ABSTRACT
Introduction: Cigarette smoking (CS) is a well-known risk factor for the development of metabolic diseases, various forms of cancer as well as insulin resistance (IR). IR is considered as an underlying derangement which very commonly aggravates metabolic syndrome. Aim: This study assessed the prevalence of IR in cigarette smokers in Sokoto metropolis using selected surrogate markers. Methodology: This cross sectional study was conducted in Sokoto among 108 subjects. Fasting venous blood samples were collected for plasma glucose, triglycerides and insulin estimation. Plasma glucose and serum triglycerides were analysed using enzymatic methods while insulin was assayed using ELISA method. Homeostasis model of assessment-IR (HOMA-IR), Quantitative insulin sensitivity check index (QUICKI), Mc Auley (McA) and fasting IR index (FIRI) were calculated using standard formula and IR cut-off of >2.5, <0.339, >5.8 and >2.3 respectively were used. Results: Based on the cut off mark, the prevalence of IR for HOMA-IR, QUICKI, McA, FIRI indices were 62(57.4%), 66(61.1%), 39(36.1%) and 60(55.6%) respectively. There was a significant correlation between HOMA-IR and FIRI (p< 0.05, r = 0.999). HOMA-IR also had a significant correlation with McA (p<0.05 r = -0.506). QUICKI had a significant correlation with McA (p<0.05 and r = 0.243). Conclusion: This study established a significantly high prevalence of IR among CS. Importantly, it can be concluded that cigarette smokers may be predisposed to the development of metabolic disease.
ABSTRACT
Background: Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway (PPP) and plays an essential role in the oxidative stress response by producing Nicotinamide adenine dinucleotide phosphate (NADPH), the main intracellular reductant. Deficient individuals suffer from mild chronic haemolytic episode which could be exacerbated on exposure to oxidant drugs. Aim: The aim of the study was to determine the prevalence of G-6-PD deficiency in Sokoto, assess liver function, lipid peroxidation and antioxidants status in G-6-PD deficient individuals. Place and Duration of Study: The study was undertaken at the Department of Chemical Pathology, Faculty of Medical Laboratory Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria, between February and April 2015. Methods: G-6-PD screening in 1000 individuals (603 males and 397 females) using Methaemoglobin Reduction Method was carried out, liver function and oxidative stress biomarkers were then evaluated in 60 deficient individuals (30 males and 30 females) and 60 individuals with normal G-6-PD status as controls using standard techniques. Results: 376 (37.6%) subjects were found to be G-6-PD deficient, 128 (12.8%) of the males and 248 (24.8%) of the females screened were deficient. G-6-PD deficient individuals have significantly low (p<0.05) total protein (TP), aspartate transaminase (AST) and alkaline phosphatase activities when compared to control group but the decreases were within the reference range, while albumin (Alb), total bilirubin (TB) and conjugated bilirubin (CB), alanine transaminase (ALT) and alkaline phosphatase (ALP) values showed no significant difference (p > 0.05). Significantly high (p<0.001) malondialdehyde (MDA) and low total antioxidant potential (TAP) values were obtained in G-6-PD deficient individuals compared to controls. Conclusion: The prevalence of G-6-PD deficiency in Sokoto is high, hence screening for G-6-PD deficiency before administration of oxidant drugs in G-6-PD deficient subjects may be necessary. G-6-PD deficient individuals may also be at the risk of developing oxidative stress induced diseases.