title: Impact of a lifestyle program on vascular insulin resistance in metabolic syndrome subjects: the RESOLVE study.
abstract: OBJECTIVE
  Impaired insulin-dependent vasodilation might contribute to microvascular dysfunction of metabolic syndrome (MetS). The aims of this study were to assess the insulin vasoreactivity in MetS, and to evaluate the effects of a lifestyle program. DESIGN, SETTING, PARTICIPANTS, AND OUTCOME MEASURES: Laser Doppler measurements were used to assess cutaneous blood flux (CBF) and flowmotion in response to iontophoresis of insulin and acetylcholine (ACh) in 38 MetS and 18 controls. Anthropometric, plasma insulin, glycemia, and inflammatory markers were measured. MetS subjects (n = 24) underwent a 6-month lifestyle intervention (M6) with a 3-week residential program (D21).
  
  
  RESULTS
  The absolute and relative peak insulin and ACh CBF were significantly higher in controls than in MetS subjects. Significant inverse correlations were found between peak insulin CBF and glycemia, insulin and glycated hemoglobin, active plasminogen activator inhibitor-1 (PAI-1), C-reactive protein (CRP), and IL-6. With respect to flowmotion, MetS subjects showed lower values in total spectrum CBF and in all its components (except respiratory one). At D21 and M6, peak insulin CBF increased and was no longer different from control values whereas peak ACh CBF did not change. From D21, all the different components and the total CBF spectrum became similar to the control values. The changes in peak insulin CBF and in endothelial component between M6 and baseline were inversely correlated with the change in CRP and PAI-1.
  
  
  CONCLUSIONS
  The local vasodilatory effects to insulin and its overall flowmotion are impaired in MetS subjects in relation to inflammation. The lifestyle intervention reversed this insulin-induced vascular dysfunction in parallel to decreased inflammation level.
authors.affiliation: Avignon University (A.V., P.O., L.D., G.W.), LAPEC EA4278, F-84000 Avignon, France; School of Exercise Science (P.O., F.D., D.C.), Australian Catholic University, Melbourne, 3065 Australia; Laboratory of Metabolic Adaptations to Exercise in Physiological and Pathological Conditions (F.D., B.L., D.C.), EA3533, F-63000 Clermont-Ferrand, France; University Hospital of Clermont-Ferrand (F.D., B.L.), CHU G. Montpied, F-63000 Clermont-Ferrand, France; and Omental (R.C.)-Thermalia Center, F-63140 Châtelguyon, France.
authors.forename: Agnes
authors.initials: A
authors.lastname: Vinet
authors.forename: Philippe
authors.initials: P
authors.lastname: Obert
authors.forename: Frederic
authors.initials: F
authors.lastname: Dutheil
authors.forename: Lamine
authors.initials: L
authors.lastname: Diagne
authors.forename: Robert
authors.initials: R
authors.lastname: Chapier
authors.forename: Bruno
authors.initials: B
authors.lastname: Lesourd
authors.forename: Daniel
authors.initials: D
authors.lastname: Courteix
authors.forename: Guillaume
authors.initials: G
authors.lastname: Walther
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D006293:Health Promotion; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D015850:Interleukin-6 / Q000097:blood; D008019:Life Style; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012039:Regional Blood Flow / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D001786:Blood Glucose; D007328:Insulin; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D002097:C-Reactive Protein