title: HbA1c levels and erythrocyte transport functions in complication-free type 1 diabetic children and adolescents.
abstract: Higher erythrocyte sodium-lithium countertransport activity (SLC) is implicated in the development of diabetic nephropathy. Altered glucose homeostasis and genetic susceptibility are claimed to play a role in the elevation of SLC. We aimed to test whether metabolic control or the genetic variants of G protein beta 3 (Gb3) subunits determine SLC and other erythrocyte transport activities in complication-free stage of type 1 diabetes. A total of 96 complication-free type 1 diabetic children and adolescents were enrolled. SLC, Na(+)/K(+)-ATPase (NAK) and Ca(2+)-ATPase (CA) were measured by functional assays in erythrocytes. Gb3-C825T polymorphism was determined by PCR-RFLP. Results were related to HbA(1c) and were compared to those of 97 healthy controls. SLC activity was higher in diabetics (387+/-146 vs. 280+/-65 mmol/RBC. hour) and correlated with HbA(1c) levels (y=0.004x+6.42, r=0.33, n=96, p<0.01). NAK and CA activities were unaltered. The prevalence of (825)T allele was similar in the patient and control groups (0.34 vs 0.37) and no differences in enzyme activities were observed between the (825)T allele-positive and negative subjects. Although metabolic control correlated with SLC, other membrane functions were not affected. Therefore we hypothesize that the relationship between advanced glycation and SLC elevation is not causative. Rather, a genetic susceptibility for the coexistence of poor metabolic control and higher SLC is more likely. However, the presence of Gb3-C825T variant is not likely to be a risk factor for SLC-elevation and altered metabolic control diabetes.
authors.affiliation: First Department of Pediatrics, Semmelweis University, Budapest, Hungary.
authors.forename: B
authors.initials: B
authors.lastname: Deák
authors.forename: M
authors.initials: M
authors.lastname: Dobos
authors.forename: I
authors.initials: I
authors.lastname: Kocsis
authors.forename: D
authors.initials: D
authors.lastname: Krikovszky
authors.forename: A
authors.initials: A
authors.lastname: Tordai
authors.forename: L
authors.initials: L
authors.lastname: Madácsy
authors.forename: T
authors.initials: T
authors.lastname: Tulassay
authors.forename: B
authors.initials: B
authors.lastname: Vásárhelyi
mesh_terms: D000293:Adolescent; D000483:Alleles; D017920:Antiporters / Q000097:blood*; D000252:Calcium-Transporting ATPases / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000235:genetics*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D044387:GTP-Binding Protein beta Subunits / Q000235:genetics*; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006442:Glycated Hemoglobin / Q000032:analysis*; D006801:Humans; D008297:Male; D011110:Polymorphism, Genetic; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood
chemical_list: D017920:Antiporters; D000252:Calcium-Transporting ATPases; D044387:GTP-Binding Protein beta Subunits; D006442:Glycated Hemoglobin; D000254:Sodium-Potassium-Exchanging ATPase; C045885:sodium-lithium countertransporter