Dr. Girish C. Melkani

Dr. Girish C. Melkani |Clyto Access

San Diego State University, USA




Dr. Melkani received his Ph.D. from Central Drug Research Institute, Lucknow, India. Currently, he is an Assistant Professor (Research) at San Diego State University, San Diego, CA. He is an Adjunct faculty at Sanford Burnham Prebys Medical Discovery Institute and Salk Institute of Biological Studies, LA Jolla. His lab is examining the molecular basis of cardiac and skeletal muscle dysfunction associated metabolic and circadian rhythm dysregulation in diet and genetic obesity, and how time-restricted feeding (TRF) mitigates these defects. He has developed Drosophila models to delay age and diet-induced cardiac dysfunction with TRF and discovered novel pathways which prevent age-associated deterioration of cardiac muscle under TRF conditions (Gill et al. Science 2015; 347:1265-9). He has obtained research grants from the National Institutes of Health and the American Heart Association to run projects in my research lab. Dr. Melkani is the member of the Biophysical Society, Protein Society, American Society for Biochemistry and Molecular Biology, American Society for Cell Biology, American Association for the Advancement of Science and the American Heart Association.



Title: Restoration of Metabolic Rhythms Attenuates Diabetes and Obesity-Induced Cardiometabolic Disorders


The diabetes and obesity epidemic is associated with a number of metabolic diseases, including elevated risk for cardiovascular disease (CVD), insulin resistance in cardiac and skeletal muscle and diabetes. Chronic disruption of circadian clock by erratic eating pattern or sleep deprivation can increase predisposition to obesity and metabolic diseases. Therefore, interventions that improve molecular circadian and metabolic rhythms are potential entry points for prevention and prognosis of cardiometabolic diseases. Taking advantage of the short lifespan and extensive genetic tools available in the Drosophila melanogaster (fruit fly) model, we have recently shownthat imposing a daily rhythm of eating and fasting by time-restricted feeding (TRF) attenuates age-related or high fat diet inducedcardiac dysfunction(Gill et al. Science, 2015). TRF does not trigger a gene expression signature of caloric restriction and its metabolic benefits require an intact circadian clock. To test whether circadian eating pattern can alleviate some of the genetic obesity-induced comorbidities, we subject young Drosophila to TRF.Obese mutant flies showed age-dependent deterioration of cardiac and skeletalmuscle performance followed by increase triglycerides level and compromised insulin sensitivity. They also exhibitsleep perturbation similar to that in humans.Interestingly, obese flies under TRF showed attenuated obesity-induced cardiac and skeletal muscle senescence, possibly by decreasing lipid accumulation, increased insulin sensitivity and by maintaining metabolic homeostasis due to improved sleep.Our findings are potentially applicable to human health such as in community-based approaches to improve cardiovascular and other health matrix outcomes linked with slowing or preventing obesity-induced cardiac disorders and other comorbidities.


Related Conferences :

International Diabetes and Degenerative Diseases Conference