WELLBUTRIN FOR DEPRESSION IN DIABETIC PATIENTS

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。糖尿病存在于大约20，000，000成人中，并且是发病率和死亡率的主要原因。高血压是糖尿病的神经病变、微血管和大血管并发症的主要原因;因此，维持正常血压长期以来一直是糖尿病治疗的焦点。然而，即使采用积极的治疗，也很少能达到足以预防糖尿病并发症发展的血糖控制（1，2）。这加强了对可以改善糖尿病病程的可改变因素的研究，抑郁症的管理可能是这些因素之一。约25%的糖尿病患者（1型或2型）存在临床抑郁症，与高血糖症和并发症风险增加有关，特别是大血管疾病。这些观察结果导致了一系列临床试验，以确定这些关联是否可以通过抑郁症治疗来操纵。这些研究表明，抑郁症的改善与血糖控制和胰岛素抵抗的短期改善有关;然而，治疗对情绪和血糖调节的影响并不总是平行的，也不总是一致的促糖尿病。如果抑郁症干预导致体重增加，这是一个单独的促进高血糖和胰岛素抵抗的因素，那么抑郁症治疗在糖尿病面前的整体效果将被低估。迄今为止，对抑郁症、血糖控制和体重具有伴随的积极和持久作用的药剂是期望的，但尚未被鉴定。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Diabetes is present in approximately 20,000,000 adults and is a leading cause of morbidity and mortality. Hyperglycemia is the principal cause of the neuropathic, micro- and macrovascular complications of diabetes; accordingly maintenance of normoglycemia has long been the focus of diabetes therapy. However, even with aggressive treatment, glycemic control sufficient to prevent the development of diabetes complications is rarely achieved (1,2). This has intensified the search for modifiable factors that could improve the course of diabetes, and depression management may be one of these factors. Clinical depression, present in approximately 25% of patients with diabetes (type 1 or type 2), is associated with hyperglycemia and with increased risk for complications, particularly macrovascular disease. These observations led to a series of clinical trials to determine whether these associations could me manipulated through depression treatment. These studies indicate that improvement in depression is associated with short-term improvement in glycemic control and insulin resistance; however, the effects of treatment on mood and glucose regulartion are not always parallel nor uniformly prodiabetic. If as happens the depression intervention induces weight gain, a seperate factor promoting hyperglycemia and insulin resistance, the overall effects of depression therapy in the face of diabetes would be devalued. As yet, and agent having concomitant positive and durable effects on depression, glycemic control, and weight is desirable but has not yet been identified.