Centre for Eye Research Ireland, School of Physics, Clinical & Optometric Sciences, Environmental Sustainability and Health Institute, Technological University Dublin, Dublin, Republic of Ireland.
African Vision Research Institute, University of KwaZulu-Natal, Durban, South Africa.
Nutr Res Rev. 2019 Dec;32(2):247-264. doi: 10.1017/S095442241900012X. Epub 2019 Aug 14.
Macular pigment (MP) confers potent antioxidant and anti-inflammatory effects at the macula, and may therefore protect retinal tissue from the oxidative stress and inflammation associated with ocular disease and ageing. There is a body of evidence implicating oxidative damage and inflammation as underlying pathological processes in diabetic retinopathy. MP has therefore become a focus of research in diabetes, with recent evidence suggesting that individuals with diabetes, particularly type 2 diabetes, have lower MP relative to healthy controls. The present review explores the currently available evidence to illuminate the metabolic perturbations that may possibly be involved in MP's depletion. Metabolic co-morbidities commonly associated with type 2 diabetes, such as overweight/obesity, dyslipidaemia, hyperglycaemia and insulin resistance, may have related and independent relationships with MP. Increased adiposity and dyslipidaemia may adversely affect MP by compromising the availability, transport and assimilation of these dietary carotenoids in the retina. Furthermore, carotenoid intake may be compromised by the dietary deficiencies characteristic of type 2 diabetes, thereby further compromising redox homeostasis. Candidate causal mechanisms to explain the lower MP levels reported in diabetes include increased oxidative stress, inflammation, hyperglycaemia, insulin resistance, overweight/obesity and dyslipidaemia; factors that may negatively affect redox status, and the availability, transport and stabilisation of carotenoids in the retina. Further study in diabetic populations is warranted to fully elucidate these relationships.
黄斑色素（MP）在黄斑处具有强大的抗氧化和抗炎作用，因此可以保护视网膜组织免受与眼病和衰老相关的氧化应激和炎症。有大量证据表明，氧化损伤和炎症是糖尿病视网膜病变的潜在病理过程。因此，MP 已成为糖尿病研究的焦点，最近的证据表明，糖尿病患者，尤其是 2 型糖尿病患者，其 MP 相对健康对照组较低。本综述探讨了目前可用的证据，以阐明可能涉及 MP 耗竭的代谢紊乱。与 2 型糖尿病相关的代谢合并症，如超重/肥胖、血脂异常、高血糖和胰岛素抵抗，可能与 MP 有相关和独立的关系。肥胖和血脂异常的增加可能通过损害这些膳食类胡萝卜素在视网膜中的可用性、运输和同化来对 MP 产生不利影响。此外，糖尿病的饮食缺陷可能会影响类胡萝卜素的摄入，从而进一步破坏氧化还原平衡。解释糖尿病患者 MP 水平较低的候选因果机制包括氧化应激增加、炎症、高血糖、胰岛素抵抗、超重/肥胖和血脂异常；这些因素可能会对氧化还原状态以及类胡萝卜素在视网膜中的可用性、运输和稳定性产生负面影响。需要在糖尿病患者中进一步研究这些关系。
