糖尿病可造成許多併發症，其中大血管的併發症如冠狀動脈疾病、中風和周邊動脈疾病，小血管的併發症則有視網膜、腎臟及神經病變等。許多大型研究( 如DCCT，EDIC，UKPDS) 都發現，在糖尿病早期，如給予積極血糖控制，相較於一般控制組，糖尿病的部份併發症（尤其是小血管併發症）顯著的減少。值得注意的是，在研究結束後的追蹤觀察，雖然兩組的糖化血色素數值已無差異，但是一開始即接受積極血糖控制的病患，各式大血管與小血管併發症以及死亡率仍然較低。部份學者提出「代謝記憶」(metabolic memory) 的概念來解釋此一現象。近年來，發現高血糖會影響表觀遺傳(epigenetic) 機制，如導致DNA甲基化，改變組蛋白(histone) 結構或微型RNA (microRNAs) 的表現，使細胞訊息傳遞下游發炎基因的表現增加，而造成糖尿病的併發症。另外，此一高血糖所導致的細胞遺傳物質改變，還會傳遞給新生細胞。藉由對血糖的「代謝記憶」之分子機制的了解，將有助於發展新的治療方式並減少或預防糖尿病各種併發症。

It is well established that patients with diabetes mellitus suffered from a variety of diabetes associated complications, including macrovascular diseases such as coronary artery disease, stroke, and peripheral arterial
disease, as well as microvascular complications such as diabetic retinopathy, nephropathy, and neuropathy.Findings from multiple major clinical interventional trials (i.e. DCCT, EDIC, and UKPDS) have consistently demonstrated that early glycemic control could lead to reduction of long-term complications, in particularly microvascular complications. Subsequent following up studies in the EDIC and UKPDS expanded and further concreted these observations that subjects originally assigned in the intensive treatment group continued to have
significant lower diabetic macro- and micro-vascular complications as well as all-cause mortality as compared to patients who were in the conventional treatment group. These findings have led to the proposed hypothesis of“metabolic memory”. In recent years, it is suggested that hyperglycemia might cause alteration of epigenetic,such as DNA methylation, histone structure or microRNAs expression, and then cause increase proinflammatory genes expression and associate with various diabetic complications. In addition, the epigenome that has been
modified by hyperglycemia can be transmitted through replication. Based on the further understanding of the molecular mechanisms of“metabolic memory”, it is hope to discover new therapeutic targets to reduce or prevent the development of diabetic complications.