title: Associations of leptin with body fat distribution and metabolic parameters in non-insulin-dependent diabetic patients: no effect of apolipoprotein E polymorphism.
abstract: Leptin levels have been shown previously to be associated with anthropometric parameters such as the body mass index (BMI), total body fat, and subcutaneous fat. Since apolipoprotein E (apoE) polymorphism is known to be a genetic marker affecting the relationship between certain anthropometric and metabolic parameters, we evaluated whether the leptin level and/or associations between the leptin level and body composition in non-insulin-dependent diabetic patients could be determined by apoE polymorphism. In 171 type 2 diabetic patients (105 male and 66 female), body composition (BMI, waist to hip ratio [WHR], fat mass, and visceral fat) was measured and fasting blood samples were obtained to determine the apoE genotype, leptin, glucose, and insulin levels, and the lipid profile. The mean leptin level for the whole group was 11.7 +/- 9.3 ng/mL, with a significant difference (P < .001) between men (7.1 +/- 4.9 ng/mL) and women (19.0 +/- 10.1 ng/mL). No difference was found for leptin levels or anthropometric variables between the 3 different apoE genotypes (E3/E3 homozygotes, E2 carriers, and E4 carriers). Only low-density lipoprotein (LDL) cholesterol was significantly different between the 3 apoE subgroups. The correlations of leptin with anthropometric variables, especially visceral fat, tended to be different between the 3 apoE groups, but this was not independent and no effect was found after controlling for the other parameters in the model. A multiple regression model containing gender, subcutaneous fat, fasting glucose, triglycerides, and high-density lipoprotein (HDL) cholesterol explained 81% of the variance in leptin levels. We conclude that apoE polymorphism has no effect on the leptin level or its associations with other anthropometric and metabolic parameters.
authors.affiliation: Department of Endocrinology, Metabolism, and Clinical Nutrition, University Hospital Antwerp, Belgium.
authors.forename: M
authors.initials: M
authors.lastname: Wauters
authors.forename: R
authors.initials: R
authors.lastname: Considine
authors.forename: A
authors.initials: A
authors.lastname: Löfgren
authors.forename: C
authors.initials: C
authors.lastname: Van Broeckhoven
authors.forename: J C
authors.initials: JC
authors.lastname: Van der Auwera
authors.forename: I
authors.initials: I
authors.lastname: De Leeuw
authors.forename: L
authors.initials: L
authors.lastname: Van Gaal
mesh_terms: D001057:Apolipoproteins E / Q000235:genetics*; D001823:Body Composition / Q000235:genetics; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005838:Genotype; D006801:Humans; D020738:Leptin / Q000097:blood*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012044:Regression Analysis
chemical_list: D001057:Apolipoproteins E; D020738:Leptin; D008055:Lipids