Leptin and smoking cessation: secondary analyses of a randomized controlled trial assessing physical activity as an aid for smoking cessation

Gonseth, Semira; Locatelli, Isabella; Bize, Raphaël; Nusslé, Sébastien; Clair, Carole; Pralong, François P.; Cornuz, Jacques

doi:10.1186/1471-2458-14-911

Cited by 18 publications

(11 citation statements)

References 51 publications

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“…The reduction in body weight is supported by previous studies that reported lower body weight among smokers compared to non-smokers and weight gain in most subjects who quit smoking [22] [23] [24]. Gonseth and his colleagues suggested a hormonal mechanism related to disturbed dynamics of leptin secretion after smoking cessation [25]. We found that co-exposure to nicotine and vitamin C failed to correct the nicotine-induced decrease in total body weight.…”

Section: Discussionsupporting

confidence: 73%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

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Abstract:Objective: Vitamin Methods: Animals were divided into four groups; (C) saline-treated, (VC) vitamin C-treated, (NIC) nicotinetreated, all were for 3 weeks, and (NIC+VC) is given vitamin C for 3 days prior, with nicotine injection and 2 days thereafter. Results: Present work showed that nicotine exposure caused significant reduction in total body weight, relative liver and kidney weights, elevated malondialdehyde (MDA), alanine transaminase (ALT), aspirate transaminase (AST), and alkaline phosphatase (ALP) in both hepatic and renal tissues. Co-exposure to nicotine and vitamin C maintained normal liver and kidney weight, significantly lowered MDA, ALT, AST, ALP and elevated glutathione in both hepatic and renal tissues compared NIC group as well as controls. Nicotine administration resulted in shedding, necrosis, and loss of brush border of cells covering proximal and distal convoluted tubules of kidney. The liver in the nicotine-treated group showed vacuolated cytoplasm of hepatocytes, with dilated central vein and sinusoids and mitochondrial destruction. Immunohistochemistry showed dense PCNA immunostaining in the livers of nicotine-treated rats. Vitamin C induced partial correction of nicotine-induced histopathological damage of liver and kidney and significant elevation in PCNA expression. Conclusion:The results of present work suggested that vitamin C has a promising prophylactic effect against nicotine-induced oxidative damage of liver and kidney.

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Section: Discussionsupporting

confidence: 73%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

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“…A significant increase in serum leptin levels one year after smoking cessation was reported in a recent study by Gonseth et al [22].…”

Section: Discussionmentioning

confidence: 51%

“…Having in mind that hypadiponectinemia in overweight individuals and in type II diabetic patients is closely associated with insulin resistance and hyperinsulinemia [55], we excluded subjects with type II diabetes and severe obesity. Nevertheless, the lack of insulin data must be considered a limitation of our study since it has been suggested recently that insulin may be involved in the association of smoking and leptin [22]. Further research on this subject is needed.…”

Section: Discussionmentioning

confidence: 89%

“…Leptin and adiponectin can be considered markers of subclinical inflammation with opposing effects and it is well appreciated that plasma levels of C-reactive protein have a positive correlation with plasma leptin and a negative correlation with plasma adiponectin [14][15][16]. Despite the well known inverse association between smoking and body weight, there have been conflicting reports on the effects of smoking on serum leptin and adiponectin levels [17][18][19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

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Effects of smoking cessation on serum leptin and adiponectin levels

Kryfti

Galenterides

Dimakou

et al. 2015

6.3 Tobacco, Smoking Control and Health Education

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Background: Evidence on the association of leptin and adiponectin and smoking is limited and discordant. Leptin and adiponectin represent the most abundant adipokines in human plasma that play crucial roles in the pathophysiology of metabolic syndrome, atherosclerosis and insulin resistance. Leptin up-regulates the expression of several pro-inflammatory cytokines and is increased upon weight gain. Adiponectin has been shown to possess insulin sensitizing, anti -inflammatory and anti-atherogenic properties and is increased upon weight reduction. Our aim was to assess the effects of smoking cessation on serum leptin and adiponectin levels. Methods: We assessed the changes in serum leptin and adiponectin levels, serum CRP levels and BMI in apparently healthy smokers after 3 and 6 months of abstinence from smoking. Successful cessation was confirmed by an exhaled carbon monoxide measurement. 26 healthy non-smokers were recruited as controls. Results: Among the sample group, 32 subjects had quitted smoking at 3 months and 29 subjects at 6 months. Conclusions: Smoking quitters' leptin levels appear to increase 3 months after smoking cessation and then decrease from 3 to 6 months of abstinence from smoking. Adiponectin levels increase during the first trimester of smoking cessation. The decrease in CRP levels indicates that the low grade inflammation observed in smokers is gradually restored. The alterations of serum leptin and adiponectin after 6 months of smoking cessation suggest the same but do not reach statistically significant levels. Weight gain and changes in fat distribution may attenuate the beneficial effects of smoking cessation.

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“…Recently, some reports have linked leptin to tobacco craving and withdrawal-related symptoms. [19][20][21] Very few studies have examined leptin levels prospectively in accordance to the smoking habits in healthy individuals of both genders and in patients with COPD. In such a prospective study Lemieux A et al have found that leptin concentration en-hances during a period of 48 hours in females after quitting smoking, but remains stable in blood of non-smokers, in relapsers and in male abstainers.…”

Section: Discussionmentioning

confidence: 99%

Possible Role of Serum Leptin as Biomarker in COPD

Zhelyazkova

Tacheva

Dimov

et al. 2019

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Citation: Zhelyazkova YA, Tacheva TT, Dimov DM, Vlaykova DG, Bivolarska AV, Vlaykova TI. Possible role of serum leptin as biomarker in COPD. Folia Med (Plovdiv) 2019;61(4):512-21. AbstractLeptin is one of the adipokines shown to exert a significant effect in respiratory diseases, including chronic obstructive pulmonary disease (COPD).The aim of the present study was to evaluate the possible role of serum leptin as biomarker in COPD.The serum leptin levels were assessed in 58 patents with stable COPD and 21 controls applying ELISA method.The leptin levels were higher, although not significantly, in COPD patients than in controls (221.52±24.28(SE) vs. 165.04±26.01 pg /ml, p=0.197). This tendency turned out significant when only females were compared (414.60±60.63 vs. 219.40±44.15 pg/ml, p=0.038). The levels of leptin were highly dependent on the BMI both in COPD patients (p<0.001) and in controls (p=0.024): they were the highest in obese individuals and decreased with reducing the BMI.In the COPD group, women had significantly higher leptin levels than men (p<0.0001) independent of the BMI. The non-smoking patients had significantly higher leptin levels than ex-smokers (р=0.007) and current smokers (р=0.007). In patients with BMI above 25, several associations were observed: patients with mild COPD had higher serum leptin level than those with severe or very severe COPD (р=0.038); the leptin levels correlated positively with FEV 1 % (r= 0.304, р=0.045) and FEV 1 /FVC ratio (r= 0.348, p=0.021), and tended to correlate negatively with ABCD GOLD groups (Rho=-0.300, p=0.043) and with the CAT points (Rho=-0.258, p=0.091); the leptin levels below 300 ng/ml determined 4.08-fold higher risk for more severe COPD.The results of our study confirm that the serum leptin levels depend significantly on the BMI and are interfered by gender and smoking habits. However, this adipokine cannot be used as a serum biomarker for distinguishing COPD patients, but its decrease might be associated with aggravation of the disease.

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Leptin and smoking cessation: secondary analyses of a randomized controlled trial assessing physical activity as an aid for smoking cessation

Cited by 18 publications

References 51 publications

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Effects of smoking cessation on serum leptin and adiponectin levels

Possible Role of Serum Leptin as Biomarker in COPD

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