beta 3-adrenoreceptor gene polymorphism and leptin. Lack of relationship in type 2 diabetic patients

Citation
J. Vendrell et al., beta 3-adrenoreceptor gene polymorphism and leptin. Lack of relationship in type 2 diabetic patients, CLIN ENDOCR, 49(5), 1998, pp. 679-683
Citations number
17
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
CLINICAL ENDOCRINOLOGY
ISSN journal
03000664 → ACNP
Volume
49
Issue
5
Year of publication
1998
Pages
679 - 683
Database
ISI
SICI code
0300-0664(199811)49:5<679:B3GPAL>2.0.ZU;2-D
Abstract
INTRODUCTION The beta(3)-Adrenergic receptor (beta(3)AR) and leptin are mol ecules involved in the regulation of energy balance. Recently, a mutation i n the PEAR gene (Trp64Arg) has been reported to be associated with features of insulin resistance, weight gain and early onset of Type 2 Diabetes Mell itus, The aim of this study was to determine the frequency and clinical cha racteristics of the Trp64Arg mutation in the beta(3)AR gene in Type 2 diabe tic patients, its relationship with leptin levels, and its role in microang iopathic complications. SUBJECTS AND METHODS 187 Type 2 diabetic patients and 100 unrelated non-dia betic subjects were studied. There was no difference between the diabetic a nd nondiabetic subjects in the frequency of the Trp64 and Arg64 alleles (92 .5% vs. 92.3% and 7.5% vs. 7.7%, respectively), Type 2 diabetic patients we re divided into two groups according to the presence (n = 27) or absence of the mutation (n = 160). RESULTS Mutation of the beta(3)AR gene was not associated with any differen ces either in the clinical and metabolic parameters or microangiopathic com plications. Type 2 diabetic patients carrying the Arg64 allele tended to ha ve a lower diabetes duration, but this was not statistically significant. P lasma leptin levels were not different according to the beta(3)AR genotype. CONCLUSIONS The Trp64Arg mutation is not a major determinant of Type 2 diab etes and its microangiopathic complications. Moreover, this mutation was no t clinically relevant in leptin regulation.