title: Weight loss may reverse blunted sympathetic neural responsiveness to glucose ingestion in obese subjects with metabolic syndrome.
abstract: OBJECTIVE
  The purpose of this study was to examine the effects of weight loss on sympathetic nervous system responsiveness to glucose ingestion in obese subjects with metabolic syndrome, in whom such responses are reportedly blunted.
  
  
  METHODS
  Thirty four subjects, 19 insulin resistant and 15 insulin sensitive and aged 55 +/- 1 years (mean +/- SE) with BMI 31.6 +/- 0.6 kg/m2, who fulfilled the Adult Treatment Panel III criteria for metabolic syndrome participated. Simultaneous measurements of whole-body norepinephrine spillover rate, calf blood flow, and intra-arterial blood pressure were made at times 0, 30, 60, 90, and 120 min postglucose (75 g). The experiment was repeated after a 3-month hypocaloric diet with or without an exercise program.
  
  
  RESULTS
  Body weight decreased by 8.1 +/- 0.9 and 8.4 +/- 1.1 kg and resting norepinephrine spillover by 94 +/- 31 and 166 +/- 58 ng/min (all P < or = 0.01) in insulin-resistant and insulin-sensitive subjects, respectively. Weight loss was accompanied by a marked increase in sympathetic responsiveness after glucose but only in insulin-resistant subjects. In this subgroup, comparative increases in norepinephrine spillover rates at baseline and after weight loss averaged -3 +/- 25 versus 73 +/- 24 ng/min at 30 min (P = 0.039), 36 +/- 21 versus 115 +/- 28 ng/min at 60 min (P = 0.045), 9 +/- 21 versus 179 +/- 50 ng/min at 90 min (P < 0.001), and 40 +/- 48 versus 106 +/- 39 ng/min at 120 min (P = 0.24).
  
  
  CONCLUSIONS
  Weight loss reverses blunted sympathetic responsiveness to glucose ingestion in insulin-resistant subjects with metabolic syndrome, which is relevant to postprandial energy utilization and body weight homeostasis.
authors.affiliation: Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia. nora.straznicky@bakeridi.edu.au
authors.forename: Nora E
authors.initials: NE
authors.lastname: Straznicky
authors.forename: Gavin W
authors.initials: GW
authors.lastname: Lambert
authors.forename: Mariee T
authors.initials: MT
authors.lastname: McGrane
authors.forename: Kazuko
authors.initials: K
authors.lastname: Masuo
authors.forename: Tye
authors.initials: T
authors.lastname: Dawood
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Nestel
authors.forename: Nina
authors.initials: N
authors.lastname: Eikelis
authors.forename: Markus P
authors.initials: MP
authors.lastname: Schlaich
authors.forename: Murray D
authors.initials: MD
authors.lastname: Esler
authors.forename: Florentia
authors.initials: F
authors.lastname: Socratous
authors.forename: Reena
authors.initials: R
authors.lastname: Chopra
authors.forename: Elisabeth A
authors.initials: EA
authors.lastname: Lambert
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002149:Energy Intake; D004837:Epinephrine / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D007866:Leg / Q000098:blood supply; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control*; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control*; D017698:Postmenopause; D012039:Regional Blood Flow; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D015431:Weight Loss / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D005947:Glucose; D004837:Epinephrine