WELLBUTRIN FOR DEPRESSION IN DIABETIC PATIENTS

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。糖尿病在大约2000万成年人中存在，是发病率和死亡率的主要原因。高血糖是糖尿病神经病变、微血管和大血管并发症的主要原因，因此维持正常血糖一直是糖尿病治疗的重点。然而，即使在积极治疗的情况下，也很少实现足以预防糖尿病并发症发展的血糖控制(1，2)。这加剧了对可以改善糖尿病病程的可修改因素的寻找，而抑郁症的管理可能是这些因素之一。临床抑郁存在于大约25%的糖尿病患者(1型或2型)中，与高血糖和增加并发症，特别是大血管疾病的风险有关。这些观察结果导致了一系列临床试验，以确定这些联系是否可以通过抑郁症治疗来操纵。这些研究表明，抑郁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。如果抑郁干预导致体重增加，这是一个单独的促进高血糖和胰岛素抵抗的因素，那么面对糖尿病，抑郁治疗的整体效果将被低估。到目前为止，对抑郁、血糖控制和体重有伴随的积极和持久影响的药物是可取的，但尚未确定。

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.