Ultraviolet Radiation Suppresses Obesity and Symptoms of Metabolic Syndrome Independently of Vitamin D in Mice Fed a High-Fat Diet
Ultraviolet Radiation Suppresses Obesity and Symptoms of Metabolic Syndrome Independently of Vitamin D in Mice Fed a High-Fat Diet
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DOI：
10.2337/db13-1675
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发表时间：
2014-11-01
期刊：
影响因子：
7.7
通讯作者：
Gorman, Shelley
中科院分区：
文献类型：
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作者：
Geldenhuys, Sian;Hart, Prue H.;Gorman, Shelley
最近，维生素D在减少肥胖和代谢综合征（MetS）和2型糖尿病等合并症的发展方面的作用受到了广泛关注。然而，临床试验未能最终证明补充维生素D的好处。在大多数研究中，血清25-羟基维生素D [25(OH)13]随着BMI高于正常体重的增加而降低。这些较低的25(OH)D水平也可能是暴露于阳光衍生的紫外线辐射（UVR）减少的代表。在这里，我们研究了UVR和/或维生素D补充剂是否会改变肥胖小鼠模型中肥胖和2型糖尿病的发展。长期红斑下和红斑性紫外线照射可显著抑制体重增加、葡萄糖耐受不良、胰岛素抵抗、非酒精性脂肪肝等指标；C57BL/6雄性小鼠的空腹胰岛素、葡萄糖和胆固醇水平。然而，紫外线辐射的许多好处并不能通过补充维生素D来重现。在进一步的机制研究中，皮肤诱导UVR诱导的介质一氧化氮（NO）再现了UVR的许多效应。这些研究表明，UVR（阳光照射）可能是抑制肥胖和MetS发展的有效手段，其机制不依赖于维生素D，但依赖于其他UVR诱导的介质，如NO。
The role of vitamin D in curtailing the development of obesity and comorbidities such as the metabolic syndrome (MetS) and type 2 diabetes has received much attention recently. However, clinical trials have failed to conclusively demonstrate the benefits of vitamin D supplementation. In most studies, serum 25-hydroxyvitamin D [25(OH)13] decreases with increasing BMI above normal weight. These low 25(OH)D levels may also be a proxy for reduced exposure to sunlight-derived ultraviolet radiation (UVR). Here we investigate whether UVR and/or vitamin D supplementation modifies the development of obesity and type 2 diabetes in a murine model of obesity. Long-term suberythemal and erythemal UVR significantly suppressed weight gain, glucose intolerance, insulin resistance, nonalcoholic fatty liver disease measures; and serum levels of fasting insulin, glucose, and cholesterol in C57BL/6 male mice fed a high-fat diet. However, many of the benefits of UVR were not reproduced by vitamin D supplementation. In further mechanistic studies, skin induction of the UVR-induced mediator nitric oxide (NO) reproduced many of the effects of UVR. These studies suggest that UVR (sunlight exposure) may be an effective means of suppressing the development of obesity and MetS, through mechanisms that are independent of vitamin D but dependent on other UVR-induced mediators such as NO.