LEARNING OBJECTIVESAfter reading the following article, the reader will be able to answer the following: 1. Identify the major contribution to our understanding of obesity and metabolic syndrome by each of the following researchers: Gerald Reaven, Norman Kaplan, Richard Unger, and Jeffery Friedman. 2. Identify the criteria used for diagnosis of metabolic syndrome (MSX). 2. Identify and describe three outcomes of normal leptin feedback to hypothalamus and three outcomes related to leptin resistance. 3. Describe the relationship between free fatty acids (FFAs) and ceramide and their significance in lipotoxicity and apoptosis. 4. Describe four destructive outcomes of elevated FFAs leading to disease and apoptosis. 5. Identify a proposed physiologic role for leptin that is independent of hypothalamus. 6. List four differences between metabolically healthy obese individuals and those with metabolic syndrome. The Focus section seeks to publish relevant and timely continuing education for clinical laboratory practitioners. Section editors, topics, and authors are selected in advance to cover current areas of interest in each discipline. Readers can obtain continuing education credit (CE) through P.A.C.E. ® by completing the continuing education registration form, recording answers to the examination, and mailing a photocopy of it with the appropriate fee to the address designated on the form. Suggestions for future Focus topics and authors, and manuscripts appropriate for CE credit are encouraged. Direct all inquiries to the Clin Lab Sci Editorial Office, Westminster Publishers, 315 Westminster Court, Brandon MS 39047. (601) 214-5028, (202) 315-5843 (fax). westminsterpublishers@comcast.net.
ABSTRACTMetabolic syndrome (MSX) identifies clinical symptoms and lab results, including abdominal obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hypertension, that lead to an increased risk of cardiovascular disease (CVD). Obesity typically results in insulin and leptin resistance and a shift from expansion of subcutaneous fat to deposition of abdominal and ectopic fat. These conditions cause metabolic dysregulation, elevated fatty acids (FFA), and increased secretion of pro-inflammatory "adipokines". Left untreated, these conditions cause lipotoxicity, chronic inflammation, hypertension, atherosclerosis, and CVD.