Cardiac Mitochondrial Alterations Observed in Hyperglycaemic Rats - What Can We Learn From Cell Biology?

摘要

Diabetes mellitus is one of the most common metabolic diseases in the world. The complications associatednwith this disease are often responsible for a decreased quality of life in many patients. For example, the diabeticnpopulation has a greater probability to suffer from cardiovascular problems and heart failure than the general population.nDue to the importance heart mitochondria have in the context of the bioenergetics of the myocardium, it appears logical tonexplore mitochondrial dysfunction as an important link between hyperglycaemia and heart alterations observed duringndiabetes. One important factor that can lead to mitochondrial dysfunction is the mitochondrial permeability transitionn(MPT), caused by the formation of poly-protein pores (MPT pores), occurring with mitochondrial calcium overload andnincreased oxidative stress, conditions already described to exist in myocytes exposed to hyperglycaemia. The MPT hasnbeen involved as determinant in the survival of myocytes after anoxia and reoxigenation, as well as in triggering cellndeath.nThe present review deals with cardiac mitochondrial alterations observed in drug-induced hyperglycaemic animals or innthe GK rat, a hereditary model of hyperglycaemia. Respiration rates, susceptibility to oxidative stress, protein expressionnand MPT induction are altered in hyperglycaemic animals, which in extreme conditions can alter the bioenergetics of thendiabetic myocardium and even cause myocardial cell death. The study of the cardiac mitochondrial function ofnhyperglycaemic animals offer an important insight, not only to explain cardiac alterations found in diabetic patients, butnalso in the design of new therapeutic approaches to reduce mitochondrial dysfunction and cell death typically associatednwith diabetes.