1999
DOI: 10.2337/diabetes.48.2.420
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Diabetic nephropathy is not associated with the dinucleotide repeat polymorphism upstream of the aldose reductase (ALR2) gene but with erythrocyte aldose reductase content in Japanese subjects with type 2 diabetes.

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Cited by 42 publications
(29 citation statements)
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“…This effect is enhanced when peripheral blood mononuclear cells (PBMCs) from those patients with diabetic microvascular complications are cultured in high glucose compared with those without complications or normal control subjects (13,14). Patients with diabetic microvascular complications also have raised enzymatic activity of AKR1B1 compared with those without microvascular complications (15)(16)(17). Several groups have shown that AKR1B1 mRNA levels can be induced under hyperglycemic and hypertonic conditions (6,14,18,19).…”
mentioning
confidence: 99%
“…This effect is enhanced when peripheral blood mononuclear cells (PBMCs) from those patients with diabetic microvascular complications are cultured in high glucose compared with those without complications or normal control subjects (13,14). Patients with diabetic microvascular complications also have raised enzymatic activity of AKR1B1 compared with those without microvascular complications (15)(16)(17). Several groups have shown that AKR1B1 mRNA levels can be induced under hyperglycemic and hypertonic conditions (6,14,18,19).…”
mentioning
confidence: 99%
“…The association was also observed in another Caucasian type 1 population [17], however it could not be confirmed by others [21, 22]. Most of the studies performed in type 2 diabetes did not show an association between diabetic nephropathy and the polymorphic (CA) n dinucleotide microsatellite [23,24,25]. …”
Section: Discussionmentioning
confidence: 82%
“…Gene polymorphism of angiotensin-converting enzyme, angiotensinogen, and AR is relevant to the onset of diabetic nephropathy [9,17,21,25]. Erythrocyte AR protein levels or its enzyme activities correlate with the high incidence of diabetic neuropathy, retinopathy, and nephropathy [15,16,30,31,36].…”
Section: Discussionmentioning
confidence: 99%
“…Experimental studies with AR inhibitors have implicated the accelerated flux of glucose through the polyol pathway in the pathogenesis of diabetic complications [10,34,39]. In diabetic patients, the incidence of chronic complications is associated with high AR activity or AR protein levels in erythrocytes [15,16,25,30,36]. The transgenic expression of human AR has also been shown to elicit severe neuropathic changes under a galactosemic condition [40].…”
Section: Introductionmentioning
confidence: 99%