Chrysostomou Vicki, van Wijngaarden Peter, Steinberg Gregory R, Crowston Jonathan G
Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, 32 Gisborne Street, East Melbourne VIC 3002, Australia; Ophthalmology, University of Melbourne, Department of Surgery, 32 Gisborne Street, East Melbourne VIC 3002, Australia.
Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, 32 Gisborne Street, East Melbourne VIC 3002, Australia; Ophthalmology, University of Melbourne, Department of Surgery, 32 Gisborne Street, East Melbourne VIC 3002, Australia.
Exp Eye Res. 2017 Sep;162:104-109. doi: 10.1016/j.exer.2017.07.015. Epub 2017 Jul 27.
The aim of the current work was to test whether increased intake of dietary fat and sucrose in mice modifies the response of retinal ganglion cells (RGCs) of the optic nerve to injury, and whether any effects of diet are influenced by physical activity levels. C57BL/6J mice were given a high-fat high-sucrose (HFS) diet for 7 weeks, with or without exposure to regular exercise by swimming (60 min/day, 5 days/week). Injury to RGCs was subsequently induced by acute elevation of intraocular pressure (IOP) and retinas were assessed for function and structure. We report that mice on a HFS diet had similar body mass and blood glucose levels compared to mice on a control diet but suffered a 30% greater loss of RGC function following injury, as measured in vivo with the electroretinogram. RGC dysfunction in retinas from mice on the HFS diet was accompanied by activation of retinal macroglia but was not associated with neuronal cell loss. Exercising mice by swimming did not prevent HFS-induced RGC dysfunction in response to injury. This study shows for the first time that a short term increase in dietary fat and sucrose enhances the vulnerability of RGCs to dysfunction and cell stress after an acute injury, and that this is independent of obesity or hyperglycemia. Furthermore, our results suggest that detrimental effects of diet predominate over protective effects of exercise.
当前研究的目的是测试增加小鼠饮食中脂肪和蔗糖的摄入量是否会改变视神经视网膜神经节细胞（RGCs）对损伤的反应，以及饮食的任何影响是否受身体活动水平的影响。将C57BL/6J小鼠给予高脂高糖（HFS）饮食7周，有无通过游泳进行规律运动（每天60分钟，每周5天）。随后通过急性眼压升高诱导RGCs损伤，并评估视网膜的功能和结构。我们报告，与对照饮食的小鼠相比，HFS饮食的小鼠体重和血糖水平相似，但损伤后RGC功能丧失增加了30%，这是通过视网膜电图在体内测量的。HFS饮食小鼠视网膜中的RGC功能障碍伴随着视网膜大胶质细胞的激活，但与神经元细胞丢失无关。通过游泳锻炼小鼠并不能预防HFS诱导的RGC对损伤的功能障碍。这项研究首次表明，饮食中脂肪和蔗糖的短期增加会增强RGCs在急性损伤后功能障碍和细胞应激的易感性，且这与肥胖或高血糖无关。此外，我们的结果表明饮食的有害影响超过运动的保护作用。
