生活習慣病薬物治療に対する肥満遺伝子の影響

抄録

The development of risk factors, such as obesity, for lifestyle-related vascular disease is heterogeneous. In this regard, recent studies have shown that mutation of the β₃-adrenoceptor gene, involving replacement of tryptophan by arginine at position 64 (Trp 64 Arg) of encoding amino acid residues (obesity gene), was associated with increased susceptibility to obesity and insulin resistance, and affected obesity treatment in humans. In the present study, we tested for the presence of the obesity gene and examined its influence on pharmacotherapy for lifestyle-related vascular disease.
Our study investigated 92 persons receiving medication (depressors, lipid-lowering drugs, oral agents for diabetes; medication group) for a lifestyle-related illness among 2453 persons who consented to β₃-adrenoceptor gene determination. There was no difference in the prevalence of the obesity gene between those receiving medicine and those not receiving any. In the medication group, there were no significant differences in the average T-C, TG, LDL-C, RLP-C, glucose, HbAic and BMI measurements among subjects who had the obesity gene. Also, when the minimal cholesterol target following therapy was set to 220 mg or less, this was achieved in all subjects without the obesity gene (wild group). In subjects with the obesity gene, there were many cases in which RLP-C was over 8 mg/dL.
These results suggest that the obesity gene would enhance resistance to pharmacotherapy intended to improve lipid levels in the treatment of lifestyle-related vascular disease.