Diabetic Cardiomyopathy Essay

Background: Diabetic cardiomyopathy (DCM) describes diabetes-associated changes in the structure and function of the myocardium, in the absence of coronary atherosclerosis and hypertension. Cardiovascular complications (hypertrophy, oxidative stress, inflammation and fibrosis) are the major cause of mortality and morbidity in diabetic patients. Ample of evidence have indicated that 11β-HSD1-mediated intracellular cortisol production may have a pathogenic role in type 2 diabetes mellitus (T2DM) and its co-morbidities. Inhibition of the enzyme 11β-HSD1 has been proposed as a novel therapeutic target for the treatment of T2DM. Recently, numerous compounds targeting 11β -HSD1 have been developed but none of the compound has been marketed yet.
They were randomly assigned to three groups, which received 21 days of either vehicle, 11β-HSD1 inhibitor (TR-013A 30mg/kg BD) and standard drug (RU38486 10mg/kg BD). Aged matched mice without HFD and STZ was used as normal control. Blood glucose was monitored at specific time interval during the study period.
Results: TR-013A treated group have shown significantly lower plasma glucose level, lipidemic parameters compared to diabetes control group. The blood glucose lowering effect is comparable to RU38486. Further, cardiac remodeling events such as inflammation, fibrosis, hypertrophy and oxidative stress were reversed by both TR-013A and RU38486 treatment in comparison to diabetic control. In addition, the TR-013A treated group did not gain any weight throughout the treatment period. Nevertheless, there is no significant difference between diabetes control group and TR-013A treated group.
Conclusion: Our results demonstrate that TR-013A does exhibit anti-diabetic, anti-hypertrophic, anti-oxidative. anti-inflammatory and anti-fibrotic activity. Thus, inhibition of 11β-HSD1 can be an attractive therapeutic target for