Effects of smoking status and smoking cessation on leptin levels

Perkins, Kenneth A.; Fonte, Carolyn

doi:10.1080/1462220021000018434

Cited by 46 publications

(61 citation statements)

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“…In addition, nicotine could induce the release of corticoids from the adrenal glands, influencing, in turn, leptinemia, in a complicated self-regulation system. (40) Another explanation for higher levels of leptin in smokers could be the decreased hypothalamic sensitivity to the hormone, as a resistance mechanism, leading to a rupture in the self-regulation system. (39) Various reports corroborate this possibility.…”

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

Tabagismo e variação ponderal: a fisiopatologia e genética podem explicar esta associação?

Chatkin

2007

J. bras. pneumol.

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Tobacco use is the leading preventable cause of death in most countries, including Brazil. Smoking cessation is an important strategy for reducing the morbidity and mortality associated with tobacco-related diseases. An inverse relationship between nicotine use and body weight has been reported, in which body weight tends to be lower among smokers than among nonsmokers. Smoking abstinence results in an increase in body weight for both males and females. On average, sustained quitters gain from 5 to 6 kg, although approximately 10% gain more than 10 kg. Pharmacological treatment for smoking cessation attenuates weight gain. The importance of smoking cessation as a contributing cause of the current obesity epidemic has been little studied. In the USA, the rate of obesity attributable to smoking cessation has been estimated at approximately 6.0 and 3.2% for males and females, respectively. Although the mechanisms are unclear, there is evidence that dopamine and serotonin are appetite suppressants. The administration of nicotine, regardless of the delivery system, acutely raises the levels of these neurotransmitters in the brain, reducing the need for energy intake and consequently suppressing appetite. In addition, nicotine has a direct effect on adipose tissue metabolism, influencing the rate of weight gain following smoking cessation. Leptin, ghrelin and neuropeptide Y are substances that might constitute factors involved in the inverse relationship between nicotine and body mass index, although their roles as determinants or consequences of this relationship have yet to be determined. Smoking and body weightThe inter-relationship between smoking and body weight has been well established in various well-designed studies, most of which were published in the 1990s. (10,11) The body mass index (BMI) of smokers is frequently present lower than that of age-and gender-matched nonsmokers. In addition, comprehensive cross-sectional epidemiological studies, some of which considered to be classical on this subject, showed a significant inverse relationship between the regular tobacco use and body weight, which tends to be lower among smokers than among nonsmokers. (12,13) Smoking cessation results in weight gain both in males and females, and over 75% of smokers gain weight when they become abstinent. (14,15) Mean weight gain attributable to smoking cessation is 2.8 and 3.8 kg in males and females, respectively. In a systematic review of the literature, it was estimated that the mean body weight gain in individuals who quit smoking can reach 5-6 kg, and 13% of ex-smokers can gain more than 10 kg. (10) Although most reports on smoking cessation have indicated mid-and long-term weight gain, other studies have shown that the most critical period is immediately after smoking cessation. (10) In one study, (16) the increase in body weight was 5.2 and 4.9 kg in females and males, respectively, during the first year after cessation, with an increase of 3.4 and 2.6 kg, respectively, in the following years. In the same stud...

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Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

Tabagismo e variação ponderal: a fisiopatologia e genética podem explicar esta associação?

Chatkin

2007

J. bras. pneumol.

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“…43,44 The finding of elevated leptin levels among chronic smokers could link hunger to addiction. 45,46 A functional neuroimaging investigation into the neuroendocrine regulation of leptin among chronic smokers would have a two-fold purpose: not only would such a study further specify the mechanisms by which leptin may mediate satiety, but the potential of leptin for mediating signaling among reward circuitry would be assessed. Research into the direct interaction of hunger and reward circuitry is essential for pinning down the transitional boundaries between biology and psychology, with investigations of this nature shedding light upon the brain modulation of reward by emotion and obesity.…”

Section: Brain Modulation Of Reward In Obese Tobacco Usersmentioning

confidence: 99%

Interaction of Satiety and Reward Response to Food Stimulation

James

Gold

Liu

2004

Journal of Addictive Diseases

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SUMMARY.Obesity is among the most pressing health issues affecting developed countries. The etiology of obesity remains unclear despite its associated health risks and problems. We propose a framework for obesity modeled upon overeating as a substance dependence disorder arising from a combination of abnormal cognitive and neuroendocrine processes. While significant work has investigated the body's regulation of satiety signals, fewer studies have focused on the mechanisms by which these two seemingly disparate (cognitive and neuroendocrine) systems interact. Although emotional states have been shown to mediate reward processing, the implications for hunger mediating reward have not previously been addressed. We review the interaction between cen-

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“…Sétimo dia de adaptação os animais nadaram 30 minutos, em água profunda. Oitavo dia os animais nadaram 40 minutos, nono dia 50 minutos e no décimo dia atingiram os 60 minutos de treinamento 8 . Ao final do período de adaptação, iniciou-se o período de treinamento, que perdurou até o final do período experimental de três meses.…”

Section: Protocolo De Treinamentounclassified

“…O uso crônico de tabaco poder aumentar a concentração sérica da leptina por dois principais mecanismos: sua maior produção e/ou a diminuição de sua depuração renal 6,8,9 . Os fumantes tendem a apresentarem menores índices de massa corporal, em comparação com indivíduos não fumantes.…”

Section: Introductionunclassified

Influência da exposição à fumaça de cigarro e do treinamento físico no apetite e desenvolvimento corporal em ratos

et al. 2016

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O fumo apresenta potencial para promover alterações no sistema hormonal, apetite e, consequentemente, na ingestão alimentar. Por sua vez, o treinamento físico amplia a demanda metabólica, exerce efeito substancial sobre o balanço energético. Objetivou-se verificar a influência do tabagismo e do treinamento físico no apetite e no desenvolvimento do peso corporal em ratos. Utilizou-se ratos Wistar (n=40, entre 200g e 250g) distribuídos em quatro grupos: Controle (C); Controle Treinado (CT); Exposto (E); Treinado/Exposto (TE). A exposição à fumaça de cigarro (EFC) e treinamento (natação) durou 15 semanas. Os animais foram pesados semanalmente e a ingestão alimentar pesada diariamente. Analisou-se com ANOVA de duas vias e adotou-se nível de significância de 5%. A ingestão nos ratos EFC foi menor, comparado com os não EFC (p=0,001). Os ratos treinados apresentaram menores valores na ingestão em relação aos não treinados (p=0,044). A interação estatística entre os fatores (fumo e natação) interferiu na ingestão (p=0,013). As curvas de crescimento apresentaram valores inferiores de peso corporal nos grupos EFC. Houve interação estatística entre os fatores fumo e natação para o peso corporal (p=0,046). Ocorreu diferença estatística com maiores valores para os pesos do coração, pulmão e tíbia nos grupos não EFC, em comparação aos ratos EFC. Conclui-se que a EFC inibe o apetite e promove prejuízo no desenvolvimento corporal. E, o treinamento físico apresenta influência no balanço energético negativo cronicamente, com diminuição no ganho de peso. Porém, não interfere no desenvolvimento corporal, sendo benéfico diferentemente da exposição à fumaça de cigarro. Palavras-chave:Fumo. Tabagismo. Ingestão alimentar. Atividade física. Apetite.The tobacco has the potential to cause changes in the hormonal system, appetite and therefore food intake. In turn, physical training increases metabolic demand, exerts a substantial effect on the energy balance. This study aimed to verify the influence of smoking and physical training in appetite and the development of body weight in rats. Rats Wistar were used (n=40, between 200g and 250g) rats were distributed into four groups: control (C); Trained control (TC); Exposure (E); Trained / exposure (TE). Exposure to cigarette smoke (ECS) and training (swimming) lasted 15 weeks. The animals were weighed weekly and food intake weighed daily. Analyzed with two-way ANOVA and was adopted a significance level of 5%. The ECS intake in rats was lower compared to the non ECS (p=0.001). The trained rats had lower values in intake compared to untrained (p=0.044). The statistical interaction between factors (smoking and swimming) interfered with the intake (p=0.013). The growth curves showed lower body weight in the groups ECS. Was no statistical interaction between smoking and factors swimming to body weight (p=0.046). Statistical difference with higher values for the weights of the heart, lung, and tibia in group no ECS, compared to rats ECS. We conclude that ECS inhibits appetite and promotes l...

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Effects of smoking status and smoking cessation on leptin levels

Cited by 46 publications

References 0 publications

Tabagismo e variação ponderal: a fisiopatologia e genética podem explicar esta associação?

Tabagismo e variação ponderal: a fisiopatologia e genética podem explicar esta associação?

Interaction of Satiety and Reward Response to Food Stimulation

Influência da exposição à fumaça de cigarro e do treinamento físico no apetite e desenvolvimento corporal em ratos

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