Sphingolipids and Metabolic Disease

  • L. Ashley Cowart

Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 721)

Table of contents

  1. Front Matter
    Pages i-xvii
  2. Sarah E. Brice, L. Ashley Cowart
    Pages 1-17
  3. Marcin Baranowski, Jan Górski
    Pages 41-56
  4. Fahumiya Samad, Leylla Badeanlou, Charmi Shah, Guang Yang
    Pages 67-86
  5. Benjamin T. Bikman, Scott A. Summers
    Pages 87-97
  6. Johannes M. Aerts, Rolf G. Boot, Marco van Eijk, Johanna Groener, Nora Bijl, Elisa Lombardo et al.
    Pages 99-119
  7. Andrew R. Mather, Leah J. Siskind
    Pages 121-138
  8. Back Matter
    Pages 149-152

About this book


Current thinking holds that obesity derives primarily from overnutrition (though compelling arguments for other mechanisms, like endocrine disruption by environmental pollutants, also gain support from the literature). In animals, overnutrition is initially handled by adipose tissue expansion; however, exhaustion of this route of lipid sequestering results in oversupply of lipid to other tissues including skeletal muscle, heart, liver, and others. Failure of these tissues to clear excess lipids through either metabolism or sequestration into putatively inert triacylglycerols results in perturbation of bioactive lipid metabolism in cells. In particular, aberrant generation of bioactive sphingolipids is implicated in a multitude of pathological outcomes of metabolic disease including insulin resistance, inflammation, cardiomyopathy, and others. This volume addresses not only the fundamentals of sphingolipid metabolism and analysis, but also the roles of sphingolipids in these disease processes.


Cowart Disease Metabolic Obesity Sphingolipid

Editors and affiliations

  • L. Ashley Cowart
    • 1
  1. 1.Department of Biochemistry and Molecular BiologyMedical University of South Carolina, and Ralph H. Johnson Veteran’s AdministrationCharlestonUSA

Bibliographic information