Plasma leptin concentrations and lipid profiles during nicotine abstinence

Background: Weight gain is a frequent consequence of smoking cessation. Lep tin, the protein product of the obese gene, seems to regulate appetite and body fat stores. The purpose of this study was to assess changes in circula ting leptin levels and lipid metabolism during nicotine abstinence (NA) and their role in post-cessation weight gain. Methods: Six sedentary, weight-s table, nonobese adult smokers were studied before and after 7 days of NA wh ile following a weight-maintenance diet of standard composition. All subjec ts refrained from smoking overnight (as assessed by breath CO) and were ins tructed to chew nicotine polacrilex gum (4 mg) hourly from 7:00 AM to 8:00 PM [nicotine intake (NI) day]. Venous blood samples were collected at 7:00 AM (after an overnight fast) and 5:00 PM (pre-supper) on NI day and again a fter 7 days of NA. Results: Body weight did not change after 7 days of NA ( 72.0 +/- 2.8 versus 71.8 +/- 2.7 kg). Serum cotinine levels declined from 2 07 +/- 40 ng/mL during NI to undetectable levels during NA (P <0.01). Fasti ng plasma leptin was similar during NI and NA (5.7 +/- 1.4 versus 6.4 +/- 1 .9 ng/mL; P = NS). Moreover, plasma concentrations of glucose, insulin, and free fatty acids were unaffected by 7 days of NA. Although plasma triglyce rides, total cholesterol, and low-density lipoprotein cholesterol were simi lar during NI and NA, high-density lipoprotein cholesterol increased by 15% after 7 days of NA (P <0.05). Conclusions: In this group of nonobese, adul t smokers consuming an isocaloric diet, NA for 7 days did not affect body w eight or circulating concentrations of leptin, glucose, insulin, or free fa tty acids. In contrast, HDL cholesterol increased significantly after NA. T hese results indicate that under controlled dietary conditions, changes in leptin expression do not contribute to the weight gain that commonly accomp anies smoking cessation.