Study of glucose-6-phosphate dehydrogenase in different ethenic groups with type 2diabetes

Abstract EN

Abstract: Background Existence of oxidative stress in diabetes type 2 is revealed by enhanced lipid peroxidation, an impaired glutathione system and decreased activity of G6PD, which may contribute to the initiation and/or progression of diabetes and its complications.

The close association of cardiovascular risk factors such as hypertension, diabetes, atherosclerosis, obesity, and hyperlipidemia in blacks suggest a common causative mechanism.

Genes and environment appear to join forces for the increased expression of these diseases in blacks.

Objective is to study the possible relationship between G6PD and type 2 diabetes in different ethenic groups Study Design 60 subjects classified into 10 white subjects as white control group,10 black subjects as black control group, 20 white diabetic patients with type 2 diabetes and 20 black diabetic patients with type 2 diabetes.

They were subjected to full clinical history and thorough clinical examination.

They were also subjected to laboratory investigations including fasting blood glucose, post-prandial blood glucose, glycated hemoglobin (HbA1C), G6PD enzyme and urinary albumin excretion levels.

Results There was significant decrease of G6PD level among diabetics [186±127.2] compared to controls[309.4±135.4.]p=0.002.G6PD level was lower in black diabetic group [139.3 ± 87.4] compared to white control group [323.4±152.9], black control group [295.5±122.04] and white diabetic group [232.7± 45.1] p=0.001 but urinary albumin excretion level was higher in black diabetics [70.2 ± 25.2] compared to white controls [4.5 ± 1.7], black control [9.76 ±3.2 ] and white diabetics [24.81 ± 8.5] p<0.001with highly significant difference between the studied groups.

There was a highly significant inverse correlation between G6PD versus HbA1C [r=-0.7,p<0.001] among all studied groups.

There was highly significant positive correlation between HbA1C versus urinary albumin excretion among black diabetic group [r=0.72, p=0.001] and significant positive correlation between HbA1C versus urinary albumin excretion among white diabetic group [r=0.67, p=0.002].

Conclusion: The increased susceptibility of ?-cells to oxidative damage by G6PD deficiency may be an important mechanism in pathogenesis of type 2 diabetes and deficiencies in this enzyme among people of African descent, may contribute to the high number of diabetic cases seen among them, this together with other environmental factors.

G6PD deficiency may be a risk factor for development and progression of type 2 diabetic nephropathy.