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Effect of PPAR-gamma agonist on exercise capacity in relation to body fat distribution in men with type 2 diabetes mellitus and coronary artery disease: a 1 year randomized study

Session Moderated Posters Session 5

Speaker Marie-Eve Piche

Congress : EuroPrevent 2019

  • Topic : preventive cardiology
  • Sub-topic : Secondary Prevention
  • Session type : Moderated Posters
  • FP Number : 643

Authors : ME Piche (Quebec,CA), M Bastien (Quebec,CA), P Brassard (Quebec,CA), BJ Arsenault (Quebec,CA), OF Bertrand (Quebec,CA), JP Despres (Quebec,CA), O Costerousse (Quebec,CA), P Poirier (Quebec,CA)

Authors:
ME Piche1 , M Bastien1 , P Brassard1 , BJ Arsenault1 , OF Bertrand1 , JP Despres1 , O Costerousse1 , P Poirier1 , 1Quebec Heart and Lung Institute - Quebec - Canada ,

Citation:

Background: The therapeutic opportunities for targeting metabolic determinants of exercise performance with pharmacological agents that would mimic or potentiate the effects of exercise represent an attractive clinical alternative to counterbalance the poor exercise capacity in patients with type 2 diabetes mellitus (T2DM). Of this, the insulin sensitizer peroxisome proliferator-activated receptor (PPAR)-gamma agonists have been proposed as potential exercise mimetic candidates.

Purpose: We examined the effect of a 1-year treatment with the insulin sensitizer PPAR-gamma agonist rosiglitazone in addition to standard care on exercise capacity and body fat composition/distribution in men with T2DM and coronary artery disease (CAD).

Methods: A total of 104 men (age: 64±7 years; body mass index: 30.0±4.4 kg/m2) with T2DM (mean duration: 7.5 years) and CAD were randomized to receive rosiglitazone or placebo for 1 year. Exercise capacity (exercise duration) was assessed with a maximal treadmill test and body composition/distribution were assessed by dual-energy X-ray absorptiometry (DEXA)/computed tomography prior the intervention and at 1-year follow-up.

Results: At 1 year, patients with T2DM under PPAR-gamma agonist treatment showed a reduction in exercise capacity compared to the control group (exercise duration change, -31 ± 8 vs. 7 ± 11 s, p=0.009). Significant increases in body fat mass (3.1 ± 0.4 kg, 12%), abdominal and mid-thigh subcutaneous adipose tissue (AT) levels, and mid-thigh skeletal muscle fat were found (all p <0.01), whereas no effect on visceral AT levels was observed following treatment (p >0.05). PPAR-gamma agonist treated patients showed significant improvements in insulin sensitivity (HOMA-IR) and fasting blood glucose despite weight gain and body fat mass expansion (all p <0.05). Subcutaneous fat mass gained under PPAR-gamma agonist was the strongest predictor of the worsening in exercise capacity in a multivariate model (p ?0.0001); no association was found with skeletal muscle fat infiltration nor visceral AT levels.

Conclusions: Treatment with the insulin sensitizer PPAR-gamma agonist rosiglitazone in patients with T2DM and stable CAD is associated with a worsening in exercise capacity, which seems to be mainly attributable to subcutaneous fat mass expansion.



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