Day 3 :
Maria Derylo, DNP, MSN, APN-BC, received her BSN degree from Ryerson University, Toronto, Ontario, Canada, Master’s at D’Youville College in Buffalo, NY, Post-master’s Adult Nurse Practitioner Certifi cate from University of Nebraska Medical Center, Omaha, and her Doctor of Nursing Practice from Case Western Reserve University in Cleveland, Ohio. She worked as Nursing Faculty at University of Nebraska Medical Center, and in Northern Illinois University, DeKalb, IL. Currently, she serves as full time faculty at the Loyola University. She practices as Adult Nurse Practitioner at the family practice comprehensive health services, primary care centers in Chicago, Illinois. She served as a speaker and poster presenter at the numerous national and international conferences. Her research interests are obesity, diabetes, cardiovascular diseases, carcinoid and health care system.
Obesity is a global epidemic with far reaching medical and social consequences. Th is presentation will provide participants with the opportunity to explore every facet of obesity care in one place operational, scientifi c, clinical and business. The goal of this presentation is to engage health care providers in learning about the medical wellness, weight loss and expose them to cutting-edge clinical and research approaches for the recognition, treatment and prevention of obesity. The information is focused on improving patient’s total wellness by utilizing clinical research and evidence-based strategies to address the myriad of comorbid conditions related to obesity to help practitioners to treat the whole person, not just obesity. Resources and tools that are needed to develop comprehensive weight management program will be presented. Th e following topics will be addressed: Basic Science and Obesity, Obesity Algorithm, Obesity defi ned as a disease, Obesity as a multifactorial disease, Obesity Management Goals, Obesity Classifi cation, Adiposopathy, Stress and Obesity, Patient Evaluation: history, physical exam, laboratory and diagnostic testing, Treatment, concurrent medications, The impact of the Aff ordable Care Act on obesity treatment, Health risks associated with obesity, Weight-management technologies, Endocrine disorders and obesity, Pharmacologic options for obesity, Addiction related strategies that can be used to improve weight loss outcomes, Comprehensive, evidence-based, personalized care for patients to reverse diabetes, cardiovascular issues, and many other high risk, high cost medical conditions.
North West University, South Africa
Keynote: Calmodulin dependent protein kinase (CaMK)II activation by exercise regulates NRF-1 and its target lipid oxidizing target gene, Cpt-1 in rat skeletal muscle
Time : 11:05-11:45
Emmanuel Mukwevho has completed his PhD in 2010 from University of Cape Town, South Africa in Anatomy and Cell Biology. He is an Associate Professor of Biochemistry at North West University, South Africa. He has published both nationally and internationally in reputed journals and his specialty is in Obesity and Diabetes where he led the Diabetes & Obesity Therapeutics Research group at North West University.
Regular exercise increases oxidation of fatty acids in skeletal muscle. Exercise activates Calmodulin-dependent protein kinase (CaMK)II, resulting in increased mitochondrial oxidative capacity. As such, exercise can curb accumulation of excess lipids in adipose and intramuscular tissues that may result in obesity/type 2 diabetes. Lipid metabolism mainly occurs in mitochondria regulated by NRF-1 and is controlled by a set of mitochondrial enzymes. For example, Carnitine palmitoyltransferase (CPT)-1 is a rate-limiting enzyme in mitochondrial lipid oxidation that regulates the transport of long chain fatty acids across the mitochondrial membrane, resulting in ATP synthesis. On the other hand, acetyl-CoA carboxylase (ACC)-1 is a mitochondrial enzyme that promotes lipid synthesis by providing malonyl CoA substrate for the biosynthesis of fatty acids. NRF-1 is the major transcriptional factor of the mitochondria, the site for ATP generation from carbohydrates and lipids. As such, mitochondrial dysfunction is crucial in metabolism of the cell. In order to investigate the amount of NRF-1 bound Cpt-1, ChIP assay performed. Exercise showed that the amount of NRF-1 bound Cpt-1 was ~1.3 fold increase compared with the control group. The exercise + KN93 group did not show any signifi cant change compared with the exercise group. This result indicates that exercise-induced CaMKII activation increase the amount of NRF-1 bound Cpt-1. With respective to
gene transcription, exercise group showed ~7.8 fold increase compared with the control group. Cpt-1 gene expression of the exercise + KN93 group showed signifi cant decrease compared with the exercise group. Cpt-1 gene expression of the exercise + KN93 was similar to the control group. Th is result shows that CaMKII activation increase Cpt-1 gene expression in rat skeletal muscle. With respect to mitochondrial integrity, mitochondria size of the exercise group increased by ~3.0 fold compared with the control group, whereas the exercise + KN93 group showed signifi cant decrease compared with the exercise group. Using TEM we show that exercise-induced CaMKII activation increases mitochondria size in rat skeletal muscle and its integrity.