Abstract
HypothesisPrevious studies provide evidence that glycated haemoglobin (HbA1c) and fasting plasma glucose (FPG) should not be considered as interchangeable alternatives in the diagnosis of the same type 2 diabetes, but as indicators of its different pathogenetic subtypes. This study was conducted to determine whether a particularly high amount of glucose in either HbA1c form or in fasting plasma would be found in diabetic patients genetically predisposed for either intensive cognitive or intensive muscle metabolic activity, respectively.MethodsHbA1c and FPG levels, polymorphisms of genes indicating the predisposition to different cognitive activity (the dopamine D2 receptor (DRD2/ANKK1)), muscle activity (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC1A(PPARGC1A))), and vascular regulation of general metabolic activity (the angiotensin 1 converting enzyme (ACE)) were assessed in diabetic patients and nondiabetic controls.ResultsDRD2/ANKK1 polymorphism that affects baseline central arousal determined HbA1c variations uncorrelated with FPG in total and clinical groups. The mutation of PGC1A mainly affecting peripheral glucose metabolism had an effect on FPG correlated or uncorrelated with HbA1c depending on the effect assessment in the total sample or in the nondiabetic group, respectively. ACE insertion/deletion (I/D) gene polymorphism was associated with both HbA1c and FPG fluctuations, but only in diabetic patients.ConclusionThe findings provide evidence that the HbA1c and FPG may predict the risks for different subtypes of type 2 diabetes associated with either brain or muscle metabolic activity in genetically vulnerable people.
Highlights
Despite the known limitations of diagnostic criteria and early risk for type 2 diabetes derived from fasting (FPG) and/or 2-h plasma glucose levels, they are still widely accepted
The distributions of all three genetic loci in the total sample were significantly different from the expectations of Hardy–Weinberg equilibrium (HWE), our additional findings attribute this departure to the association of polymorphisms with generations overlapping and the rate of surviving to old age
This is consistent with the genetic models of morbidity and mortality protection effects of PGC1A gene GG genotype, angiotensin converting enzyme (ACE) I allele, and DRD2/ANKK1 gene polymorphism depending on sex [45, 46, 47, 48, 49, 50]
Summary
Despite the known limitations of diagnostic criteria and early risk for type 2 diabetes derived from fasting (FPG) and/or 2-h plasma glucose levels, they are still widely accepted. It was concluded that HbA1c and FPG display a different sensitivity versus specificity in identifying people at risk for later development of diabetes, and Expert Committees in diabetes consider that a better biochemical marker should be selected as a more reliable diagnostic tool [1, 2]. This discordance may occur because HbA1c and FPG each measure different physiological processes associated with the risk for type 2 diabetes.
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