Journal of Medicine and Medical Science Vol. 2(8) pp. 1017-1021, August 2011 Available online@ http://www.interesjournals.org/JMMS Copyright © 2011 International Research Journals Full Length Research Paper G-6-PD deficiency - a potential risk factor for development of diabetes mellitus M. B. Adinortey 1* , R. K. Owusu 4 , I. K. A. Galyuon 2 , W. Ekloh 1 , I. Owusu 1 and D. A. Larbi 3 1 Department of Biochemistry, School of Biological Sciences, University of Cape Coast, Cape Coast, Ghana. 2 Department of Molecular Biology and Biotechnology, School of Biological Sciences, University of Cape Coast, Cape Coast, Ghana 3 Department of Biochemistry, School of Medical Sciences, University of Cape Coast, Cape Coast, Ghana 4 Department of Obs/Gyn, Komfo Anokye Teaching Hospital, Kumasi, Ghana. Accepted 10 August, 2011 Glucose-6-phosphate dehydrogenase (G-6-PD), an enzyme expressed in most human tissues is important in the generation of reduced glutathione - a key product in the control of oxidative stress. A low activity of this enzyme in red blood cells leads to Glucose-6-phosphate dehydrogenase deficiency (G-6-PDD). This disease has been overlooked as one of the causes of increased oxidative stress; a risk factor for diabetes mellitus-a disease which is a threat to the health of many populations. This study aimed at an evaluation of the relationship between G-6-PD deficiency and Type 2 diabetes mellitus in Ghanaians and also to determine whether G-6-PD deficient individuals are at risk of developing diabetes mellitus. The prevalence of G-6-PD deficiency was analyzed in a total of 422 individuals – both diabetic and non-diabetic controls. The study showed that G-6-PD deficiency (severe and moderate defect) was significantly (p < 0.001) higher (50.7%) in diabetic individuals compared to non diabetics (22.3%). The odds ratio for diabetes mellitus was 1.61 (95% confidence interval = 1.55-1.67) (p < 0.001). The study confirmed the association between G-6-PD deficiency and diabetes mellitus and that G-6-PD deficiency (moderate and severe) is a risk factor for diabetes mellitus. Treatments that directly prevent a decrease in G-6-PD activity or promote G-6-PD activity or directly reduce G-6-PD deficiency induced oxidative stress could hold a great promise in reducing the risk of developing diabetes mellitus among G-6-PD deficiency individuals. Key words: Diabetes mellitus, oxidative stress, G-6-PD deficiency, Ghana. INTRODUCTION Glucose-6-phosphate dehydrogenase (G-6-PD) defi- ciency is one of the most common enzymopathies in humans affecting over 400 million people worldwide (Cappellini and Fiorelli, 2008). The disorder is an X- linked, hereditary genetic defect caused by mutations in the G-6-PD gene, resulting in protein variants with different levels of enzyme activity, that are associated with a wide range of biochemical and clinical manifest- tations. Glucose-6-phosphate dehydrogenase (G-6-PD), an enzyme produced in all tissues, is important in the generation of reduced glutathione, a key product in *Corresponding Author: Email: Michaelbuenor@gmail.com; Tel: +233-332136922 the control of oxidative stress (Mehta et al., 2000). Oxidative stress results from an imbalance between radical-generating and radical-scavenging systems. It is characterized by an increased concentration of oxygen- derived products that provoke irreversible cell injury in cells of liver, kidney, brain, lung, skeletal muscle, heart muscle, adrenal gland, pituitary gland and pancreas (Halliwell and Gutteridge, 1989). A study by Donde et al (1985) has shown elevated levels of glycosylated haemoglobin and reduced levels of reduced glutathionine (GSH) in the blood of G-6-PD-deficient subjects compared to G-6-PD-normal subjects. This implies that G-6-PD deficiency individuals have increased oxidative stress in their cells due to the major biochemical dysfunction in the G-6-PD enzyme to generate adequate amount of reduced nicotinamide adenine dinucleotide phosphate (NADPH) the essential reducing agent for