title: Improvements in glycemic control after gastric bypass occur despite persistent adipose tissue inflammation.
abstract: Type 2 diabetes commonly goes into remission following Roux-en-Y gastric bypass (RYGB). As the mechanisms remain incompletely understood, a reduction in adipose tissue inflammation may contribute to these metabolic improvements. Therefore, whether RYGB reduces adipose tissue inflammation compared with equivalent weight loss from an intensive lifestyle intervention was investigated.
  
  
  
  Sixteen people with obesity and type 2 diabetes were randomized to RYGB or lifestyle intervention. Fasting blood and subcutaneous abdominal adipose tissue were obtained before and after the loss of ∼7% of baseline weight. Adipose tissue inflammation was assessed by whole-tissue gene expression and flow cytometry-based quantification of tissue leukocytes.
  
  
  
  At 7% weight loss, insulin and metformin use were reduced among the RYGB but not the Lifestyle cohort, while fasting glucose and insulin declined in both. Adipose tissue inflammation increased modestly after RYGB and to a similar extent following nonsurgical weight loss. In both groups, the number of neutrophils increased severalfold (P < 0.001), mRNA levels of the proinflammatory cytokine interleukin-1β increased (P = 0.037), and mRNA expression of the anti-inflammatory and insulin-sensitizing adipokine adiponectin decreased (P = 0.010).
  
  
  
  A reduction in adipose tissue inflammation is not one of the acute weight loss-independent mechanisms through which RYGB exerts its antidiabetes effects.
authors.affiliation: Division of Public Health Sciences, Cancer Prevention Program, Fred Hutchinson Cancer Research Center (FHCRC), Seattle, Washington, USA.|Department of Medicine, Division of Metabolism, Endocrinology & Nutrition, University of Washington, Seattle, Washington, USA.|Department of Epidemiology, University of Washington, Seattle, Washington, USA.
authors.forename: Mario
authors.initials: M
authors.lastname: Kratz
authors.affiliation: Division of Public Health Sciences, Cancer Prevention Program, Fred Hutchinson Cancer Research Center (FHCRC), Seattle, Washington, USA.
authors.forename: Derek K
authors.initials: DK
authors.lastname: Hagman
authors.affiliation: Division of Public Health Sciences, Cancer Prevention Program, Fred Hutchinson Cancer Research Center (FHCRC), Seattle, Washington, USA.
authors.forename: Jessica N
authors.initials: JN
authors.lastname: Kuzma
authors.affiliation: Department of Medicine, Division of Metabolism, Endocrinology & Nutrition, University of Washington, Seattle, Washington, USA.
authors.forename: Karen E
authors.initials: KE
authors.lastname: Foster-Schubert
authors.affiliation: Department of Surgery, University of Washington, Seattle, Washington, USA.
authors.forename: Chun P
authors.initials: CP
authors.lastname: Chan
authors.affiliation: Department of Surgery, University of Washington, Seattle, Washington, USA.
authors.forename: Skye
authors.initials: S
authors.lastname: Stewart
authors.affiliation: Diabetes Research Center, Virus Vector and Transgenic Mouse Core, University of Washington, Seattle, Washington, USA.
authors.forename: Brian
authors.initials: B
authors.lastname: van Yserloo
authors.affiliation: Group Health Research Institute, Seattle, Washington, USA.
authors.forename: Emily O
authors.initials: EO
authors.lastname: Westbrook
authors.affiliation: Group Health Research Institute, Seattle, Washington, USA.
authors.forename: David E
authors.initials: DE
authors.lastname: Arterburn
authors.affiliation: Department of Epidemiology, University of Washington, Seattle, Washington, USA.|Department of Surgery, University of Washington, Seattle, Washington, USA.
authors.forename: David R
authors.initials: DR
authors.lastname: Flum
authors.affiliation: Department of Medicine, Division of Metabolism, Endocrinology & Nutrition, University of Washington, Seattle, Washington, USA.
authors.forename: David E
authors.initials: DE
authors.lastname: Cummings
mesh_terms: D052242:Adiponectin / Q000235:genetics; D000273:Adipose Tissue / Q000503:physiopathology*; D001786:Blood Glucose / Q000032:analysis*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology; D005260:Female; D015390:Gastric Bypass; D006801:Humans; D007249:Inflammation; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D053583:Interleukin-1beta / Q000235:genetics; D008019:Life Style; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D012333:RNA, Messenger / Q000032:analysis; D015431:Weight Loss
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D053583:Interleukin-1beta; D012333:RNA, Messenger