Omega-3/Omega-6 Long-Chain Fatty Acid Imbalance in Phase I Retinopathy of Prematurity
Zhongjie Fu; Wenjun Yan; Chuck T. Chen; Anders K. Nilsson; Edward Bull; William Allen; Jay Yang; Minji Ko; John Paul SanGiovanni; James D. Akula; Saswata Talukdar; Ann Hellström; Lois E. H. Smith
There is a gap in understanding the effect of the essential &omega:-3 and &omega:-6 long-chain polyunsaturated fatty acids (LCPUFA) on Phase I retinopathy of prematurity (ROP), which precipitates proliferative ROP. Postnatal hyperglycemia contributes to Phase I ROP by delaying retinal vascularization. In mouse neonates with hyperglycemia-associated Phase I retinopathy, dietary &omega:-3 (vs. &omega:-6 LCPUFA) supplementation promoted retinal vessel development. However, &omega:-6 (vs. &omega:-3 LCPUFA) was also developmentally essential, promoting neuronal growth and metabolism as suggested by a strong metabolic shift in almost all types of retinal neuronal and glial cells identified with single-cell transcriptomics. Loss of adiponectin (APN) in mice (mimicking the low APN levels in Phase I ROP) decreased LCPUFA levels (including &omega:-3 and &omega:-6) in retinas under normoglycemic and hyperglycemic conditions. &omega:-3 (vs. &omega:-6) LCPUFA activated the APN pathway by increasing the circulating APN levels and inducing expression of the retinal APN receptor. Our findings suggested that both &omega:-3 and &omega:-6 LCPUFA are crucial in protecting against retinal neurovascular dysfunction in a Phase I ROP model: adequate &omega:-6 LCPUFA levels must be maintained in addition to &omega:-3 supplementation to prevent retinopathy. Activation of the APN pathway may further enhance the &omega:-3 and &omega:-6 LCPUFA&rsquo:s protection against ROP.
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