Increased leptin and decreased ghrelin level after smoking cessation

Lee, Heejin; Joe, Keun Ho; Kim, Won; Park, Jae-Woo; Lee, Do‐Hoon; Sung, Ki-Wug; Kim, Daijin

doi:10.1016/j.neulet.2006.09.013

Cited by 63 publications

(62 citation statements)

References 24 publications

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“…(57) More recently, it has been demonstrated that, after smoking cessation, the serum concentration of leptin increases, whereas that of ghrelin decreases. (47) These results, which are contrary to what would be expected, induce further speculation: changes in the leptin-ghrelin-NPY system produced in peripheral tissues might be the consequence, and not the cause, of the changes in body weight after smoking cessation, possibly related to the direct effects of the lack of nicotine in the central nervous system. (47) The role of genetic polymorphisms…”

Section: Leptin Ghrelin Neuropeptide Y and Their Relationships Withmentioning

confidence: 83%

“…Some studies have demonstrated a significant increase, rather than the expected decrease, in post-cessation serum levels of leptin. (40,47) Neither could the inverse relationship between leptin levels and gradation of appetite after smoking cessation be demonstrated. (14) It is possible that biases in the various studies, such as in the design of the investigation project, which disregarded the possible role of different ethnicities, age brackets and health status of participants, among others, can explain these discrepancies.…”

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

“…(14) It is possible that biases in the various studies, such as in the design of the investigation project, which disregarded the possible role of different ethnicities, age brackets and health status of participants, among others, can explain these discrepancies. (47) Neither has the potential relationship between serum levels of leptin and the dose of inhaled nicotine been considered, that is, no correction was made regarding the number of cigarettes consumed per day and the number of deep inhalations per cigarette (puffs).…”

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

“…In one study, (47) when trying to explain the findings of high leptin and low ghrelin levels two months after smoking cessation, the authors speculated that those findings were not the cause, but the result of the increase in fat mass caused by smoking abstinence.…”

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

“…(52) Conflicting findings have been reported, not only regarding the relationship between smoking and serum levels of leptin but also regarding the levels of other peptides that regulate food intake, such as NPY, (53) orexins (54) and ghrelin. (47) The parenteral administration of nicotine, as well as the administration of inhaled nicotine, has been shown to markedly reduce food intake in rats by inhibiting the synthesis of NPY, one of the hormones that increase appetite. (31,55) In addition, there might be a direct inter-relation between leptin and NPY: when the level of one increases, that of the other tends to decrease, in a feedback loop.…”

Section: Final Considerationsmentioning

confidence: 99%

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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: Leptin Ghrelin Neuropeptide Y and Their Relationships Withmentioning

confidence: 83%

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

Section: Mechanisms Of Weight Gain During Smoking Cessationmentioning

confidence: 99%

Section: Final Considerationsmentioning

confidence: 99%

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

Chatkin

2007

J. bras. pneumol.

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Elevated serum insulin‐like growth factor 1 in recurrent aphthous stomatitis

Baccaglini

Shuster

Theriaque

et al. 2019

Clinical & Exp Dental Res

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Over 100 million Americans experience recurrent aphthous stomatitis (RAS) at some point in life. To develop targeted drugs for RAS treatment, it is critical to identify its etiology. We determined if serum insulin‐like growth factor 1 (IGF‐1) and related factors are associated with RAS, because both RAS prevalence and IGF‐1 are highest during puberty. We analyzed data from 1,480 Third National Health and Nutrition Examination Survey participants aged 20–40 years. Participants with a history of diabetes or lupus, cotinine levels 6 ng/ml or higher or glycemia 110 mg/dl or higher were excluded. We compared levels of IGF‐1, IGFBP‐3, leptin, and insulin in participants with a positive vs. negative RAS history in the prior 12 months. We used logistic regression in SAS/SUDAAN to account for the complex sampling design. The odds of a positive RAS history were 1.31 times higher for every 100 ng/ml increase in serum IGF‐1. This association persisted after adjustment for age, race/ethnicity, medication intake, body mass index, insulin, leptin, glycemia, and income (adjusted OR = 1.30, 95% CI [1.06, 1.60]; p = 0.013). The odds of a positive RAS history were also higher among non‐Hispanic white compared with non‐Hispanic black participants (adjusted OR = 4.37, 95% CI [3.00, 6.38]). Leptin, IGFBP‐3, and insulin levels did not differ by RAS status. The significantly higher IGF‐1 levels in participants with a positive RAS history compared with controls suggest a possible role of the IGF‐1 pathway in RAS etiology.

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Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

Fischer

Völzke

Kassubek

et al. 2020

Obesity

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Objective: This study provides a comprehensive overview of the associations of five adipokines (adiponectin, chemerin, galectin-3, leptin, and resistin) with fat deposits, behavioral risk factors, and metabolic phenotypes. Methods: Using multivariable linear and logistic regression models, cross-sectional data from 4,116 participants of the population-based Study of Health in Pomerania were analyzed. Results: Participants with obesity showed higher chemerin, galectin-3, and leptin but showed lower adiponectin concentrations. Independently of other fat compounds, liver fat content, visceral adipose tissue, and subcutaneous adipose tissue (SAT) were inversely associated with adiponectin. Independent positive associations of liver fat content and SAT with chemerin as well as of SAT with galectin-3 and leptin were observed. Physically inactive participants had higher chemerin and leptin concentrations. Smokers had higher chemerin and galectin-3 as well as lower leptin. Alcohol consumption was associated with adiponectin (positive) and resistin (inverse). All adipokines were associated with at least one lipid marker. Associations with glucose metabolism were seen for adiponectin, chemerin, galectin-3, and leptin. Conclusions: High adiponectin concentrations were related to favorable metabolic conditions, whereas high chemerin, galectin-3, and leptin were associated with an unfavorable metabolic profile. High leptin seems to be primarily indicative of obesity, whereas high adiponectin and chemerin are associated with a broader range of metabolic phenotypes.

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Increased leptin and decreased ghrelin level after smoking cessation

Cited by 63 publications

References 24 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?

Elevated serum insulin‐like growth factor 1 in recurrent aphthous stomatitis

Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

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