Table 1: Main cardiovascular findings in genetic models of metabolic syndrome.

ModelsCardiovascular changes

db/db mouse(i) Increased vascular contractility
(ii) High blood pressure levels (14-15 weeks of age)
(iii) Sympathetic denervation (14-15 weeks of age)

KKAy mice(i) High blood pressure levels
(ii) Sympathetic alterations

ob/ob mice(i) Hypotensive with low sympathetic nerve activity
(ii) Cardiac fibrosis (20 weeks of age)
(iii) Left ventricular hypertrophy (24 weeks of age)
(iv) Decreased cardiac function (24 weeks of age)

db/db mice(i) Vascular endothelial dysfunction
(ii) No or low blood pressure changes
(iii) No changes in heart rate variability
(iv) No changes in spontaneous baroreflex sensitivity

Wistar Ottawa Karlsburg W(i) Impaired coronary function
(ii) Increased alpha(1)-adrenoceptor-mediated coronary constriction (3 and 10 months of age)
(iii) Seriously blunted beta-adrenoceptor-mediated coronary relaxation (16 months of age)

Zucker obese rats(i) Diastolic dysfunction with preserved ejection fraction (9 weeks of age)
(ii) High blood pressure levels (12 weeks of age)
(iii) High resting sympathetic nerve activity
(iv) Reduced heart rate variability

Zucker Diabetic Fatty (i) Increased myocardial fatty acid oxidation
(ii) Reduction of insulin-mediated myocardial glucose utilization (14 weeks of age)
(iii) Reduction of left ventricular chamber

DahlS.Z-Leprfa/Leprfa(i) Diastolic dysfunction
(ii) Marked left ventricle hypertrophy and fibrosis
(iii) Myocardial oxidative stress

Otsuka Long-Evans Tokushima Fatty (i) Diastolic dysfunction (15 weeks)
(ii) No changes in the blood pressure and heart rate
(iii) Extracellular fibrosis and abundant transforming growth factor-β1 receptor II in the left ventricle
(iv) Low coronary flow reserve
(v) Increased coronary vascular resistance

Goto-Kakizaki(i) Left ventricle remodeling with marked hypertrophy
(ii) Increased extracellular matrix deposition
(iii) Mild hypertension
(iv) Blunted vascular relaxation by acetylcholine and sodium nitroprusside