糖尿病性心肌病是指發生在糖尿病中，不能用高血壓病、冠心病、心臟瓣膜病及其他心臟病來解釋的心肌疾病。心肌壁內微血管病變、血管周邊間質纖維化可能是產生糖尿病心肌病（Diabetic Cardiomyopathy）的原因。
該病在代謝紊亂及微血管病變之基礎上引發心肌廣泛灶性壞死，出現亞臨床的心功能異常，最終進展為心力衰竭、心律失常及心源性休克，重症患者甚至猝死。
2型糖尿病也叫成人發病型糖尿病，多在35~40歲之後發病，佔糖尿病患者90%以上。2007年，我國大陸地區（不包括港、澳、臺）已經成為僅次於印度（4085萬人）的糖尿病第二大國，患者3981萬人，患病率4.3%；預計2025年達到5927萬人，患病率達5.6%。
導致II型糖尿病患者死亡的主要原因是心臟病，但迄今為止糖尿病性心肌病的確切分子機制仍不甚明了。近日，來自德克薩斯大學西南醫學研究中心的Joseph Hill等研究人員通過小鼠動物試驗證實：一種新的治療方法或許能緩解糖尿病患者心力衰竭的症狀，提高II型糖尿病患者的存活率。
許多因素能誘發糖尿病性相關心臟病，其中最具代表的是糖尿病性心肌病包括高血壓依賴性的心臟功能衰竭以及主動脈血管疾病。早期研究已發現FoxO1轉錄因子的活化能誘發心肌疾病的發生，敲除心肌細胞FoxO1能顯著抑制心肌病的發生。這項研究運用患II型糖尿病的小鼠動物模型證實糖尿病患者的心臟FoxO1轉錄因子能保持激活狀態，這或許是糖尿病患者伴發心肌病的主要原因。
研究人員表示：FoxO1活化是糖尿病患者伴發心肌病的關鍵因素，因此FoxO1將來或許能成為糖尿病性心肌病的一個潛在治療靶標。(生物谷 Bioon.com)
Metabolic stress–induced activation of FoxO1 triggers diabetic cardiomyopathy in mice
Pavan K. Battiprolu1, Berdymammet Hojayev1, Nan Jiang1, Zhao V. Wang1, Xiang Luo1,et al.
The leading cause of death in diabetic patients is cardiovascular disease; diabetic cardiomyopathy is typified by alterations in cardiac morphology and function, independent of hypertension or coronary disease. However, the molecular mechanism that links diabetes to cardiomyopathy is incompletely understood. Insulin resistance is a hallmark feature of diabetes, and the FoxO family of transcription factors, which regulate cell size, viability, and metabolism, are established targets of insulin and growth factor signaling. Here, we set out to evaluate a possible role of FoxO proteins in diabetic cardiomyopathy. We found that FoxO proteins were persistently activated in cardiac tissue in mice with diabetes induced either genetically or by high-fat diet (HFD). FoxO activity was critically linked with development of cardiomyopathy: cardiomyocyte-specific deletion of FoxO1 rescued HFD-induced declines in cardiac function and preserved cardiomyocyte insulin responsiveness. FoxO1-depleted cells displayed a shift in their metabolic substrate usage, from free fatty acids to glucose, associated with decreased accumulation of lipids in the heart. Furthermore, we found that FoxO1-dependent downregulation of IRS1 resulted in blunted Akt signaling and insulin resistance. Together, these data suggest that activation of FoxO1 is an important mediator of diabetic cardiomyopathy and is a promising therapeutic target for the disease.