title: Compromised responses to dietary methionine restriction in adipose tissue but not liver of ob/ob mice.
abstract: OBJECTIVE
  Dietary methionine restriction (MR) reduces adiposity and hepatic lipids and increases overall insulin sensitivity in part by reducing lipogenic gene expression in liver, inducing browning of white adipose tissue (WAT), and enhancing the lipogenic and oxidative capacity of the remodeled WAT.
  
  
  METHODS
  Ob/ob mice have compromised β-adrenergic receptor expression in adipose tissue and were used to test whether MR could ameliorate obesity, insulin resistance, and disordered lipid metabolism.
  
  
  RESULTS
  In contrast to responses in wild-type mice, MR failed to slow accumulation of adiposity, increase lipogenic and thermogenic gene expression in adipose tissue, reduce serum insulin, or increase serum adiponectin in ob/ob mice. However, MR produced comparable reductions in hepatic lipids and lipogenic gene expression in both genotypes. In addition, MR was fully effective in increasing insulin sensitivity in adiponectin(-/-) mice.
  
  
  CONCLUSIONS
  These findings show that diet-induced changes in hepatic lipid metabolism are independent of weight loss and remodeling of WAT and are not required for insulin sensitization. In contrast, the failure of ob/ob mice to mount a normal thermogenic response to MR suggests that the compromised responsiveness of adipose tissue to SNS input is an important component of the inability of the diet to correct their obesity and insulin resistance.
authors.affiliation: Laboratory of Nutrient Sensing and Adipocyte Signaling, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
authors.forename: Kirsten P
authors.initials: KP
authors.lastname: Stone
authors.affiliation: Laboratory of Nutrient Sensing and Adipocyte Signaling, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
authors.forename: Desiree
authors.initials: D
authors.lastname: Wanders
authors.affiliation: Laboratory of Nutrient Sensing and Adipocyte Signaling, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
authors.forename: Lucie F
authors.initials: LF
authors.lastname: Calderon
authors.affiliation: Department of Internal Medicine, Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.|Department of Cell Biology, Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Spurgin
authors.affiliation: Department of Internal Medicine, Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.|Department of Cell Biology, Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
authors.forename: Philipp E
authors.initials: PE
authors.lastname: Scherer
authors.affiliation: Laboratory of Nutrient Sensing and Adipocyte Signaling, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Gettys
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D050154:Adiposity / Q000235:genetics*; D000818:Animals; D007333:Insulin Resistance / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D008297:Male; D008715:Methionine / Q000235:genetics*; D051379:Mice; D009765:Obesity / Q000378:metabolism
chemical_list: D008715:Methionine