Type 2 diabetes (DT2) increases the risk of cardiovascular events and cardiac insufficiency. This insufficiency is mostly post-ischaemic in nature, but other aetiologies are possible in this high-risk population. In patients with DT2, diabetic cardiomyopathy is a recognized cause of cardiac insufficiency secondary to chronic hyperglycaemia and myocardial lipotoxicity, which promotes cardiomyocyte hypertrophy (and, frequently, apoptosis of these cells), interstitial fibrosis and a decrease in myocardial contractile performance. Several studies have shown that diabetic cardiomyopathy is associated with modifications to the intestinal microbiota, and changes in the synthesis of bacterial metabolites and their diffusion into the host, some of which appear to have direct deleterious effects on cardiac contractility. These findings open up new perspectives for pathophysiological studies by establishing the presence of a ‘microbiota–myocardium’ axis and raising the possibility of innovative new treatments. Correction of intestinal dysbiosis in patients with cardiac insufficiency could, therefore, constitute an innovative therapeutic approach to cases of this disease with a poor prognosis.