title: Rates of lipid fluxes in adipose tissue in vivo after a mixed meal in morbid obesity.
abstract: OBJECTIVE
  Although insulin resistance in obesity is established, information on insulin action on lipid fluxes, in morbid obesity, is limited. This study was undertaken in morbidly obese women to investigate insulin action on triacylglycerol fluxes and lipolysis across adipose tissue.
  
  
  METHODS
  A meal was given to 26 obese (age 35+/-1 years, body mass index 46+/-1 kg m(-2)) and 11 non-obese women (age 38+/-2 years, body mass index 24+/-1 kg m(-2)). Plasma samples for glucose, insulin, triglycerides and non-esterified fatty acids (NEFAs) were taken for 360 min from a vein draining the abdominal subcutaneous adipose tissue and from the radial artery. Adipose tissue blood flow was measured with (133)Xe.
  
  
  RESULTS
  In obese vs non-obese: (1) Arterial glucose was similar, but insulin was increased (P=0.0001). (2) Adipose tissue blood flow was decreased (P=0.0001). (3) Arterial triglycerides (P=0.0001) and NEFAs (P=0.01) were increased. (4) Lipoprotein lipase was decreased (P=0.0009), although the arteriovenous triglyceride differences were similar. (5) Veno-arterial NEFA differences across the adipose tissue were similar. (6) NEFA fluxes and hormone-sensitive lipase-derived glycerol output from 100 g adipose tissue were not different. (7) Total adipose tissue NEFA release was increased (P=0.02).
  
  
  CONCLUSIONS
  In morbid obesity: (a) hypertriglycerinemia could be attributed to a defect in the postprandial dynamic adjustment of triglyceride clearance across the adipose tissue, partly caused by blunted BF; and (b) postprandially, there is an impairment of adipose tissue to buffer NEFA excess, despite hyperinsulinemia.
authors.affiliation: Hellenic National Center for Research, Prevention and Treatment of Diabetes Mellitus and its Complications, Athens, Greece (H.N.D.C).
authors.forename: P
authors.initials: P
authors.lastname: Mitrou
authors.forename: E
authors.initials: E
authors.lastname: Boutati
authors.forename: V
authors.initials: V
authors.lastname: Lambadiari
authors.forename: E
authors.initials: E
authors.lastname: Maratou
authors.forename: V
authors.initials: V
authors.lastname: Komesidou
authors.forename: A
authors.initials: A
authors.lastname: Papakonstantinou
authors.forename: L
authors.initials: L
authors.lastname: Sidossis
authors.forename: N
authors.initials: N
authors.lastname: Tountas
authors.forename: N
authors.initials: N
authors.lastname: Katsilambros
authors.forename: T
authors.initials: T
authors.lastname: Economopoulos
authors.forename: S A
authors.initials: SA
authors.lastname: Raptis
authors.forename: G
authors.initials: G
authors.lastname: Dimitriadis
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D005260:Female; D006801:Humans; D015228:Hypertriglyceridemia / Q000209:etiology; D007328:Insulin / Q000502:physiology*; D008066:Lipolysis; D008071:Lipoprotein Lipase / Q000378:metabolism*; D009767:Obesity, Morbid / Q000378:metabolism*; D019518:Postprandial Period; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D008071:Lipoprotein Lipase