PDF(Pubmed)
Abstract：
Common psychiatric disorders (CPDs) and depression contribute significantly to the global epidemic of type 2 diabetes (T2D). We postulated a possible pathophysiological mechanism that through Bridge-Symptoms present in depression and CPDs, promotes the establishment of emotional eating, activation of the reward system, onset of overweight and obesity and, ultimately the increased risk of developing T2D. The plausibility of the proposed pathophysiological mechanism is supported by the mechanism of action of drugs such as naltrexone-bupropion currently approved for the treatment of both obesity/overweight with T2D and as separate active pharmaceutical ingredients in drug addiction, but also from initial evidence that is emerging regarding glucagon-like peptide 1 receptor agonists that appear to be effective in the treatment of drug addiction. We hope that our hypothesis may be useful in interpreting the higher prevalence of CPDs and depression in patients with T2D compared with the general population and may help refine the integrated psychiatric-diabetic therapy approach to improve the treatment and or remission of T2D.
摘要：
常见的精神疾病（CPD）和抑郁症是2型糖尿病（T2D）全球流行的重要原因。我们推测了一种可能的病理生理机制，通过抑郁症和CPDs中存在的桥症状，促进情绪化饮食的建立，激活奖励系统，超重和肥胖的发作，最终增加患T2D的风险。拟议的病理生理机制的合理性得到了纳曲酮-安非他酮等药物的作用机制的支持，这些药物目前已被批准用于治疗T2D肥胖/超重以及作为药物成瘾中的单独活性药物成分，但也有初步证据表明，胰高血糖素样肽1受体激动剂似乎在药物成瘾的治疗中有效。我们希望我们的假设可能有助于解释与一般人群相比，T2D患者中CPD和抑郁症的患病率更高，并可能有助于完善综合精神病-糖尿病治疗方法，以改善T2D的治疗和/或缓解。
