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 and Aim: Different parts of Phyllanthus amarus are being used in the treatment of different diseases in several parts of Nigeria without considering its safety. This study was aimed at investigating the effect of ingestion of methanolic leaf extract of Phyllanthus amarus on the liver of Wistar rats. Materials and Methods: The acute oral toxicity of the leaf extract (LD50) was determined in 9 Wistar rats divided into 3 groups of 3 rats per group. Group 1 was the control and received distilled water. Different doses of 2000 mg/kg and 5000 mg/kg were administered orally once to the study groups 2 and 3 respectively. A sub-chronic toxicity study was carried out in 25 Wistar rats, divided into five groups of 5 rats per group. Group 1 served as control and received distilled water. The remaining 4 groups (2, 3, 4 and 5) served as the study groups and were administered different doses of 250 mg/kg, 500 mg/kg, 750 mg/kg and 1000 mg/kg of methanolic leaf extract of Phyllanthus amarus respectively on a daily basis for 28 days. Total protein (TP), albumin (ALB), total and conjugated bilirubin (TB and CB), aspartate and alanine transaminase (AST and ALT), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) were assayed using standard techniques. Results: In the acute oral toxicity study, no death or any sign of toxicities were recorded in the rats after 24 hours and up to 14 days post oral administration and there was no significant difference (P>0.05) in all the parameters analysed between the control and the study groups. In sub-chronic toxicity study, there was no significant difference (P>0.05) in all parameters analysed between the control and study groups. Histology of the liver of the rats in both the acute and sub-chronic study showed normocytic and normochromic cells. Conclusion: Methanolic leaf extract of Phyllanthus amarus is relatively non-toxic and is not likely to induce liver damage.
ABSTRACT
Background: Glucose-6-phosphate dehydrogenase deficiency is one of the most common enzyme defects affecting all races and particularly in malaria-endemic areas. This study aimed at determining G6PD deficiency, bilirubin and oxidative stress biomarkers in G6PD deficient neonates among neonates in UDUTH, Sokoto. Methods: Samples of cord blood were collected at delivery, in the Labour Room, from 300 neonates made up of 131 (43.7%) males and 169 (56.3%) females. Methaemoglobin reduction method was used for the screening of G6PD deficiency; total bilirubin level was estimated using bilirubinometer, total antioxidant capacity (TAC) was measured using TAC Assay Kit, and malondialdehyde (MDA) using thiobarbituric acid method. Results: Of the 300 neonates tested, a total of 90(30%) were G6PD-deficient while 210(70%) had normal G6PD status. Of the 90 G6PD-deficient neonates, 41(45.6%) were males and 49(54.4%) were females. The prevalence was 31.3% among male population and 29.0% among female population. The mean ± standard error of total bilirubin (mg/dL), TAC (uM CRE), and MDA (nmol/L) in G6PD-deficient and G6PD-normal neonates were 6.63 ± 0.12 and 6.11 ± 0.06, 364.34 + 18.76 and 390.99 + 24.18, 26.15 + 1.22 and 23.35 + 1.15 respectively. The total bilirubin was significantly higher (p<0.05) in G6PD-deficient neonate than in G6PD-normal neonates, both TAC and MDA values showed no significant difference between the G6PD deficient and G6PD normal neonates. Conclusion: From this study, there is a high prevalence of G6PD deficiency among neonates in UDUTH, Sokoto. G6PD deficiency is a known cause of neonatal jaundice hence it is recommended G6PD screening be made routine for all neonates born in UDUTH, Sokoto.
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.