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 Ca2+-ATPase (CA) were measured by functional assays in erythrocytes. Gb3-C825T polymorphism was determined by PCR-RFLP. Results were related to HbA1c 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 HbA1c levels (y=0.004x+6.42, r=0.33, n=96, p<0.01). NAK and CA activities were unaltered. The prevalence of 825T allele was similar in the patient and control groups (0.34 vs 0.37) and no differences in enzyme activities were observed between the 825T 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.
- Diabetes mellitus
- G-protein beta 3 subunit polymorphism
- Na/ K-ATPase
- Na/Li-counter transporter
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism