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Zhongjie Fu, Chatarina Lofqvist, Aimee Juan, Zhenghao Cui, Dorothy Pei, Christian Hurst, Lucy Evans, Jing Chen, Ann Hellström, Lois Smith; Adiponectin mediates protective effect of omega-3 long-chain polyunsaturated fatty acid in retinopathy of prematurity. Invest. Ophthalmol. Vis. Sci. 2013;54(15):615.
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Retinopathy of prematurity (ROP) is a blinding disease caused by inadequate retinal vascularization after premature birth resulting in retinal ischemia, which stimulates vision-threatening proliferative ROP. Lack of factors normally available in the third trimester of pregnancy, such as omega-3 long-chain polyunsaturated fatty acid (ω-3 LCPUFA), is associated with development of retinopathy, and dietary supplement of ω-3 LCPUFA is protective in a mouse model of ROP. Our preliminary data show that adiponectin (APN), an adipocytokine abundantly expressed in adipose tissue, is significantly lower in serum from preterm infants who develop ROP compared with those without ROP. We aimed to determine whether decreased APN levels in ROP is associated with deficiency of ω-3 LCPUFA, and if APN mediates in part the protective effect of ω-3 LCPUFA in ROP.
Longitudinal serum APN levels in 46 infants (ROP: n=18; no ROP, n=28) with gestational age (GA) <29 weeks was measured weekly using ELISA. The serum levels of arachidonic acid (AA) and docosahexaenoic acid (DHA) were analyzed by capillary gas-liquid chromatography at 30 weeks GA. For the animal study, adiponectin knockout (APN-/-) and wild-type (WT) mice were fed from birth isocaloric diet enriched with either ω-3 or ω-6 LCPUFA in a mouse model of oxygen-induced retinopathy (OIR). Pups were analyzed at P17 for serum adiponectin levels and retinal vaso-obliteration and neovascularization. APN and its receptor adipoR1 were examined with immunohistochemistry.
Significantly lower serum APN levels were observed in preterm infants at the induction of proliferative ROP (33-36 weeks GA) compared with those with no ROP. Serum APN levels were correlated with serum DHA, but not with AA. In the mouse model of ROP, dietary ω-3 LCPUFA feed increased serum APN level at P17 compared with ω-6 feed. Moreover, the vaso-protective effect of ω-3 LCPUFA in OIR observed in WT retinae compared with omega-6 feed was abolished in APN-/- retinae. APN and its receptor adipoR1 were localized in endothelial cells and macrophages in both neovascular areas and inner retina in OIR.
Dietary ω-3 LCPUFA may regulate production of serum APN in ROP and APN likely mediates in part the protective effects of ω-3 LCPUFA in OIR.
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