In rats, 7-week exposure to isolated hyperinsulinaemia increased left ventricular mass by 17% and total peripheral resistance (P<0.001), while lowering cardiac output and stroke volume by 30-40%.
Does isolated hyperinsulinaemia increase myocardial mass and alter haemodynamic regulation in rats?
Long-term exposure to isolated hyperinsulinaemia in rats leads to increased myocardial mass, elevated peripheral resistance, and decreased cardiac output, suggesting a direct trophic effect of insulin.
Left ventricular hypertrophy is a condition with high mortality. An association with insulin resistance and hyperinsulinaemia has recently been suggested. The aim of this study was to examine the effects of isolated hyperinsulinaemia on cardiac weight and haemodynamic regulation. Rats were exposed to hyperinsulinaemia for 7 weeks after adrenalectomy with corticosterone substitution and continuous infusion of propranolol to control counter-regulatory mechanism (n = 15) (AIP group). Hypoglycaemia was prevented by glucose in the drinking water. Hyperinsulinaemic (AIP) rats were heavier and had increased relative masses of the myocardium (left ventricle 17% and right ventricle 20%), kidneys and adipose tissues in comparison with normoinsulinaemic adrenalectomized, corticosterone- and propranolol-treated controls (AP) (n = 10). Blood pressure in the insulin-exposed animals, measured weekly by the tail-cuff method in conscious rats, was not different from (AP) controls over 5 weeks, but increased in the sixth week. At the end of the seventh experimental week, blood pressure measured intra-arterially was also found to be elevated. Heart rate was not changed but total peripheral resistance was about twice that of controls (P < 0.001). Cardiac output and stroke volume was 30-40% lower in the AIP rats (P < 0.05). It is concluded that exposure to elevated insulin levels with control of counter-regulating mechanisms from beta-adrenergic mechanisms and adrenals is not immediately followed by blood pressure elevation. It is, therefore, suggested that early onset of blood pressure elevation after insulin exposure might be caused by insulin counter-regulatory events, causing both insulin resistance and blood pressure elevation. The long-term adaptations may involve a direct influence by insulin as a 'trophic factor' on myocardial and on peripheral resistance levels, followed by increased blood pressure, decreased cardiac and stroke volume.
Ng et al. (1996) studied Hyperinsulinaemia (n=25). Hyperinsulinaemia vs. Normoinsulinaemic controls was evaluated on Cardiac weight and haemodynamic regulation. In rats, 7-week exposure to isolated hyperinsulinaemia increased left ventricular mass by 17% and total peripheral resistance (P<0.001), while lowering cardiac output and stroke volume by 30-40%.