title: Failure to increase postprandial blood flow in subcutaneous adipose tissue is associated with tissue resistance to adrenergic stimulation.
abstract: OBJECTIVE
  Adequate adipose tissue blood flow (ATBF) is essential for its metabolic and endocrine functions. From a metabolic point of view, sufficient increases in ATBF after meals permits full storage of excess energy into fat, thus protecting other tissues against the toxic effects of fatty acids and glucose spillover. It was previously shown that postprandial increases in ATBF are blunted in obese and insulin-resistant subjects, and that much of the postprandial ATBF response is the result of β-adrenergic activation. Examination of previously recorded data on postprandial ATBF responses revealed an underlying heterogeneity, with postprandial ATBF being largely unresponsive to food stimuli in a substantial proportion of normal weight healthy people (low responders). Our study tests the hypothesis that this unresponsive pattern is due to resistance to β-adrenergic stimulation in adipose tissue.
  
  
  METHODS
  Five responders and five low responders were selected from a previously studied cohort and matched for BMI (20.5±0.7 vs 22±1 kg/m(2), respectively), gender (male/female: 2/3) and age (30±3 vs 37±6 years). Subcutaneous adipose tissue microinfusions of stepwise increasing doses of isoproterenol were performed with concomitant monitoring of blood flow, using the (133)Xenon washout technique.
  
  
  RESULTS
  Although BMI was similar between responders and low responders, there were significant differences in fat mass (9.9±1.6 vs 14.4±1.6 kg; P<0.05) and four-point skinfold thickness (33±4 vs 52±16 mm; P<0.05). Lack of ATBF response to oral glucose was confirmed in the low responder group. In responders, ATBF was higher at baseline (5.4±1 vs 3.4±1 mL/min/100 g of tissue) and responded more distinctly to increasing isoproterenol doses (10(-8) M: 7.6±1.4 vs 4.9±1; 10(-6) M: 12.5±1.7 vs 7.5±1.6; and 10(-4) M: 20 ±1.7 vs 9±0.9 mL/min/100 g of tissue).
  
  
  CONCLUSIONS
  These data suggest that the lack of glucose-stimulated ATBF is associated with resistance to sympathetic activation in adipose tissue.
authors.affiliation: Division of Endocrinology, Department of Medicine, Université de Sherbrooke, 3001, 12th Avenue North, J1H 5N4 Sherbrooke, Quebec, Canada. Jean-Luc.Ardilouze@USherbrooke.ca
authors.forename: J-L
authors.initials: JL
authors.lastname: Ardilouze
authors.forename: R
authors.initials: R
authors.lastname: Sotorník
authors.forename: L A
authors.initials: LA
authors.lastname: Dennis
authors.forename: B A
authors.initials: BA
authors.lastname: Fielding
authors.forename: K N
authors.initials: KN
authors.lastname: Frayn
authors.forename: F
authors.initials: F
authors.lastname: Karpe
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology*; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D015331:Cohort Studies; D004351:Drug Resistance; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D019518:Postprandial Period / Q000502:physiology; D012039:Regional Blood Flow; D012885:Skinfold Thickness; D050151:Subcutaneous Fat / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D011795:Surveys and Questionnaires; D013564:Sympathetic Nervous System / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology
chemical_list: D000322:Adrenergic Agonists; D001786:Blood Glucose; D007328:Insulin