We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Ultraviolet Radiation Suppresses Obesity and Symptoms of Metabolic Syndrome Independently of Vitamin D in Mice Fed a High-Fat Diet.
- Authors
Geldenhuys, Sian; Hart, Prue H.; Endersby, Raelene; Jacoby, Peter; Feelisch, Martin; Weller, Richard B.; Matthews, Vance; Gorman, Shelley
- Abstract
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)D] 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.
- Subjects
PHYSIOLOGICAL effects of ultraviolet radiation; PHYSIOLOGICAL effects of vitamin D; PREVENTION of obesity; METABOLIC syndrome; TYPE 2 diabetes; NITRIC oxide; HIGH-fat diet; LABORATORY mice
- Publication
Diabetes, 2014, Vol 63, Issue 11, p3759
- ISSN
0012-1797
- Publication type
Article
- DOI
10.2337/db13-1675