Dr Andrew Butler

Associate Professor, Department of Metablolism and Aging, The Scripps Research Institute - Scripps Florida, USA

Dr Butler completed graduate training at the University of Auckland’s School of Medicine in 1995 in New Zealand. He moved to the United States for post doctoral training, spending two years in Derek LeRoith’s laboratory studying the biology of the insulin like growth factor-1 receptor at the Diabetes Branch of the National Institutes of Diabetes, Digestive and Kidney Disease in Bethesda, Maryland. He then relocated to Dr Roger Cone’s laboratory at the Vollum Institute for Advanced Biomedical Research on the campus of the Oregon Health & Science University in Portland, Oregon. Dr Butler’s interest in melanocortin biology began in Dr Cone’s laboratory, and the control of homeostasis by the melanocortin-3 receptor (MC3R) remains one of the central themes in the laboratory. In 2001, Dr Butler moved to the Pennington Biomedical Research Center in Baton Rouge, Louisiana. At that time, the Pennington was the only center in the world dedicated exclusively to the study of the conditions associated with the Western lifestyle: obesity and diseases of the Metabolic Syndrome. During his tenure at this center, Dr Butler created an independent laboratory focused on how organisms maintain body weight and the homeostatic control of glucose and lipid metabolism. Dr Butler’s group investigated the role of MC3Rs in regulating the anticipatory response to nutrient intake, developing a sophisticated conditional genetic strain (the LoxTB MC3R mouse) that is being used to dissect the neural and non-neural pathways involved. Dr Butler’s laboratory also made important contributions to studies examining the regulation of glucose homeostasis by melanocortin-4 receptors. While studying the regulation of peripheral metabolism by melanocortins, Dr Butler’s laboratory identified a peptide hormone named adropin (“sets fire to fat”) encoded by the Energy Homeostasis Associated gene. The naming of the protein and gene was based on the dramatic improvements in steatosis and delayed obesity observed with adropin treatment. Delivery of adropin, either by injection of the synthetic peptide or transgenic over expression, improves the metabolic condition of obese mice. Dr Butler’s laboratory has developed a new genetic model to further investigate adropin function. Flanking the adropin open reading frame with loxP sites allows for tissue-selective deletion of adropin production. Analysis of the whole-body adropin knockout by removing the adropin open reading frame from the germline is consistent with functions related to homeostasis. The knockouts display a 1.5 to 2.0-fold increase in fat mass compared to wild type controls, and also exhibit hepatic steatosis and dyslipidemia. The whole body knockouts display hyperinsulinemia and hepatic insulin resistance, as assessed using the hyperinsulinemic-euglycemic clamp in conscious mice. In 2009, Dr Butler moved to the Florida Campus of The Scripps Research Institute. Dr Butler’s laboratory continues to investigate MC3R function, while also maintaining an interest in a peptide hormone with important but poorly undefined functions in homeostasis.