title: Effect of telmisartan on selected adipokines, insulin sensitivity, and substrate utilization during insulin-stimulated conditions in patients with metabolic syndrome and impaired fasting glucose.
abstract: OBJECTIVE
  Telmisartan improves glucose and lipid metabolism in rodents. This study evaluated the effect of telmisartan on insulin sensitivity, substrate utilization, selected plasma adipokines and their expressions in subcutaneous adipose tissue (SAT) in metabolic syndrome.
  
  
  METHODS
  Twelve patients with impaired fasting glucose completed the double-blind, randomized, crossover trial. Patients received telmisartan (160 mg/day) or placebo for 3 weeks and vice versa with a 2-week washout period. At the end of each period, a hyperinsulinemic euglycemic clamp (HEC) combined with indirect calorimetry was performed. During HEC (0, 30, and 120 min), plasma levels of adipokines were measured and a needle biopsy (0 and 30 min) of SAT was performed.
  
  
  RESULTS
  Fasting plasma glucose was lower after telmisartan compared with placebo (P<0.05). There were no differences in insulin sensitivity and substrate utilization. We found no differences in basal plasma adiponectin, resistin and tumour necrosis factor α (TNFα), but an increase was found in basal leptin, after telmisartan treatment. Insulin-stimulated plasma adiponectin (P<0.05), leptin and resistin (P<0.001) were increased, whereas TNFα was decreased (P<0.05) after telmisartan treatment. Expression of resistin, but not adiponectin, TNFα and leptin was increased after telmisartan treatment.
  
  
  CONCLUSIONS
  Despite the decrease in fasting plasma glucose, telmisartan does not improve insulin sensitivity and substrate utilization. Telmisartan increases plasma leptin as well as insulin-stimulated plasma adiponectin, leptin and resistin, and decreases plasma TNFα during HEC. Changes in plasma adipokines cannot be explained by their expressions in SAT. The changes in plasma adipokines might be involved in the metabolic effects of telmisartan in metabolic syndrome.
authors.affiliation: Diabetes Center, Institute for Clinical and Experimental Medicine, Vídenská 1958/4, Prague, Czech Republic.
authors.forename: Petr
authors.initials: P
authors.lastname: Wohl
authors.forename: Eva
authors.initials: E
authors.lastname: Krusinová
authors.forename: Martin
authors.initials: M
authors.lastname: Hill
authors.forename: Simona
authors.initials: S
authors.lastname: Kratochvílová
authors.forename: Katerina
authors.initials: K
authors.lastname: Zídková
authors.forename: Jan
authors.initials: J
authors.lastname: Kopecký
authors.forename: Tomás
authors.initials: T
authors.lastname: Neskudla
authors.forename: Michal
authors.initials: M
authors.lastname: Pravenec
authors.forename: Marta
authors.initials: M
authors.lastname: Klementová
authors.forename: Jana
authors.initials: J
authors.lastname: Vrbíková
authors.forename: Pavel
authors.initials: P
authors.lastname: Wohl
authors.forename: Petr
authors.initials: P
authors.lastname: Mlejnek
authors.forename: Terezie
authors.initials: T
authors.lastname: Pelikánová
mesh_terms: D054392:Adipokines / Q000097:blood*; D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D015309:Glucose Clamp Technique; D018149:Glucose Intolerance / Q000097:blood / Q000188:drug therapy*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000188:drug therapy*; D008875:Middle Aged; D000077333:Telmisartan
chemical_list: D054392:Adipokines; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001565:Benzoates; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D000077333:Telmisartan