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A single prior bout of exercise protects against palmitate-induced insulin resistance despite an increase in total ceramide content.

Abstract
Ceramide accumulation has been implicated in the impairment of insulin-stimulated glucose transport in skeletal muscle following saturated fatty acid (FA) exposure. Importantly, a single bout of exercise can protect against acute lipid-induced insulin resistance. The mechanism by which exercise protects against lipid-induced insulin resistance is not completely known but may occur through a redirection of FA toward triacylglycerol (TAG) and away from ceramide and diacylglycerol (DAG). Therefore, in the current study, an in vitro preparation was used to examine whether a prior bout of exercise could confer protection against palmitate-induced insulin resistance and whether the pharmacological [50 μM fumonisin B(1) (FB1)] inhibition of ceramide synthesis in the presence of palmitate could mimic the protective effect of exercise. Soleus muscle of sedentary (SED), exercised (EX), and SED in the presence of FB1 (SED+FB1) were incubated with or without 2 mM palmitate for 4 h. This 2-mM palmitate exposure impaired insulin-stimulated glucose transport (-28%, P < 0.01) and significantly increased ceramide, DAG, and TAG accumulation in the SED group (P < 0.05). A single prior bout of exercise prevented the detrimental effects of palmitate on insulin signaling and caused a partial redistribution of FA toward TAG (P < 0.05). However, the net increase in ceramide content in response to palmitate exposure in the EX group was not different compared with SED, despite the maintenance of insulin sensitivity. The incubation of soleus from SED rats with FB1 (SED+FB1) prevented the detrimental effects of palmitate and caused a redirection of FA toward TAG accumulation (P < 0.05). Therefore, this research suggests that although inhibiting ceramide accumulation can prevent the detrimental effects of palmitate, a single prior bout of exercise appears to protect against palmitate-induced insulin resistance, which may be independent of changes in ceramide content.
AuthorsA Brianne Thrush, Ewa Harasim, Adrian Chabowski, Roberto Gulli, Leslie Stefanyk, David J Dyck
JournalAmerican journal of physiology. Regulatory, integrative and comparative physiology (Am J Physiol Regul Integr Comp Physiol) Vol. 300 Issue 5 Pg. R1200-8 (May 2011) ISSN: 1522-1490 [Electronic] United States
PMID21325642 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Ceramides
  • Diglycerides
  • Enzyme Inhibitors
  • Fumonisins
  • Insulin
  • Triglycerides
  • fumonisin B1
  • Palmitic Acid
  • Oxidoreductases
  • dihydroceramide desaturase
  • Glucose
Topics
  • Animals
  • Ceramides (metabolism)
  • Diglycerides (metabolism)
  • Energy Metabolism (drug effects)
  • Enzyme Inhibitors (pharmacology)
  • Female
  • Fumonisins (pharmacology)
  • Glucose (metabolism)
  • In Vitro Techniques
  • Insulin (metabolism)
  • Insulin Resistance
  • Muscle Contraction
  • Muscle, Skeletal (drug effects, metabolism, physiopathology)
  • Oxidation-Reduction
  • Oxidoreductases (antagonists & inhibitors, metabolism)
  • Palmitic Acid (metabolism)
  • Physical Exertion
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors
  • Triglycerides (metabolism)
  • Up-Regulation

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