The LIPID Metabolites and Pathway Strategy (MAPS) Annual Meeting was held at UCSD in La Jolla, CA from03-04 May 2010. LIPID MAPS was created in 2003 as a multidisciplinary effort to identify and quantitate all of the major (and some minor) lipid species in mammalian cells and how they change in response to diseases such as atherosclerosis, diabetes, obesity, stroke, cancer, arthritis, Alzheimer’s, inflammatory, and other lipid-based diseases. The meeting presented intriguing results and new methods in the growing lipodomics field. Findings on lipid structure and experimental data demonstrated the broad impact that lipids have on multiple disease indications.
All of the presentations during the 2-day conference were outstanding, but two of them were of particular interest to me. A novel method of cell and tissue imaging was described by Dr. Roger Tsien, UCSD, 2008 winner of the Nobel Prize in Chemistry. This methodology uses both light and fluorescence to detect and allow the surgical removal of solid tumors in cancer. This same technique can also be used in the detection of atherosclerosis and, importantly, will preferentially target vulnerable plaques. This type of breakthrough will be of great benefit in treating cases of advanced atherosclerosis. Dr. Ronald Tomkins (MA General Hospital) discussed inflammation and host response to injury in a large‑scale collaborative program aiming to uncover the biological reasons why patients can have dramatically different outcomes after suffering a traumatic injury. Inflammation plays a major role in these injuries, and an understanding of the body’s mechanisms of inflammation in fighting infection after trauma or burn injury and an understanding of the individual genome will ultimately enable treatment tailored to that specific genome.
One especially intriguing poster presentation was related to the role of macrophages and inflammation in diabetes. The poster was authored by researchers from the University of North Carolina at Chapel Hill (UNC), Duke University, and Vanderbilt University, and entitled “Metabolomic and Genomic Analysis of Cafeteria-Diet Induced Macrophage Infiltration of Adipose Tissue Reveals a Robust Model of Obesity, Inflammation, and Glucose Intolerance.” The poster demonstrated the deleterious effects of a standard high fat (HF) diet and the even greater negative effects of a “cafeteria diet” (CD) that included a random sampling of foods rich in fat, salt, and sugar, and low in fiber and nutrients (e.g., cookies, chips, etc.) that were included as part of the rats’ diet. Dr. Brante Sampey of UNC explained that the CD consists of rat chow plus a daily excess of 3 varied human snacks.
In this study the CD was compared to a traditional Western diet of 45% high fat in rodent models. Male rats were fed either the HF or CD for 15 weeks. The body weight of rats on the CD increased significantly at 2 weeks and remained elevated while the rats on the HF diet did not become obese relative to controls. Glucose levels were higher and insulin responses were lower in the CD than in the HF fed rats. In addition rats fed the CD showed a greater change in genes associated with increased glucose metabolism and the immune response. The CD provided a more potent and robust model of diet-induced obesity compared with the traditional HF diet. Further, there was an increased infiltration of macrophages in fat from the CD, creating an exaggerated obesity with glucose intolerance and inflammation. This model can be used to further study the mechanisms of obesity and obesity-related disease states that are currently rampant in Western civilization. So, next time you reach for a snack, be sure to choose something healthy!
This is a post by Kathy Grako, Ph.D., PMP. Kathy is a Clinical Strategy Scientist in Cato Research’s San Diego, CA office.
