title: Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease.
abstract: BACKGROUND
  Liposuction has been proposed as a potential treatment for the metabolic complications of obesity. We evaluated the effect of large-volume abdominal liposuction on metabolic risk factors for coronary heart disease in women with abdominal obesity.
  
  
  METHODS
  We evaluated the insulin sensitivity of liver, skeletal muscle, and adipose tissue (with a euglycemic-hyperinsulinemic clamp procedure and isotope-tracer infusions) as well as levels of inflammatory mediators and other risk factors for coronary heart disease in 15 obese women before and 10 to 12 weeks after abdominal liposuction. Eight of the women had normal glucose tolerance (mean [+/-SD] body-mass index, 35.1+/-2.4), and seven had type 2 diabetes (body-mass index, 39.9+/-5.6).
  
  
  RESULTS
  Liposuction decreased the volume of subcutaneous abdominal adipose tissue by 44 percent in the subjects with normal glucose tolerance and 28 percent in those with diabetes; those with normal oral glucose tolerance lost 9.1+/-3.7 kg of fat (18+/-3 percent decrease in total fat, P=0.002), and those with type 2 diabetes lost 10.5+/-3.3 kg of fat (19+/-2 percent decrease in total fat, P<0.001). Liposuction did not significantly alter the insulin sensitivity of muscle, liver, or adipose tissue (assessed by the stimulation of glucose disposal, the suppression of glucose production, and the suppression of lipolysis, respectively); did not significantly alter plasma concentrations of C-reactive protein, interleukin-6, tumor necrosis factor alpha, and adiponectin; and did not significantly affect other risk factors for coronary heart disease (blood pressure and plasma glucose, insulin, and lipid concentrations) in either group.
  
  
  CONCLUSIONS
  Abdominal liposuction does not significantly improve obesity-associated metabolic abnormalities. Decreasing adipose tissue mass alone will not achieve the metabolic benefits of weight loss.
authors.affiliation: Center for Human Nutrition, Washington University School of Medicine, St. Louis 63110, USA.
authors.forename: Samuel
authors.initials: S
authors.lastname: Klein
authors.forename: Luigi
authors.initials: L
authors.lastname: Fontana
authors.forename: V Leroy
authors.initials: VL
authors.lastname: Young
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Coggan
authors.forename: Charles
authors.initials: C
authors.lastname: Kilo
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Patterson
authors.forename: B Selma
authors.initials: BS
authors.lastname: Mohammed
mesh_terms: D000005:Abdomen; D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D001824:Body Constitution; D015992:Body Mass Index; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D005260:Female; D015309:Glucose Clamp Technique; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D015187:Lipectomy; D008099:Liver / Q000378:metabolism; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000378:metabolism* / Q000601:surgery; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss / Q000502:physiology
chemical_list: D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol