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Dietary omega-3 polyunsaturated fatty acids decrease retinal neovascularization by adipose-endoplasmic reticulum stress reduction to increase adiponectin

Artikel i vetenskaplig tidskrift
Författare Z. J. Fu
Chatarina Löfqvist
Z. Shao
Y. Sun
J. S. Joyal
C. G. Hurst
R. Z. Cui
L. P. Evans
K. Tian
J. P. Sangiovanni
J. Chen
D. Ley
I. H. Pupp
Ann Hellström
L. E. H. Smith
Publicerad i American Journal of Clinical Nutrition
Volym 101
Nummer/häfte 4
Sidor 879-888
ISSN 0002-9165
Publiceringsår 2015
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 879-888
Språk en
Länkar dx.doi.org/10.3945/ajcn.114.099291
Ämnesord omega-3 long-chain polyunsaturated fatty acids, adiponectin, endoplasmic reticulum stress, OXYGEN-INDUCED RETINOPATHY, ENDOTHELIAL-CELL APOPTOSIS, MOLECULAR-WEIGHT, FORM, PATHOLOGICAL ANGIOGENESIS, PRETERM INFANTS, NITRIC-OXIDE, FISH-OIL, PREMATURITY, MOUSE, SUPPRESSION, Nutrition & Dietetics
Ämneskategorier Näringslära

Sammanfattning

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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