Beyond Obesity: The Diagnosis and Pathophysiology of Metabolic Syndrome

Wayne Gade; Jessica Schmit; Melissa Collins; Jean Gade

doi:10.29074/ascls.23.1.51

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Wayne Gade, PhD, MT(ASCP)⇑
1. Associate Professor, Clinical Lab Science Program, University of Illinois Springfield, Springfield, IL
Jessica Schmit
1. Student, Clinical Lab Science Program, University of Illinois Springfield, Springfield, IL
Melissa Collins, MLS (ASCP)
1. Medical Lab Scientist, Skokie Hospital, 9600 Gross Point Rd, Skokie, IL
Jean Gade, MS, BS(RN)
1. Nurse Educator, Lincoln Prairie Behavioral Health, Springfield, IL

Address for Correspondence: Wayne Gade, Clinical Laboratory Science & Chemistry Departments, HSB Rm 314, One University Place, Springfield, IL 62703, wgade1{at}uis.edu, 217-725-6384.

After 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.
7. Describe “lipid buffering”and how the development of leptin resistance allows fat deposition into non-adipocytes (ectopic fat).
8. Describe why glyceroneogenesis and PEPCK activity are required for “lipid buffering” or fatty acid re-esterification.
9. Describe the signal transduction resulting from leptin binding (JAK/STATsystem), which exerts both transcriptional level control (PPARs) and control of pre-existing enzyme activities through the AMPK system.
10. Discuss the importance of adiponectin (ADN) as an “adipokine” in relation to obesity and metabolic syndrome.
11. Describe the development of atherosclerosis including the inflammatory process that recruits macrophages and list three ways that ADN helps prevent this process.

Abstract

Metabolic 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.