Does troglitazone reduce myocardial collagen accumulation in a prediabetic rat model?
Troglitazone decreases myocardial interstitial fibrosis and collagen accumulation in a prediabetic rat model, suggesting a potential role in preventing early diabetic cardiomyopathy.
Diabetic cardiomyopathy can be a major complication of diabetes. This complication is not only present in established diabetes but also in prediabetes. Increased diastolic stiffness develops early in experimental diabetic animals which is associated with interstitial accumulation of connective tissue.1 2 The Otsuka Long-Evans Tokushima Fatty (DM) strain of rat was established as an animal model of congenital diabetes, manifesting stable clinical and pathological features that resemble human non-insulin dependent diabetes mellitus (NIDDM).3 In our previous study we found alteration in left ventricular diastolic function and accumulation of myocardial collagen in prediabetic rats.4 Troglitazone, an insulin sensitising thiazolidinedione, improves metabolic deterioration in diabetic animal models, obese subjects, and patients with NIDDM.5 The drug has an acute effect on cultured cardiac myocytes, on isolated rat hearts, and prevents high glucose induced insulin resistance in cultured rat fibroblasts. Our study aimed to examine the long term effects of troglitazone on myocardial collagen content using histopathological methods in prediabetic rats. Male DM rats and age matched male non-DM rats were randomly divided into two groups, respectively: (1) treated DM (n = 10); (2) untreated DM (n =10); (3) treated non-DM (n = 10); (4) untreated non- DM …
Li Yao (2000) studied this question.