title: Duodenal-jejunal bypass surgery induces hepatic lipidomic alterations associated with ameliorated hepatic steatosis in mice.
abstract: Bariatric surgery induces weight loss and improvement of insulin resistance; one aspect of both is an amelioration of hepatic steatosis. This study was undertaken to assess the changes in the hepatic lipidome after duodenal-jejunal bypass (DJB) surgery.
  
  
  
  A DJB surgical model was developed and characterized in diet-induced obese mice. In comparison with sham-operated mice, an unbiased lipidomic profiling of hepatic lipids was performed together with measurements of gene expression within key pathways of hepatic lipid metabolism.
  
  
  
  In the liver of DJB mice, a dramatic reduction (by 77%) in hepatic triacylglycerols was observed. Global lipidomic profiling identified marked decreases of triacylglycerols comprised of medium length fatty acids and with low double bond content. Specific diacylglycerol species were also among the most dramatic decreases in hepatic lipids, whereas lysophosphatidic acids and phosphatidic acids were increased. Expression of fatty acid transporter and lipogenic genes was down-regulated.
  
  
  
  From in-depth analysis of hepatic lipid composition, specific lipid intermediates were identified that are preferentially changed following DJB surgery. These changes were most likely due to DJB-induced weight loss, and only further studies will be able to distinguish weight loss-dependent from weight loss-independent changes.
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Jin
authors.initials: J
authors.lastname: Shang
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Jose M
authors.initials: JM
authors.lastname: Castro-Perez
authors.affiliation: Safety Assessment and Laboratory Animal Resource, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Xiaolan
authors.initials: X
authors.lastname: Shen
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Yonghua
authors.initials: Y
authors.lastname: Zhu
authors.affiliation: Imaging, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Haiying
authors.initials: H
authors.lastname: Liu
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Ying
authors.initials: Y
authors.lastname: Qian
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Stephen
authors.initials: S
authors.lastname: Previs
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Howard
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Mark
authors.initials: M
authors.lastname: Erion
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: David E
authors.initials: DE
authors.lastname: Kelley
authors.affiliation: Cardiometabolic Disease, Merck Research Laboratories, Kenilworth, New Jersey, USA.
authors.forename: Liangsu
authors.initials: L
authors.lastname: Wang
mesh_terms: D000818:Animals; D050110:Bariatric Surgery; D001786:Blood Glucose / Q000378:metabolism; D004386:Duodenum / Q000601:surgery*; D005234:Fatty Liver / Q000378:metabolism* / Q000601:surgery; D015390:Gastric Bypass / Q000379:methods; D007333:Insulin Resistance; D007583:Jejunum / Q000601:surgery*; D008297:Male; D051379:Mice
chemical_list: D001786:Blood Glucose