Olga Tarasova is an Associate Professor of Hospital, Therapy department of RUDN University, Doctor-hepatologist of the Liver Research Center of the Medical Institute of RUDN University. She repeatedly spoke at international conferences of the American and European, Pacific associations for the study of liver diseases (DDW, AASLD, EASL, APASL) including Singapore, New York and Chicago. She has 15 years of experience in the treatment of patients with chronic and severe liver damage, hepatitis and cirrhosis based on the university's clinic. She has published more than 25 scientific and educational-methodical works
Aim: To decide whether adding metformin an agent reducing insulin resistance (IR), improves treatment effi cacy of chronic hepatitis C (genotype 1) in naïve patients. Methods: 133 treatment-naïve patients were tested: 70 patients with IR and 63 patients without it. 28 of 70 patients with IR received metformin. Metformin was added to a standard Peg-IFNα-2b/ribavirin therapy at the very start of treatment or 3-6 months before the start and continued throughout the whole course of treatment. Patients in the second control group with IR did not receive metformin (n=42). Patients in both groups receiving and not receiving metformin did not diff er signifi cantly in viral load, the degree of liver fi brosis (measured with FibroScan®502) and gender. Results: Among the patients with HCV-1 without IR, SVR rate was 46% (n=29/63) and in those who had IR (not receiving metformin) the rate of SVR was 42% (n=18/42), p=0.33. Among patients with HCV-1 and with IR, receiving metformin, the SVR rate was 64% (n=18/28), p=0.001. Signifi cant reduction of glucose levels among patients with IR receiving metformin was not revealed. Conclusion: Adding metformin to a standard Peg-IFNα-2b/ribavirin therapy for treatment-naïve HCV-1 patients with IR leads to an increase of SVR by 1.5 times. Metformin is safe and efficient for patients with chronic hepatitis C and IR as a drug reducing IR.
Emmanuel Mukwevho is a Professor of Biochemistry at the school of Chemical and Physical Sciences, at the NWU in South Africa. He has graduated for his PhD from University of Cape Town in June, 2010. He teaches Biochemistry in both undergraduate and postgraduate, especially Metabolism and Analytical Biochemistry. He has also obtained Certifi cates in Project Management and in Financial Management from UCT both in 2012. He is currently registered for MBA with NWU Graduate Business School.
AMPK is known to control both glucose and lipid metabolism, two main candidates critical in the development of type-2 diabetes (T2D). Studies have shown that AMPK can be activated by adiponectin. Patients suff ering from T2D are known to have low adiponectin concentration in their blood plasma. In this study, we have assessed one of the anti-diabetic compound Oleanolic acid (OA) if it could produce desirable eff ect in upregulating adiponectin concentration and the subsequent regulation of AMPK. Sprague Dawley rats were fed with high fructose diet (HFD) to induce T2D, and the rats that developed insulin resistance were considered as diseased, they were then treated with OA. Analysis of adiponectin concentration in blood plasma was done, AMPK gene expression and subsequent genes that play vital role in glucose and lipid metabolism (GLUT-4 and CPT-1) in skeletal muscle tissue was also performed. Th e results showed 1.19-fold increase in blood plasma adiponectin concentration aft er OA administration. Furthermore AMPK gene expression showed 3.98-fold increase and GLUT-4 gene expression was increased with 1.5-fold whereas CTP-1 gene expression was increased with 1.59-fold. Th ese results clearly indicate that OA produced good eff ects in ameliorating insulin resistance since it could upregulate all the genes and adiponectin concentration which are well known to be abnormally suppressed in a situation of T2D. In conclusion, these studies further confi rm that OA can be used as an eff ective therapeutic agent to ameliorate T2D and these studies also suggest that OA’s mechanism of action it could be through AMPK pathway.