title: Circulating insulin concentrations, smoking, and alcohol intake are important independent predictors of leptin in young healthy men.
abstract: OBJECTIVE
  Leptin, an adipocyte-secreted hormone, has been shown to signal the status of energy stores to the brain, regulate energy homeostasis, and mediate the neuroendocrine response to food deprivation. Obesity is associated with increased leptin levels, and several hormones, including insulin and glucocorticoids, have been associated with leptin levels and expression in rodents. Although obesity has been strongly associated with increased leptin in humans, a significant percentage of leptin's variability remains unexplained. The role of endogenous hormones, demographic factors, or certain life-style factors in explaining the residual variability of leptin levels has not yet been clarified. We performed this cross-sectional study to document the relative importance of obesity, lifestyle factor, and endogenous hormones in determining serum leptin levels.
  
  
  METHODS
  We measured serum concentrations of insulin, cortisol, testosterone, growth hormone, and dehydroepiandrosterone sulfate; ascertained anthropometric, demographic, and lifestyle characteristics; and studied these variables in relationship to serum leptin concentrations in a sample of young healthy men.
  
  
  RESULTS
  Obesity and alcohol intake were independently and positively associated with circulating leptin concentrations. Additionally, cigarette smoking was negatively and independently associated with leptin concentrations. Finally, serum insulin concentration was an independent hormonal determinant of circulating leptin concentrations, whereas serum testosterone was negatively associated with leptin only by bivariate analysis.
  
  
  CONCLUSIONS
  We conclude that, in addition to obesity, cigarette smoking, alcohol intake, and serum insulin levels are associated with leptin levels in a population of healthy young men.
authors.affiliation: Division of Endocrinology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: C S
authors.initials: CS
authors.lastname: Mantzoros
authors.forename: A D
authors.initials: AD
authors.lastname: Liolios
authors.forename: N A
authors.initials: NA
authors.lastname: Tritos
authors.forename: V G
authors.initials: VG
authors.lastname: Kaklamani
authors.forename: D E
authors.initials: DE
authors.lastname: Doulgerakis
authors.forename: I
authors.initials: I
authors.lastname: Griveas
authors.forename: A C
authors.initials: AC
authors.lastname: Moses
authors.forename: J S
authors.initials: JS
authors.lastname: Flier
mesh_terms: D000293:Adolescent; D000328:Adult; D000428:Alcohol Drinking; D015992:Body Mass Index; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood*; D020738:Leptin; D016014:Linear Models; D008297:Male; D009765:Obesity / Q000097:blood*; D011506:Proteins / Q000378:metabolism*; D012907:Smoking; D013739:Testosterone / Q000097:blood
chemical_list: D007328:Insulin; D020738:Leptin; D011506:Proteins; D019382:Human Growth Hormone; D013739:Testosterone; D019314:Dehydroepiandrosterone Sulfate; D006854:Hydrocortisone