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Central role of ceramide biosynthesis in body weight regulation, energy metabolism, and the metabolic syndrome

Academic Article
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Overview

authors

  • Yang, G.
  • Badeanlou, L.
  • Bielawski, J.
  • Roberts, Amanda
  • Hannun, Y. A.
  • Samad, F.

publication date

  • July 2009

journal

  • American Journal of Physiology-Endocrinology and Metabolism  Journal

abstract

  • Although obesity is associated with multiple features of the metabolic syndrome (insulin resistance, leptin resistance, hepatic steatosis, chronic inflammation, etc.), the molecular changes that promote these conditions are not completely understood. Here, we tested the hypothesis that elevated ceramide biosynthesis contributes to the pathogenesis of obesity and the metabolic syndrome. Chronic treatment for 8 wk of genetically obese (ob/ob), and, high-fat diet-induced obese (DIO) mice with myriocin, an inhibitor of de novo ceramide synthesis, decreased circulating ceramides. Decreased ceramide was associated with reduced weight, enhanced metabolism and energy expenditure, decreased hepatic steatosis, and improved glucose hemostasis via enhancement of insulin signaling in the liver and muscle. Inhibition of de novo ceramide biosynthesis decreased adipose expression of suppressor of cytokine signaling-3 (SOCS-3) and induced adipose uncoupling protein-3 (UCP3). Moreover, ceramide directly induced SOCS-3 and inhibited UCP3 mRNA in cultured adipocytes suggesting a direct role for ceramide in regulation of metabolism and energy expenditure. Inhibition of de novo ceramide synthesis had no effect on adipose tumor necrosis factor-alpha (TNF-alpha) expression but dramatically reduced adipose plasminogen activator inhibitor-1 (PAI-1) and monocyte chemoattactant protein-1 (MCP-1). This study highlights a novel role for ceramide biosynthesis in body weight regulation, energy expenditure, and the metabolic syndrome.

subject areas

  • Adipose Tissue
  • Animals
  • Body Weight
  • Ceramides
  • Energy Metabolism
  • Fatty Acids, Monounsaturated
  • Ion Channels
  • Lysophospholipids
  • Male
  • Metabolic Syndrome
  • Mice
  • Mice, Inbred C57BL
  • Mitochondrial Proteins
  • Obesity
  • Organ Size
  • Sphingolipids
  • Sphingosine
  • Suppressor of Cytokine Signaling Proteins
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Research

keywords

  • insulin resistance
  • leptin resistance
  • monocyte chemoattactant protein-1
  • plasminogen activator inhibitor-1
  • sphingolipids
  • suppressor of cytokine signaling-3
  • tumor necrosis factor-alpha
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Identity

PubMed Central ID

  • PMC2711669

International Standard Serial Number (ISSN)

  • 0193-1849

Digital Object Identifier (DOI)

  • 10.1152/ajpendo.91014.2008

PubMed ID

  • 19435851
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Additional Document Info

start page

  • E211

end page

  • E224

volume

  • 297

issue

  • 1

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