No Change in Serum Incretins Levels but Rise of Leptin Levels After Smoking Cessation: a Pilot Study

Abstract

The mechanisms behind the changes of body weight after smoking cessation are only partially understood. To this end, we explored the possible effects of smoking cessation on incretin hormones, leptin and selected anthropometric, biochemical and other hormonal parameters. Twenty-two non-obese male adult smokers attending an ambulatory smoking cessation program in Prague, Czech Republic, were examined at the baseline. Thirteen patients (mean age 37.92±2.66 years, mean body mass index 25.56±0.69 kg/m2) successfully quit smoking and were examined three months after smoking cessation; relapsed smokers were not followed up. The patients underwent 2-h liquid meal test with Fresubin and repeated blood sampling for measurements of blood glucose, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), amylin, insulin, leptin, peptide-YY (PYY) and pancreatic polypeptide (PP). Three months after smoking cessation, body weight increased (4.35±3.32 kg, p<0.001). Leptin levels increased significantly in all repeated samples, while levels of GIP, GLP-1, amylin, insulin, PYY and PP remained unchanged. In conclusions, smoking cessation increased leptin levels probably owing to weight gain while it did not influence incretin levels.

Effects of Smoking Versus Nonsmoking on Postprandial Glucose Metabolism in Heavy Smokers Compared With Nonsmokers

“…Similarly, our data suggest that smoking does not have a direct effect on postprandial plasma responses of the incretin hormones GIP and GLP-1. This is in line with other studies showing no effect of smoking cessation in heavy smokers on postprandial responses of GLP-1, GIP, and other gut hormones (39,40). Interestingly, the gut hormone CCK and its cellular pathways have been suspected to interact with and mediate the effects of nicotine, and studies in rats have shown nicotine and other derivatives of smoking to acutely increase CCK levels (41,42).…”

The Effect of Smoking Cessation on Body Weight and Other Metabolic Parameters with Focus on People with Type 2 Diabetes Mellitus

“…In a recent study, female smokers not only showed significantly higher serum levels of leptin compared to female non-smokers, but also compared to male smokers [ 72 ]. However, most of the studies noted a significant increase in serum leptin levels after smoking cessation [ 69 , 73 , 74 , 75 ]. This increase was positively correlated with an increase in body weight, BMI and body fat mass [ 61 , 64 , 71 , 73 , 74 ].…”

“…However, most of the studies noted a significant increase in serum leptin levels after smoking cessation [ 69 , 73 , 74 , 75 ]. This increase was positively correlated with an increase in body weight, BMI and body fat mass [ 61 , 64 , 71 , 73 , 74 ]. Gonseth et al reported a significant increase in serum leptin levels one year after smoking cessation, parallel with substantial weight in the same time period.…”

“…CCK is a peptide released by enteroendocrine cells within the small intestine in response to mixed meals, acting as a satiety signal [ 96 ]. Fasting GLP-1, visfatin and PYY levels were unchanged 3 months after smoking cessation in a study conducted by Stadler et al [ 49 ], and levels of gastric inhibitory polypeptide (GIP), GLP-1, amylin, insulin, PYY and pancreatic polypeptide (PP), measured after a meal challenge, were also not affected after 3 months of abstinence, according to Pancova et al However, changes in incretin levels earlier after smoking cessation may have occurred [ 73 ]. PYY suppresses food intake, and although no significant change was observed on its levels after smoking abstinence, according to the above-mentioned studies, body weight showed a significant increase.…”

“…Both parameters return to baseline after a few years of cessation [ 27 ]. Furthermore, a significant decrease in glycated hemoglobin (HbA1c) levels after smoking cessation has been reported [ 26 , 73 ]. Despite the association of smoking cessation with weight gain, concomitant improvements in insulin sensitivity and glucose homeostasis have been reported at the same time [ 31 , 107 ].…”