Impact of the sulfonylurea receptor 1 (SUR1) exon 16-3c/t polymorphism on acute hyperglycaemia in type 2 diabetic patients.
Epidemiological data collected over the last few decades have demonstrated the significant role of acute (especially postprandial) hyperglycaemia in the development of macrovascular complications in patients with type 2 diabetes. However, the influence of SUR1 exon 16-3c/t polymorphism on impaired insulin secretion during acute hyperglycaemic episodes has not yet been evaluated. We studied 40 type 2 diabetic patients. Single nucleotide polymorphism in the sulfonylurea receptor gene was examined by means of PCR-RLFP. In every patient, fasting insulin, proinsulin, C-peptide and 1,5-anhydro-d-glucitol concentrations were assayed as markers of insulin secretion, peripheral resistance to insulin, and acute hyperglycaemia. The distribution of SUR1 exon 16-3c/t polymorphism was tt 35%, tc -40%, and cc -25%. By means of analysis of covariance, it was revealed that 1,5-anhydro-d-glucitol plasma levels are associated with SUR1 exon 16-3c/t polymorphism. However, the HOMA(IR) score influenced 1,5-anhydro-d-glucitol levels in plasma at a higher level of statistical power than the genetic variant. Our results suggest that SUR1 exon 16-3c/t polymorphism is only a partial determinant of acute hyperglycaemia-cardiovascular risk factor in type 2 diabetes.
Dworacka
Marzena
M
Department of Pharmacology, Poznan University of Medical Sciences, ul. Rokietnicka 5a, 60-806 Poznan, Poland. mdworac@amp.edu.pl
Winiarska
Hanna
H
Jagodziński
Paweł P
PP
D018528:ATP-Binding Cassette Transporters / Q000097:blood / Q000235:genetics*; D017668:Age of Onset; D015992:Body Mass Index; D003596:Cytosine; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D003925:Diabetic Angiopathies / Q000453:epidemiology / Q000235:genetics; D005091:Exons; D006801:Humans; D007003:Hypoglycemia / Q000235:genetics*; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D015221:Potassium Channels / Q000097:blood / Q000235:genetics*; D024661:Potassium Channels, Inwardly Rectifying / Q000097:blood / Q000235:genetics*; D011955:Receptors, Drug / Q000097:blood / Q000235:genetics*; D012307:Risk Factors; D064233:Sulfonylurea Receptors; D013941:Thymine; D044465:White People
C577507:ABCC8 protein, human; D018528:ATP-Binding Cassette Transporters; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D011955:Receptors, Drug; D064233:Sulfonylurea Receptors; D003596:Cytosine; D013941:Thymine