title: Dietary intake of green tea polyphenols regulates insulin sensitivity with an increase in AMP-activated protein kinase α content and changes in mitochondrial respiratory complexes.
abstract: METHODS
  The intake of food rich in polyphenols is related to a lower incidence in almost all chronic degenerative diseases. However, relatively little is known about the molecular mechanisms involved in its antioxidant properties. The aim of this study was to determine whether the mechanism of action of polyphenols could be related to a modulation in energy uptake and metabolism, and further induced mitochondrial changes.
  
  
  RESULTS
  For this purpose, male C57BL6 mice were fed during 3 months with a tea-based beverage rich in polyphenols. Insulin sensitivity, tissue oxidative damage biomarkers, as well as energy-related signaling pathways were determined to evaluate its mechanism of action. As a result, a tissue- and protein-specific subtle reduction in oxidative damage was observed. Skeletal muscle showed mitochondrial changes in respiratory complexes and an increase in AMP-activated protein kinase α levels, suggesting reduced energy availability. These changes were also associated with adipose tissue cellular metabolism. This was confirmed by a decline in the potential of energy uptake, evidenced by a diminished intestinal and systemic absorption of carbohydrates together with an inhibition of insulin sensitivity.
  
  
  CONCLUSIONS
  Our results suggest that the mechanisms of action of green tea polyphenols may be related to their ability to modulate energy uptake leading to mitochondrial adaptations possibly responsible for the changes in protein oxidative damage.
authors.affiliation: Department of Experimental Medicine, Faculty of Medicine, University of Lleida-IRBLleida, Lleida, Spain. jceserrano@mex.udl.cat
authors.forename: José C E
authors.initials: JC
authors.lastname: Serrano
authors.forename: Hugo
authors.initials: H
authors.lastname: Gonzalo-Benito
authors.forename: Mariona
authors.initials: M
authors.lastname: Jové
authors.forename: Stéphane
authors.initials: S
authors.lastname: Fourcade
authors.forename: Anna
authors.initials: A
authors.lastname: Cassanyé
authors.forename: Jordi
authors.initials: J
authors.lastname: Boada
authors.forename: Marco A
authors.initials: MA
authors.lastname: Delgado
authors.forename: Alberto E
authors.initials: AE
authors.lastname: Espinel
authors.forename: Reinald
authors.initials: R
authors.lastname: Pamplona
authors.forename: Manuel
authors.initials: M
authors.lastname: Portero-Otín
mesh_terms: D041721:3T3-L1 Cells / Q000187:drug effects; D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D050260:Carbohydrate Metabolism / Q000187:drug effects; D002149:Energy Intake / Q000187:drug effects*; D007333:Insulin Resistance; D020738:Leptin / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D059808:Polyphenols / Q000494:pharmacology*; D021122:Protein Subunits; D011506:Proteins / Q000378:metabolism; D013662:Tea / Q000737:chemistry*
chemical_list: D000975:Antioxidants; D020738:Leptin; D059808:Polyphenols; D021122:Protein Subunits; D011506:Proteins; D013662:Tea; D055372:AMP-Activated Protein Kinases