Objective: To assess the prevalence and determinants of hyperuricemia among type 2 diabetic patients on follow-up at Jimma Medical Center from March 1 to June 30, 2019. Methods: This institution-based cross-sectional study was used to assess the level of serum uric acid in type 2 diabetic patients attending their follow-up at Jimma Medical Center chronic illness clinic. A systematic sampling technique was used to include 287 type 2 diabetic patients in the study and an interviewer-based questionnaire was used to collect important data from each participant. Five milliliters of blood were collected from each participant under sterile conditions and serum was separated by centrifugation at 3000 rpm for 10 minutes. Serum was stored at −20°C and analyzed for serum uric acid using an ABX Pentra 400 clinical chemistry analyzer. Bivariate and multivariable binary logistic regression were used to assess significant associations between hyperuricemia and independent factors. A p-value of <0.05 was considered significant in the final model. Results: The mean±SD age of the study participants was 51.79±14.36 years. The prevalence of hyperuricemia was found to be 22% (n=66/287) in the study population. Hyperuricemia was common in those aged ≥60 years and males. Obesity (AOR=7.84, 95% CI=2.005-30.666), duration of diabetes mellitus (DM) ≥10 years (AOR=3.963, 95% CI=1.902-8.259), family history of CVD (AOR=2.929, 95% CI=1.124-7.630), alcohol drinking (AOR=5.83, 95% CI=2.341-14.545) and increased DBP (AOR=4.198, 95% CI=1.772-9.949) were determinant variables for hyperuricemia in type 2 DM. Conclusion: Hyperuricemia was relatively common among type 2 diabetic patients. The prevalence of hyperuricemia was common among patients with obesity, a long duration of DM and increased diastolic blood pressure, and alcohol drinkers. There is a need to raise awareness of lifestyle modification, healthy behavior and early diagnosis of hyperuricemia in type 2 diabetic patients.

Background. Foods fried with oils at streets contain many harmful substances for health. Locally fried foods are consumed commonly in our society, yet their health effect is not studied. Objective. To assess the effect of palm oil-fried street kokor on liver and kidney biomarkers of Swiss Albino mice. Methods. Thirty-two male and female Swiss Albino mice with the age of 10-12 weeks old were divided randomly into four groups of eight members with equal male and female subgroups. The control group (group I) received only a standard pellet, and the experimental groups (group II, group III, and group IV) received 10%, 20%, and 30% kokor of their daily food consumption, respectively. At the end of the 6th week, they were sacrificed by thoracoabdominal incision after anesthetizing by diethyl ether. Blood was taken from each mouse by cardiac puncture and analyzed for liver and kidney function tests. Result. The serum levels of liver damage biomarkers (alanine transaminase (ALT) and aspartate transaminase (AST)) and kidney damage biomarkers (urea and creatinine) of experimental groups were increased significantly relative to the control groups ( P < 0.05 ). Level of biochemical profiles increased as the dose of kokor increased. Conclusions. Palm oil-fried street kokor damaged the liver and kidney of the mice, and the damage was exacerbated as the dose of kokor increased.

Introduction. Nephrotoxicity is the most common and severe side effect of cisplatin. Cisplatin causes nephrotoxicity through free radical production and debilitating cellular antioxidant capacity. Coffee is a commonly consumed drink and its ingredients have antioxidant roles that could bring benefits to patients affected by nephrotoxicity. Thus, the present study aimed to investigate the renoprotective effects of our locally grown green coffee beans against cisplatin-induced nephrotoxicity in Swiss albino mice. Methods. The posttest only control group design was employed on a total of thirty male Swiss albino mice. The mice were divided into five groups: group I (normal control group) received distilled water; group II (negative control group) received distilled water; and groups III–V (treatment groups) received 100, 200, and 300 mg/kg BW/day of green coffee bean extract for 14 days, respectively. Nephrotoxicity was induced in groups II–V by a single intraperitoneal injection of cisplatin (7.5 mg/kg). All mice were sacrificed after 14 days and blood was drawn to evaluate kidney function tests (serum creatinine and serum blood urea nitrogen). Besides, body weight, relative kidney weight, and kidney histopathology were investigated. Result. Our results showed that treatment of cisplatin alone (group II mice) significantly increased serum creatinine, serum blood urea nitrogen, relative kidney weight, and pathological damage to the kidney with a decrease in final body weight. However, low-dose green coffee beans (group III), medium-dose green coffee beans (group IV), and high-dose green coffee beans (group V) mice showed a significant dose-dependent decrease in serum creatinine, serum blood urea nitrogen, and relative kidney weight. Furthermore, the dose-dependent treatment with green coffee bean extract prevented the decrease in body weight gain and pathological damage to the kidney in mice. Conclusion. Our locally grown green coffee beans brought a dose-dependent ameliorative effect and a promising preventive approach against cisplatin-induced kidney damage in mice.

No abstract

Background: Highly Active Antiretroviral Therapy (HAART) has significantly enhanced the life expectancy of HIV-infected patients. However, utilization of HAART has been identified with adverse events including nonalcoholic fatty liver disease (NAFLD). Objectives: The Objective of this experiment was to explore the conceivable protective effect of green tea (Camellia sinensis) hydro-methonolic extract (GTE) on highly active antiretroviral therapy-induced NAFLD in albino Wistar rats. Methods: Thirty adult rats of comparative weights were chosen and divided into 5 groups of six rats each. Group-1 was a control group, Group II was given HAART and served as negative control, Groups III, IV and V were given HAART and 100, 200 and 400 mg/kg of GTE, respectively for sixty days. At the end of experiment day, the rats were fasted overnight sacrificed by cervical dislocation and blood was taken via cardiac puncture. Serum was separated and liver function test was assessed. Liver were excised from the rats, histopathological studies and lipid profiles were also investigated. Results: Elevated levels of serum TGL, total cholesterol, ALT, AST and liver TGL, TBARS and decreased levels of TAC was seen in HARRT treated rats. The amelioration potential of GTE was observed in a dose-dependent manner, the highest dose 400mg/kg more potently ameliorated HAART affected parameters near to the normal control. Conclusion: This consequence of HAART induced NAFLD may be due to oxidative stress by mitochondrial ROS that leads to increased hepatocellular oxidative damage. This may progress to hepatic inflammation and the development of NAFLD. The effect of GTE against NAFLD and oxidative stress might be due to its antioxidant activity and scavenging of reactive oxygen species induced by HAART.