Changes of cardiac function of high fat diet-induced insulin resistance rat and telmisartan intervention

Objective: To explore cardiac function and myocardial collagen type I in diet-induced insulin-resistant rats and the effect of telmisartan on cardiac diastolic function in diet-induced insulin-resistant rats. Methods: We randomized 27 Wistar rats into control group (n=9), high-fat group (n=9), and telmisartan treatment group (n=9). At the end of the study, left ventricular end diastolic pressure (LVEDP) and left ventricular systolic pressure (LVSP) of the rats and ±dp/dt were detected by carotid artery intubation. Masson cardiac staining was used to observe cardiac fibrosis, and collagen volume fraction (CVF) was measured. ELISA method was used to detect the concentration of plasma PICP and ICTP. Results: Compared with the control group, in high-fat group LVEDP was significantly higher and -dP/dtmax decreased significantly (P<0.01); the plasma PICP level and the ratio of PICP/ICTP were significantly increased (P<0.01), cardiac collagen volume fraction was significantly higher (P<0.01). After 22 weeks' telmisartan intervention, compared with the high-fat group, LVEDP and LVSP were significantly decreased (P<0.01), but -dP/dtmax significantly increased (P<0.05). The level of the plasma PICP and PICP/ICTP were significantly decreased (P<0.05); left ventricular myocardial tissue collagen volume fraction content was decreased (P<0.01). The correlation analysis showed that cardiac collagen volume fraction in insulin-resistant group was positively correlated with insulin resistance index but negatively correlated with -dp/dtmax (P<0.01). Conclusion: Insulin resistance promoted the synthesis of myocardial type I collagen, leading to increased myocardial collagen deposition and decreased cardiac diastolic function. Telmisartan may improve diastolic function partly by improving insulin resistance and reducing the deposition of myocardial collagen type I.