International Conference on Diabetes and Diabetic Nursing Care September 20-21, 2017 Charlotte, North Carolina, USA

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.

Saneh Khunkaew has completed his Master’s degree from Mälardalen University, Sweden. He is a PhD candidate from University of Wollongong School of Nursing, Australia. He is an expert on diabetic foot care.

Diabetes mellitus is the most common metabolic disease which may lead to microvascular circulation problems. A signifi cant problem associated with diabetic foot ulcers is the loss of health-related quality of life (HRQOL). Th e aim of this systematic review was to determine the factors for low health related quality of life among people living with diabetic foot ulcers. A systematic search of the medical and nursing/health content databases including MEDLINE, CINAHL, and PsycINFO was conducted. Random eff ect meta-analysis and narrative analysis were used to identify the factors for low health related quality of life. Twelve observational studies were identifi ed. Four of eight subscales in the SF-36 (physical functioning mean=44.8 (SE 2.8), role physical mean=23.5 (SE 3.9), general health mean=40.09 (SE 2.0), and vitality mean=48.65 (SE 2.2)) were poor among people with diabetic foot ulcers. People who had pain also reported low HRQOL (p<0.05). Furthermore, the biomedical indicators of poor glycaemic control (CRP, ABI, and HbA1c) were related to low HRQOL. Th e ulcers size (Wagner’s grade 2 or 3) was also associated with HRQOL impairment. Th ese fi ndings have identifi ed a number of important factors determining the low HRQOL in people with diabetic foot ulcers. Th e presentation will share the fi ndings from this review to assist health care professionals to make decisions on clinical care and education program to improve the HRQOL among people with diabetic foot ulcers.

Eleanor Cramer is a family nurse practitioner (FNP) who spent the last three semesters as a Doctor of Nursing Practice student (DNP) in the Endocrine Department at a metropolitan academic medical center in New York, NY. She collaborates with a DNP certifi ed diabetic educator and an attending endocrinologist as a consultant for endocrine services for the adult population. The endocrine team covers consultations throughout the hospital and outpatient setting. She is a DNP candidate for October 2017 at Columbia University in New York, NY. She also received her Master of Science degree in Nursing as a Family Nurse Practitioner from Columbia, and is ANCC certifi ed. She completed her Bachelor of Science in Nursing at Villanova University, Villanova, PA, after graduating from St. Joseph’s Hospital School of Nursing, Reading Pennsylvania. Prior to becoming an FNP, she spent 37 years as a critical care nurse, working in various critical care settings.

Introduction: Ketosis Prone Type 2 Diabetes (KPD) is also known as “Flatbush Diabetes”, due to the cluster of patients identifi ed in the Flatbush section of Brooklyn, NY with new onset of type 2 diabetes accompanied by Diabetic Ketoacidosis (DKA) as the fi rst manifestation. Th ese patients have an absence (A-) or presence (A+) of islet cell autoantibodies and quantitive diff erences in beta cell function. Th e A-B+ is the most frequent manifestation. Th ese patient’s parameters resemble type 2 diabetes, in that it usually occurs in the adult population, they are overweight or obese, a strong family history of type 2 diabetes, do not have islet cell autoantibodies, and have a plentiful reserve of pancreatic beta cells, which have been measured aft er the “index” case of KPD. Th ey may also have physical signs such as acanthosis nigricans and abdominal straie. Th ey have an unprovoked episode of diabetic ketoacidosis (DKA), and may have blurred vision, nausea, vomiting or abdominal pain, which bring them to the emergency department. Th ey may also have polyuria resulting in dehydration secondary to blood glucose numbers far in excess of type 1 diabetics. Treatment is the same as for any DKA patient, and they usually are treated with a basal/bolus regimen, along with metformin, which is increased as tolerated. Th ey generally have rapid beta cell recovery and many eventually stay on metformin as a preventative measure; some require only lifestyle modifi cations. Th is holiday period may last from months to years. Th e most common subtype of KPD is A- B+ (54%). Case: 33-year-old African American woman, With a BMI of 42 mg/kg m2, G 6, P 2. Her children are aged 15 and 5. She had little prenatal care with her fi rst child, and at time of labor she was found to have gestational diabetes (GDM). She was started on basal bolus insulin with levemir and lispro, which was continued post-partum, but eventually eliminated over the course of several months, and she did not require metformin. She was carefully followed with the second child, and was treaded with insulin throughout her pregnancy, and discontinued in the immediate post-partum period. In the fi ve years since, she has had no recurrence of diabetes, until this DKA event. No precipitating cause, such as infection, increased stress or steroid use was identifi ed. She had a blood glucose more 700 mg/dL, and a HBA1c of 13%. She responded rapidly to insulin and rehydration, and was weaned from insulin to metformin, and fi nally just diet control over the next three months. One year later she still has not had a recurrence of DKA or evidence of persistent diabetes, with decrease of HBA1c to high normal range. Discussion: Th is case is a good example of the need for identifi cation of presence or absence of autoantibodies in a younger patient who presents in DKA who could quite possibly have type 1 diabetes. It also shows that with careful monitoring and titration, medication can be temporary for a signifi cant amount of time. Th is patient had the desire for another pregnancy, and was referred to high risk OB care to reinforce the need for keeping with her diet to lose weight and to decrease her HBA1c to prepare her body for pregnancy and prevent the known teratogenic eff ects of hyperglycemia to the developing fetus.