Journal
AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 101, Issue 4, Pages 879-888Publisher
OXFORD UNIV PRESS
DOI: 10.3945/ajcn.114.099291
Keywords
omega-3 long-chain polyunsaturated fatty acids; adiponectin; endoplasmic reticulum stress; retinopathy of prematurity; white adipose tissue; neovascularization
Categories
Funding
- NIH/National Eye Institute [EY022275, EY017017, EY024963]
- Boston Children's Hospital Mental Retardation and Developmental Disabilities Research Center [P01 HD18655]
- project PREVENT-ROP from the Lowy Medical Research Foundation, European Commission FP7 (LEHS) [305485]
- project PREVENT-ROP from the European Commission FP7 [305485, VINNOVA 2009-01152]
- Swedish Medical Research Council [2011-2432]
- Swedish government [ALFGB2770]
- Swedish Research Council [14940]
- governmental ALF research grants
- BrightFocus Foundation Macular Degeneration research grant
- career development award from Boston Children's Hospital
- Burroughs Wellcome Fund Career Awards for Medical Scientists
- Canadian Institutes of Health Research Fellowship
- Foundation Fighting Blindness Operational grant
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Background: Retinopathy of prematurity (ROP) is a vision-threatening disease in premature infants. Serum adiponectin (APN) concentrations positively correlate with postnatal growth and gestational age, important risk factors for ROP development. Dietary omega-3 (n-3) long-chain polyunsaturated fatty acids (omega-3 LCPUFAs) suppress ROP and oxygen-induced retinopathy (OIR) in a mouse model of human ROP, but the mechanism is not fully understood. Objective: We examined the role of APN in ROP development and whether circulating APN concentrations are increased by dietary omega-3 LCPUFAs to mediate the protective effect in ROP. Design: Serum APN concentrations were correlated with ROP development and serum omega-3 LCPUFA concentrations in preterm infants. Mouse OIR was then used to determine whether omega-3 LCPUFA supplementation increases serum APN concentrations, which then suppress retinopathy. Results: We found that in preterm infants, low serum APN concentrations positively correlate with ROP, and serum APN concentrations positively correlate with serum omega-3 LCPUFA concentrations. In mouse OIR, serum total APN and bioactive high-molecular-weight APN concentrations are increased by omega-3 LCPUFA feed. White adipose tissue, where APN is produced and assembled in the endoplasmic reticulum, is the major source of serum APN. In mouse OIR, adipose endoplasmic reticulum stress is increased, and APN production is suppressed. omega-3 LCPUFA feed in mice increases APN production by reducing adipose endoplasmic reticulum stress markers. Dietary omega-3 LCPUFA suppression of neovascularization is reduced from 70% to 10% with APN deficiency. APN receptors localize in the retina, particularly to pathologic neovessels. Conclusion: Our findings suggest that increasing APN by omega-3 LCPUFA supplementation in total parental nutrition for preterm infants may suppress ROP.
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