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β3‐adrenoreceptor gene polymorphism and leptin. Lack of relationship in type 2 diabetic patients
Author(s) -
Joan Vendrell,
Cristina Gutiérrez,
Montse Broch,
José Manuel FernándezReal,
Carmen Aguilar,
C Richart
Publication year - 1998
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.1998.00599.x
Subject(s) - medicine , endocrinology , leptin , polymorphism (computer science) , gene , type 2 diabetes , biology , diabetes mellitus , obesity , genotype , genetics
The β 3 ‐Adrenergic receptor (β 3 AR) and leptin are molecules involved in the regulation of energy balance. Recently, a mutation in the β 3 AR gene (Trp64Arg) has been reported to be associated with features of insulin resistance, weight gain and early onset of Type 2 Diabetes Mellitus. The aim of this study was to determine the frequency and clinical characteristics of the Trp64Arg mutation in the β 3 AR gene in Type 2 diabetic patients, its relationship with leptin levels, and its role in microangiopathic complications. SUBJECTS AND METHODS 187 Type 2 diabetic patients and 100 unrelated non‐diabetic subjects were studied. There was no difference between the diabetic and 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 were divided into two groups according to the presence ( n = 27) or absence of the mutation ( n = 160). RESULTS Mutation of the β 3 AR gene was not associated with any differences either in the clinical and metabolic parameters or microangiopathic complications. Type 2 diabetic patients carrying the Arg64 allele tended to have a lower diabetes duration, but this was not statistically significant. Plasma leptin levels were not different according to the β 3 AR genotype. CONCLUSIONS The Trp64Arg mutation is not a major determinant of Type 2 diabetes and its microangiopathic complications. Moreover, this mutation was not clinically relevant in leptin regulation.