Exercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus

Elena Anna De Filippis, Kenneth Cusi, Gloria Ocampo, Rachele Berria, Susan Buck, Agostino Consoli, Lawrence J. Mandarino

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

Objective: The present study was undertaken to determine whether improved vasodilatory function accompanies increased insulin sensitivity in overweight, insulin-resistant subjects (OW) and type 2 diabetic patients (T2DM) who participated in an 8-wk exercise training regimen. Design: Before and after training, subjects had euglycemic clamps to determine insulin sensitivity. Brachial artery catheterization was done on another occasion for measurement of vasodilatory function. A lean, healthy, untrained group was studied as nonexercised controls. Results: Training increased oxygen consumption (VO 2) peak [OW, 29 ± 1 to 37 ± 4 ml/kg fat-free mass (FFM)·min; T2DM, 33 ± 2 to 43 ± 3 ml/kg FFM·min; P < 0.05] and improved insulin-stimulated glucose disposal (OW, 6.5 ± 0.5 to 7.2 ± 0.4 mg/kg FFM·min; T2DM, 3.8 ± 0.3 to 4.2 ± 0.3 mg/kg FFM·min; P < 0.05) in insulin resistance. OW and T2DM, before training, had decreased acetylcholine chloride (ACh)- and sodium nitroprusside-mediated vasodilation and decreased reactive hyperemia compared with lean controls. Training increased the vasodilatory response to ACh [OW (30 μg ACh/min), 12.2 ± 3.4 to 19 ± 4.2 ml/100 g·min; T2DM (30 μg ACh/min), 10.1 ± 1.5 to 14.2 ± 2.1 ml/100 g·min; P < 0.05] in both groups without affecting nitroprusside response. Conclusion: Because vasodilatory dysfunction has been postulated to contribute to insulin resistance, the exercise-induced improvement in vasodilatory function may signify changes in the endothelium that could contribute to the improvement in insulin sensitivity observed after aerobic exercise training.

Original languageEnglish (US)
Pages (from-to)4903-4910
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume91
Issue number12
DOIs
StatePublished - Dec 2006
Externally publishedYes

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Medical problems
Type 2 Diabetes Mellitus
Insulin Resistance
Obesity
Acetylcholine
Exercise
Insulin
Nitroprusside
Glucose Clamp Technique
Brachial Artery
Hyperemia
Vasodilation
Oxygen Consumption
Catheterization
Endothelium
Clamping devices
Fats
Glucose
Oxygen

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Exercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus. / De Filippis, Elena Anna; Cusi, Kenneth; Ocampo, Gloria; Berria, Rachele; Buck, Susan; Consoli, Agostino; Mandarino, Lawrence J.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 91, No. 12, 12.2006, p. 4903-4910.

Research output: Contribution to journalArticle

De Filippis, Elena Anna ; Cusi, Kenneth ; Ocampo, Gloria ; Berria, Rachele ; Buck, Susan ; Consoli, Agostino ; Mandarino, Lawrence J. / Exercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus. In: Journal of Clinical Endocrinology and Metabolism. 2006 ; Vol. 91, No. 12. pp. 4903-4910.
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abstract = "Objective: The present study was undertaken to determine whether improved vasodilatory function accompanies increased insulin sensitivity in overweight, insulin-resistant subjects (OW) and type 2 diabetic patients (T2DM) who participated in an 8-wk exercise training regimen. Design: Before and after training, subjects had euglycemic clamps to determine insulin sensitivity. Brachial artery catheterization was done on another occasion for measurement of vasodilatory function. A lean, healthy, untrained group was studied as nonexercised controls. Results: Training increased oxygen consumption (VO 2) peak [OW, 29 ± 1 to 37 ± 4 ml/kg fat-free mass (FFM)·min; T2DM, 33 ± 2 to 43 ± 3 ml/kg FFM·min; P < 0.05] and improved insulin-stimulated glucose disposal (OW, 6.5 ± 0.5 to 7.2 ± 0.4 mg/kg FFM·min; T2DM, 3.8 ± 0.3 to 4.2 ± 0.3 mg/kg FFM·min; P < 0.05) in insulin resistance. OW and T2DM, before training, had decreased acetylcholine chloride (ACh)- and sodium nitroprusside-mediated vasodilation and decreased reactive hyperemia compared with lean controls. Training increased the vasodilatory response to ACh [OW (30 μg ACh/min), 12.2 ± 3.4 to 19 ± 4.2 ml/100 g·min; T2DM (30 μg ACh/min), 10.1 ± 1.5 to 14.2 ± 2.1 ml/100 g·min; P < 0.05] in both groups without affecting nitroprusside response. Conclusion: Because vasodilatory dysfunction has been postulated to contribute to insulin resistance, the exercise-induced improvement in vasodilatory function may signify changes in the endothelium that could contribute to the improvement in insulin sensitivity observed after aerobic exercise training.",
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T1 - Exercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus

AU - De Filippis, Elena Anna

AU - Cusi, Kenneth

AU - Ocampo, Gloria

AU - Berria, Rachele

AU - Buck, Susan

AU - Consoli, Agostino

AU - Mandarino, Lawrence J.

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N2 - Objective: The present study was undertaken to determine whether improved vasodilatory function accompanies increased insulin sensitivity in overweight, insulin-resistant subjects (OW) and type 2 diabetic patients (T2DM) who participated in an 8-wk exercise training regimen. Design: Before and after training, subjects had euglycemic clamps to determine insulin sensitivity. Brachial artery catheterization was done on another occasion for measurement of vasodilatory function. A lean, healthy, untrained group was studied as nonexercised controls. Results: Training increased oxygen consumption (VO 2) peak [OW, 29 ± 1 to 37 ± 4 ml/kg fat-free mass (FFM)·min; T2DM, 33 ± 2 to 43 ± 3 ml/kg FFM·min; P < 0.05] and improved insulin-stimulated glucose disposal (OW, 6.5 ± 0.5 to 7.2 ± 0.4 mg/kg FFM·min; T2DM, 3.8 ± 0.3 to 4.2 ± 0.3 mg/kg FFM·min; P < 0.05) in insulin resistance. OW and T2DM, before training, had decreased acetylcholine chloride (ACh)- and sodium nitroprusside-mediated vasodilation and decreased reactive hyperemia compared with lean controls. Training increased the vasodilatory response to ACh [OW (30 μg ACh/min), 12.2 ± 3.4 to 19 ± 4.2 ml/100 g·min; T2DM (30 μg ACh/min), 10.1 ± 1.5 to 14.2 ± 2.1 ml/100 g·min; P < 0.05] in both groups without affecting nitroprusside response. Conclusion: Because vasodilatory dysfunction has been postulated to contribute to insulin resistance, the exercise-induced improvement in vasodilatory function may signify changes in the endothelium that could contribute to the improvement in insulin sensitivity observed after aerobic exercise training.

AB - Objective: The present study was undertaken to determine whether improved vasodilatory function accompanies increased insulin sensitivity in overweight, insulin-resistant subjects (OW) and type 2 diabetic patients (T2DM) who participated in an 8-wk exercise training regimen. Design: Before and after training, subjects had euglycemic clamps to determine insulin sensitivity. Brachial artery catheterization was done on another occasion for measurement of vasodilatory function. A lean, healthy, untrained group was studied as nonexercised controls. Results: Training increased oxygen consumption (VO 2) peak [OW, 29 ± 1 to 37 ± 4 ml/kg fat-free mass (FFM)·min; T2DM, 33 ± 2 to 43 ± 3 ml/kg FFM·min; P < 0.05] and improved insulin-stimulated glucose disposal (OW, 6.5 ± 0.5 to 7.2 ± 0.4 mg/kg FFM·min; T2DM, 3.8 ± 0.3 to 4.2 ± 0.3 mg/kg FFM·min; P < 0.05) in insulin resistance. OW and T2DM, before training, had decreased acetylcholine chloride (ACh)- and sodium nitroprusside-mediated vasodilation and decreased reactive hyperemia compared with lean controls. Training increased the vasodilatory response to ACh [OW (30 μg ACh/min), 12.2 ± 3.4 to 19 ± 4.2 ml/100 g·min; T2DM (30 μg ACh/min), 10.1 ± 1.5 to 14.2 ± 2.1 ml/100 g·min; P < 0.05] in both groups without affecting nitroprusside response. Conclusion: Because vasodilatory dysfunction has been postulated to contribute to insulin resistance, the exercise-induced improvement in vasodilatory function may signify changes in the endothelium that could contribute to the improvement in insulin sensitivity observed after aerobic exercise training.

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