Association of Retinopathy of Prematurity With Low Levels of Arachidonic Acid

Löfqvist, Chatarina; Najm, Svetlana; Hellgren, Gunnel; Engström, Eva; Sävman, Karin; Nilsson, Anders; Andersson, Mats X.; Hård, Anna‐Lena; Smith, Lois E H; Hellström, Ann

doi:10.1001/jamaophthalmol.2017.6658

Cited by 62 publications

(65 citation statements)

References 41 publications

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“…It is well-documented that in the early postnatal period of preterm infants, whole blood docosahexaenoic acid (DHA, C22:6n-3) and arachidonic acid (ARA, C20:4n-6) deficits and linoleic acid (LA, C18:2n-6) excesses occur within the first postnatal week [50]. Although these altered fatty acid profiles have been linked to the increased risk of developing bronchopulmonary dysplasia, retinopathy of prematurity, and late onset sepsis, the impact of these altered fatty acid profiles on intestinal development has just recently been described [50][51][52].…”

Section: Polyunsaturated Fatty Acidsmentioning

confidence: 99%

Breast Milk Lipids and Fatty Acids in Regulating Neonatal Intestinal Development and Protecting against Intestinal Injury

et al. 2020

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Human breast milk is the optimal source of nutrition for infant growth and development. Breast milk fats and their downstream derivatives of fatty acids and fatty acid-derived terminal mediators not only provide an energy source but also are important regulators of development, immune function, and metabolism. The composition of the lipids and fatty acids determines the nutritional and physicochemical properties of human milk fat. Essential fatty acids, including long-chain polyunsaturated fatty acids (LCPUFAs) and specialized pro-resolving mediators, are critical for growth, organogenesis, and regulation of inflammation. Combined data including in vitro, in vivo, and human cohort studies support the beneficial effects of human breast milk in intestinal development and in reducing the risk of intestinal injury. Human milk has been shown to reduce the occurrence of necrotizing enterocolitis (NEC), a common gastrointestinal disease in preterm infants. Preterm infants fed human breast milk are less likely to develop NEC compared to preterm infants receiving infant formula. Intestinal development and its physiological functions are highly adaptive to changes in nutritional status influencing the susceptibility towards intestinal injury in response to pathological challenges. In this review, we focus on lipids and fatty acids present in breast milk and their impact on neonatal gut development and the risk of disease.

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Section: Polyunsaturated Fatty Acidsmentioning

confidence: 99%

Breast Milk Lipids and Fatty Acids in Regulating Neonatal Intestinal Development and Protecting against Intestinal Injury

et al. 2020

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“…In premature infants, high triglycerides are associated with increased severity of retinopathy of prematurity (ROP; Sinclair et al , ). The ω‐6 LCPUFA, arachidonic acid, level is also significantly lower in severe ROP in premature infants at postmenstrual age of 32 weeks (Lofqvist et al , ). Although the results from many studies exploring the associations between diabetic retinopathy (DR) and lipid abnormality are inconsistent, one study found that high circulating LDL cholesterol levels are a significant risk factor for diabetic macular edema and retinal hard exudates (Chang & Wu, ).…”

Section: Dyslipidemia In Neurovascular Retinopathiesmentioning

confidence: 99%

“…Severe ROP is reduced in premature infants (GA < 32 weeks) receiving ω‐3 LCPUFA versus parenteral soybean and olive oil supplementation (Pawlik et al , ). There is also an association between low serum levels of ω‐6 LCPUFA (AA) and later development of ROP (Lofqvist et al , ). In mice, dietary ω‐3 versus ω‐6 LCPUFA suppresses retinal neovascularization (Connor et al , ; Fu et al , ).…”

Section: Dyslipidemia In Neurovascular Retinopathiesmentioning

confidence: 99%

Dyslipidemia in retinal metabolic disorders

Chen

Cagnone

et al. 2019

EMBO Mol Med

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The light‐sensitive photoreceptors in the retina are extremely metabolically demanding and have the highest density of mitochondria of any cell in the body. Both physiological and pathological retinal vascular growth and regression are controlled by photoreceptor energy demands. It is critical to understand the energy demands of photoreceptors and fuel sources supplying them to understand neurovascular diseases. Retinas are very rich in lipids, which are continuously recycled as lipid‐rich photoreceptor outer segments are shed and reformed and dietary intake of lipids modulates retinal lipid composition. Lipids (as well as glucose) are fuel substrates for photoreceptor mitochondria. Dyslipidemia contributes to the development and progression of retinal dysfunction in many eye diseases. Here, we review photoreceptor energy demands with a focus on lipid metabolism in retinal neurovascular disorders.

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“…Macronutrient transport protein expression has been associated with cellular-level placental histologic changes in preeclampsia; specifically, increased fatty acid placental transfer and maternal systemic circulation have been suggested to mediate disease in early onset preeclampsia [190]. As discussed previously, ROP development has been associated with decreased circulating fatty acids longitudinally from birth [191]. Combined, these studies suggest that an integrated systems approach, combining maternal and placental pathobiology relative to preterm infant ROP can elucidate underlying mechanisms of protection that can be therapeutically replicated post-natally or even in-utero to prevent ROP.…”

Section: A Novel Model Of Natural Rop Protectionmentioning

confidence: 99%

Current evidence and outcomes for retinopathy of prematurity prevention: insight into novel maternal and placental contributions

Carroll

Owen

2020

Exploration of Medicine

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Retinopathy of prematurity (ROP) is a blinding morbidity of preterm infants, which represents a significant clinical problem, accounting for up to 40% of all childhood blindness. ROP displays a range of severity, though even mild disease may result in life-long visual impairment. This is complicated by the fact that our current treatments have significant ocular and potentially systemic effects. Therefore, disease prevention is desperately needed to mitigate the life-long deleterious effects of ROP for preterm infants. Although ROP demonstrates a delayed onset of retinal disease following preterm birth, representing a potential window for prevention, we have been unable to sufficiently alter the natural disease course and meaningfully prevent ROP. Prevention therapeutics requires knowledge of early ROP molecular changes and risk, occurring prior to clinical retinal disease. While we still have an incomplete understanding of these disease mechanisms, emerging data integrating contributions of maternal/placental pathobiology with ROP are poised to inform novel approaches to prevention. Herein, we review the molecular basis for current prevention strategies and the clinical outcomes of these interventions. We also discuss how insights into early ROP pathophysiology may be gained by a better understanding of maternal and placental factors playing a role in preterm birth.

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Association of Retinopathy of Prematurity With Low Levels of Arachidonic Acid

Cited by 62 publications

References 41 publications

Breast Milk Lipids and Fatty Acids in Regulating Neonatal Intestinal Development and Protecting against Intestinal Injury

Breast Milk Lipids and Fatty Acids in Regulating Neonatal Intestinal Development and Protecting against Intestinal Injury

Dyslipidemia in retinal metabolic disorders

Current evidence and outcomes for retinopathy of prematurity prevention: insight into novel maternal and placental contributions

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