12 This has significant implications for the premature infant, who is in a catabolic state.Breast milk and formula are the only sources of nutrition and growth factors for the infant in the postnatal environment. Mammary epithelial cells produce leptin, 13 and leptin is secreted into term breast milk. [13][14][15] A previous study 15 showed that leptin can pass from mother's milk into the circulation of rat pups, suggesting that term breast milk is an exogenous source of leptin. Whether preterm breast milk (PBM) ...

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Section: Discussionmentioning

confidence: 99%

Leptin Levels in Preterm Human Breast Milk and Infant Formula

et al. 2001

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“…Several laboratories have attempted to test these hypotheses; overall, it appears that nicotineinduced changes in leptin levels-measured either as leptin mRNA in adipocytes or as plasma leptin concentration-are highly dependent on experimental protocol. Some studies indicate that chronic smokers have significantly higher serum leptin concentrations than nonsmokers, consistent with nicotine's hypophagic effects (Hodge et al, 1997;Wei et al, 1997;Eliasson and Smith, 1999;Nicklas et al, 1999). Other reports find no correlation (either positive or negative) between chronic nicotine exposure and serum leptin concentrations (Yoshinari et al, 1998;Donahue et al, 1999).…”

Section: Could the Anorectic Effects Of Nicotine Involve Regulation Omentioning

confidence: 99%

Nicotinic receptor‐mediated effects on appetite and food intake

Jo¹,

Talmage

Role³

2002

J. Neurobiol.

274

197

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ABSTRACT:It is well known, although not well understood, that smoking and eating just do not go together. Smoking is associated with decreased food intake and lower body weight. Nicotine, administered either by smoking or by smokeless routes, is considered the major appetite-suppressing component of tobacco. Perhaps the most renowned example of nicotine's influence on appetite and feeding behavior is the significant weight gain associated with smoking cessation. This article presents an overview of the literature at, or near, the interface of nicotinic receptors and appetite regulation. We first consider some of the possible sites of nicotine's action along the complex network of neural and non-neural regulators of feeding. We then present the hypothesis that the lateral hypothalamus is a particularly important locus of the anorectic effects of nicotine. Finally, we discuss the potential role of endogenous cholinergic systems in motivational feeding, focusing on cholinergic pathways in the lateral hypothalamus.

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“…13 The coordinated function of these two systems might be involved in controlling satiety and food intake. Serum leptin concentration in smokers has been described to be lower, 14,15 similar 16 or greater 17 than that found in nonsmokers.…”

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confidence: 91%

Smoking, fat mass and activation of the tumor necrosis factor-α pathway

et al. 2003

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OBJECTIVE: Obesity may be associated with increased markers of inflammation that could be triggered by metabolic, physical, infectious or environmental processes. As smoking significantly increases cytokine production, we aimed to study how smoking influences the relationship between fat mass and soluble tumor necrosis factor-a (TNF-a) receptors 1 and 2 (sTNFR1 and sTNFR2). DESIGN: Cross-sectional, clinical observational study. SUBJECTS: A total of 133 healthy men (age: 27-53 y, body mass index (BMI): 24-30.2 kg/m 2 ), 80 of whom were never-smokers and 53 smokers, matched for age, BMI and waist-to-hip ratio. MEASUREMENTS: Circulating soluble fractions of the TNF-a receptors sTNFR1 and sTNFR2 were measured to study their relationship with fat mass (bioelectric impedance). RESULTS: Smokers had significantly lower fat mass, lower fasting glucose, insulin and leptin concentrations than nonsmokers. Despite lower fat mass and insulin, smokers showed significantly increased circulating sTNFR2 levels (3.770.8 vs 3.470.7 ng/ ml, P ¼ 0.03). The slopes of the relationships between sTNFR1 and fat mass, and between sTNFR2 and fat mass, were significantly steeper in smokers than in nonsmokers. In a stepwise multiple linear regression analysis, both fat mass (Po0.00001) and smoking (P ¼ 0.025) independently contributed to 13% of sTNFR1 variance and to 4% of sTNFR2 variance (P ¼ 0.03). CONCLUSION: Both fat mass and smoking are related to increased activity of the TNF-a axis.

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Effects of cigarette smoking and its cessation on body weight and plasma leptin levels

Cited by 89 publications

References 24 publications

Leptin Levels in Preterm Human Breast Milk and Infant Formula

Leptin Levels in Preterm Human Breast Milk and Infant Formula

Nicotinic receptor‐mediated effects on appetite and food intake

Smoking, fat mass and activation of the tumor necrosis factor-α pathway

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