OBJECTIVE: Hyperleptinemia, a hallmark of obesity, appears to be a risk factor for coronary artery disease. However, although leptin is a vasoactive hormone, no studies addressing leptin's effect on coronary perfusion have been performed. We examined the association between circulating leptin concentration and coronary vasoreactivity in young obese and nonobese males. RESEARCH METHODS AND PROCEDURES: Myocardial blood flow was quantitated in 10 obese men (age 31 +/- 7 years, BMI 34 +/- 2 kg/m(2)) and 10 healthy matched nonobese men (age 33 +/- 8 years, BMI 24 +/- 2 kg/m(2)) using positron emission tomography and O-15-water. The measurements were performed basally and during adenosine infusion (140 micro g/kg per minute). RESULTS: Serum leptin was significantly higher in obese than nonobese subjects (10.3 +/- 5.6 vs. 4.3 +/- 2.5 ng/mL, p < 0.01). Basal myocardial blood flow was not significantly different between obese and nonobese subjects. Adenosine-stimulated flow was blunted in obese (3.2 +/- 0.6 mL/g per minute) when compared with nonobese subjects (4.0 +/- 1.1 mL/g per minute, p < 0.05). Serum leptin concentration was inversely associated with adenosine-stimulated flow in study subjects (r = -0.50, p < 0.05). This association was no longer observed after adjustment for obesity and/or hyperinsulinemia. DISCUSSION: Hyperleptinemia and reduced coronary vasoreactivity occur concomitantly in young obese but otherwise healthy men. Moreover, the adenosine-stimulated myocardial flow is inversely related to prevailing concentration of serum leptin. Although this relationship appears to be explained by obesity and/or hyperinsulinemia, leptin might have a role in regulation of myocardial blood supply.
OBJECTIVE: Hyperleptinemia, a hallmark of obesity, appears to be a risk factor for coronary artery disease. However, although leptin is a vasoactive hormone, no studies addressing leptin's effect on coronary perfusion have been performed. We examined the association between circulating leptin concentration and coronary vasoreactivity in young obese and nonobese males. RESEARCH METHODS AND PROCEDURES: Myocardial blood flow was quantitated in 10 obesemen (age 31 +/- 7 years, BMI 34 +/- 2 kg/m(2)) and 10 healthy matched nonobese men (age 33 +/- 8 years, BMI 24 +/- 2 kg/m(2)) using positron emission tomography and O-15-water. The measurements were performed basally and during adenosine infusion (140 micro g/kg per minute). RESULTS: Serum leptin was significantly higher in obese than nonobese subjects (10.3 +/- 5.6 vs. 4.3 +/- 2.5 ng/mL, p < 0.01). Basal myocardial blood flow was not significantly different between obese and nonobese subjects. Adenosine-stimulated flow was blunted in obese (3.2 +/- 0.6 mL/g per minute) when compared with nonobese subjects (4.0 +/- 1.1 mL/g per minute, p < 0.05). Serum leptin concentration was inversely associated with adenosine-stimulated flow in study subjects (r = -0.50, p < 0.05). This association was no longer observed after adjustment for obesity and/or hyperinsulinemia. DISCUSSION: Hyperleptinemia and reduced coronary vasoreactivity occur concomitantly in young obese but otherwise healthy men. Moreover, the adenosine-stimulated myocardial flow is inversely related to prevailing concentration of serum leptin. Although this relationship appears to be explained by obesity and/or hyperinsulinemia, leptin might have a role in regulation of myocardial blood supply.
Authors: Greg J Zahner; Joel L Ramirez; Kimberly A Spaulding; Sukaynah A Khetani; Warren J Gasper; Carl Grunfeld; Nancy K Hills; Anne L Schafer; S Marlene Grenon Journal: J Surg Res Date: 2019-02-06 Impact factor: 2.192
Authors: Hadi Abdul Ridha Hadi Khafaji; Abdulbari Bener; Mohammed Osman; Ajayeb Al Merri; Jassim Al Suwaidi Journal: Vasc Health Risk Manag Date: 2011-12-30
Authors: Rabia Johnson; Phiwayinkosi V Dludla; Christo J F Muller; Barbara Huisamen; M Faadiel Essop; Johan Louw Journal: Molecules Date: 2017-01-31 Impact factor: 4.411