• Mrudula Tiruvalluru, Prashanth Ananthathmakula, Vajreswari Ayyalasomayajula, Giridharan Nappanveettil, Radha Ayyagari, and Geereddy Bhanuprakash Reddy.
• Department of Biochemistry, National Institute of Nutrition, Hyderabad, India.
• Nutrition. 2013 Jan 1; 29 (1): 298-304.

ObjectiveObesity is associated with various health afflictions, including ocular complications such as diabetic retinopathy, high intraocular pressure, cataracts, and macular degeneration. We previously reported progressive retinal degeneration after the onset of obesity in the spontaneously obese rat (WNIN/Ob) model. In the present study, we investigated vitamin A supplementation to ameliorate obesity-associated retinal degeneration in the WNIN/Ob rat.MethodsFive-month-old male WNIN/Ob obese (O) and lean (L) control rats were fed with vitamin A 2.6 mg (L/O-I), 26 mg (L/O-II), 52 mg (L/O-III), and 129 mg (L/O-IV) per kilogram of diet as retinyl palmitate for 4 mo 2 wk. Retinal morphology and retinal gene expression were assessed by histologic, immunohistochemical, and real-time polymerase chain reaction methods.ResultsSupplementation of vitamin A at 26 or 52 mg significantly modulated the expression of retinal genes in the O but not in the L phenotype. Vitamin A supplementation significantly upregulated the expression of genes, such as rhodopsin, rod arrestin, phosphodiesterase, transducins, and fatty acid elongase-4, that were otherwise downregulated in O rat retina. The expression of glial fibrillary acidic protein was downregulated by vitamin A feeding in O rat retina. The immunohistochemical and histologic findings corroborated the gene expression data. The effects were significant at a 26- or 52-mg dose of vitamin A.ConclusionVitamin A supplementation alleviated obesity-associated retinal degeneration in the WNIN/Ob rat.Copyright © 2013 Elsevier Inc. All rights reserved.

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