RESUMEN
Background: Obesity is a largely neglected health problem in developing countries which leads to additional morbidities including nonalcoholic fatty liver disease (NAFLD), one of the most important causes of chronic liver disease. Central obesity is intricately related to the pathogenesis of the NAFLD, which over time could result in a fibrogenic response and end-stage liver disease. We have attempted to study the association of various risk factors and laboratory investigations with the incidence of liver involvement in obese individuals. Materials and methods: A cross-sectional study of 210 patients was carried out in a tertiary care center in Western India. Patients above 18 years of age with either general or abdominal obesity were included and their history taking and general and systemic examination was done along with laboratory investigations and ultrasonography for visualize any liver involvement. Results: Age >50 years, female gender, postmenopausal state, sedentary lifestyle, high body mass index (BMI), waist circumference (WC), and neck circumference were all risk factors for liver involvement in obese individuals. Raised C-reactive protein (CRP), serum glutamic-oxaloacetic transaminase (SGOT), triglycerides, low density lipoprotein (LDL), cholesterol, fasting blood sugar (FBS), 2-hour postprandial blood sugar (PP2BS), and low high density lipoprotein (HDL), serum protein, and albumin were significantly associated with liver disease. Patients having high NAFLD fibrosis and BMI, aminotransferace ratio and diabetes (BARD) scores, or Metabolic syndrome (MS) was at a higher risk for liver disease. Conclusion: Advancing age, postmenopausal females, and lack of physical activity are risk factors for liver disease in obesity. Raised CRP and SGOT along with impaired lipid profile and glycemic control could be used as markers for fatty liver in obese individuals. MS greatly increases the risk of liver involvement in obese individuals.
RESUMEN
The world is facing an explosive increase in the incidence of diabetes mellitus and cost-effective complementary therapies are needed. The effects of Eugenia jambolana, a household remedy for diabetes, were studied. Streptozotocin diabetic female albino Wistar rats weighing 150-200 g (N = 6) were fed E. jambolana seed powder (250, 500 or 1000 mg/kg) for 15 days. Diabetic rats fed 500 and 1000 mg/kg seed powder showed an increase in body weight on day 20 in relation to day 5 (6 ± 4.7, 9 ± 7.8 vs diabetic control -16 ± 7.1 g, P < 0.001), a decrease in fasting blood glucose (75 ± 11.9, 123 ± 14.4 vs diabetic control -34 ± 12.1 mg/dl, P < 0.001), a difference in post-treatment fasting and peak blood glucose (38 ± 11.9, 36 ± 14.2 vs diabetic control 78 ± 11.9 mg/dl, P < 0.001), and a difference in liver glycogen (50 ± 6.8, 52 ± 7.5 vs normal control 90 ± 6.6 æg/g of liver tissue, P < 0.001). Tri-terpenoids, tannins, gallic acid, and oxalic acid were the chemical constituents detected in E. jambolana seed. The best results were obtained with an oral dose of 500 mg/kg. Subacute toxicity studies with a single administration of 2.5 and 5.0 g/kg seed powder showed no mortality or abnormality. These data on the antidiabetic effect of E. jambolana seed are adequate for approval of phase 2 clinical trials to evaluate this seed powder as complementary therapy in type 2 and type 1 diabetes.