Ocular surface complications in diabetes: The interrelationship between insulin and enkephalin.
Ocular surface complications in diabetes: The interrelationship between insulin and enkephalin.
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DOI：
10.1016/j.bcp.2021.114712
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发表时间：
2021-10
影响因子：
5.8
通讯作者：
McLaughlin PJ
中科院分区：
文献类型：
--
作者：
Purushothaman I;Zagon IS;Sassani JW;McLaughlin PJ
糖尿病是一种多方面的疾病，患病率不断增加，医疗费用不断上升。糖尿病的负担增加，因为相关的并发症影响几乎所有器官，包括眼睛。这些眼表疾病发病的基础病理生理学尚不清楚。脑啡肽是一种内源性阿片类物质，起源于大脑，在人体内具有多种作用。阿片样生长因子（OGF），化学名称为[Met 5]-脑啡肽，结合到一个新的，核相关的受体和介导的细胞内稳态。血清OGF水平在糖尿病个体和糖尿病啮齿动物模型中升高。用阿片受体拮抗剂如纳洛酮（NTX）持续阻断OGF受体（OGFr）可逆转动物模型中糖尿病的许多并发症，包括皮肤伤口愈合延迟、干眼、角膜表面敏感性改变和角膜病。在糖尿病中观察到的脑啡肽水平升高提示内源性阿片肽与糖尿病的病理生理学之间存在关系。糖尿病患者通常接受胰岛素治疗以恢复正常血糖水平。然而，这种恢复并不改变OGF血清水平，也不改善糖尿病动物模型中的眼表并发症。此外，糖尿病患病率、胰岛素治疗反应和OGF-OGFr轴异常的性别差异也有报道。这篇综述强调了目前对OGF-OGFr通路失调的认识，以及胰岛素和脑啡肽与糖尿病眼表缺陷发展的可能关系。它提出，这种失调是糖尿病并发症的病理生物学的基本机制。胰岛素途径和OGF-OGFr轴在糖尿病眼表并发症的形成方面是平行的。
Diabetes is a multi-faceted disorder with increasing prevalence and rising healthcare costs. The burden of diabetes is increased because of associated complications affecting nearly all organs including the eye. The underlying pathophysiology for the onset of these ocular surface disorders is not well known. Enkephalins are endogenous opioids that originate in the brain and have numerous actions in the human body. Opioid growth factor (OGF), chemically termed [Met5]-enkephalin, binds to a novel, nuclear-associated receptor and mediates cellular homeostasis. Serum OGF levels are elevated in diabetic individuals and rodent models of diabetes. Sustained blockade of the OGF receptor (OGFr) with opioid receptor antagonists, such as naltrexone (NTX), reverses many complications of diabetes in the animal model, including delayed cutaneous wound healing, dry eye, altered corneal surface sensitivity, and keratopathy. The increased enkephalin levels observed in diabetes suggest a relationship between endogenous opioid peptides and the pathophysiology of diabetes. It is common for diabetic patients to undergo insulin therapy to restore normal blood glucose levels. However, this restoration does not alter OGF serum levels nor ameliorate ocular surface complications in the animal model of diabetes. Moreover, sex differences in the prevalence of diabetes, response to insulin therapy, and abnormalities in the OGF-OGFr axis have been reported. This review highlights current knowledge on the dysregulation of the OGF-OGFr pathway and possible relationships of insulin and enkephalins to the development of ocular surface defects in diabetes. It proposes that this dysregulation is a fundamental mechanism for the pathobiology of diabetic complications. The insulin pathway and the OGF-OGFr axis word in parallel with regard to formation of ocular surface complications in diabetes.
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DOI：
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