Association of the nitric oxide synthase gene polymorphism with an increased risk for progression to diabetic nephropathy in type 2 diabetes

被引:106
作者
Neugebauer, S
Baba, T
Watanabe, T
机构
[1] Fukushima Med Coll, Dept Internal Med 3, Fukushima 9601247, Japan
[2] Univ Tokyo, Fac Med, Dept Internal Med 1, Tokyo, Japan
关键词
D O I
10.2337/diabetes.49.3.500
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
A mutation of endothelial nitric oxide synthase (ecNOS)-a key enzyme of the endogenous nitrovasodilator system that is essential for the regulation of blood flow and blood pressure-may aggravate the progression to diabetic nephropathy and/or retinopathy. To investigate the association of ecNOS tandem repeat polymorphism with diabetic nephropathy, the ecNOS genotype was assessed in 82 Japanese type 2 diabetic patients without nephropathy, 94 patients with microalbuminuria, 39 patients with nephropathy, and 155 healthy control subjects. The analysis revealed that type 2 diabetic patients with nephropathy (not with microalbuminuria) were significantly different from type 2 diabetic patients without nephropathy and healthy control subjects in genotype distribution (P = 0.0423) and frequency of the ecNOS4a allele (19.2% vs. 7.3 and 7.1%, respectively; P = 0.0078). The odds ratio of progression to diabetic nephropathy in diabetic patients who carry the mutated allele is about 2.87 compared with noncarriers. The stepwise multiple regression analysis in these patients showed that hypertension (F = 9.760) and ecNOS gene polymorphism (F = 5.298) are the relevant variables for nephropathy. However, no association was found between the ecNOS4a allele and hypertension or diabetic retinopathy. These results imply that the ecNOS gene polymorphism may be associated with progression to diabetic nephropathy in Japanese type 2 diabetic patients.
引用
收藏
页码:500 / 503
页数:4
相关论文
共 21 条
[1]  
BONNER TI, 1991, CYTOGENET CELL GENET, V58, P1850
[2]   ACTIVATION OF PROTEIN-KINASE-C IN GLOMERULAR CELLS IN DIABETES - MECHANISMS AND POTENTIAL LINKS TO THE PATHOGENESIS OF DIABETIC GLOMERULOPATHY [J].
DERUBERTIS, FR ;
CRAVEN, PA .
DIABETES, 1994, 43 (01) :1-8
[3]  
GRAHAM A, 1991, HUM GENET, V86, P509
[4]   Polymorphism in the 5'-end of the aldose reductase gene is strongly associated with the development of diabetic nephropathy in type I diabetes [J].
Heesom, AE ;
Hibberd, ML ;
Millward, A ;
Demaine, AG .
DIABETES, 1997, 46 (02) :287-291
[5]   ROLE OF ENDOTHELIUM-DERIVED NITRIC-OXIDE IN THE PATHOGENESIS OF THE RENAL HEMODYNAMIC-CHANGES OF EXPERIMENTAL DIABETES [J].
KOMERS, R ;
ALLEN, TJ ;
COOPER, ME .
DIABETES, 1994, 43 (10) :1190-1197
[6]   Nitric oxide synthase gene polymorphisms, blood pressure and aortic stiffness in normotensive and hypertensive subjects [J].
Lacolley, P ;
Gautier, S ;
Poirier, O ;
Pannier, B ;
Cambien, F ;
Benetos, A .
JOURNAL OF HYPERTENSION, 1998, 16 (01) :31-35
[7]   PATHOBIOLOGY OF ENDOTHELIAL AND OTHER VASCULAR CELLS IN DIABETES-MELLITUS - CALL FOR DATA [J].
LORENZI, M ;
CAGLIERO, E .
DIABETES, 1991, 40 (06) :653-659
[8]  
MARSDEN PA, 1993, J BIOL CHEM, V268, P17478
[9]   PROSPECTIVE-STUDY OF MICROALBUMINURIA AS PREDICTOR OF MORTALITY IN NIDDM [J].
MATTOCK, MB ;
MORRISH, NJ ;
VIBERTI, G ;
KEEN, H ;
FITZGERALD, AP ;
JACKSON, G .
DIABETES, 1992, 41 (06) :736-741
[10]   STRUCTURAL-FUNCTIONAL RELATIONSHIPS IN DIABETIC NEPHROPATHY [J].
MAUER, SM ;
STEFFES, MW ;
ELLIS, EN ;
SUTHERLAND, DER ;
BROWN, DM ;
GOETZ, FC .
JOURNAL OF CLINICAL INVESTIGATION, 1984, 74 (04) :1143-1155