Postnatal hyperglycemia alters amino acid profile in retinas
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ABSTRACT: Nutritional deprivation occurring in most preterm infants postnatally, can induce hyperglycemia, a significant and independent risk factor for suppressing physiological retinal vascularization (Phase I retinopathy of prematurity (ROP)), leading to compensatory but pathological neovascularization. Amino acid supplementation reduces retinal neovascularization in mice. Little is known about amino acid contribution to Phase I ROP. Significant changes in retinal amino acids (including most decreased L-leucine, L-isoleucine and L-valine) were found in mice modeling hyperglycemia-associated Phase I ROP, and parenteral (i.p.) L-isoleucine suppressed physiological retinal vascularization. In premature infants, severe ROP was associated with a higher mean intake of parenteral versus enteral amino acids in the first two weeks of life after adjustment for treatment group, gestational age at birth, birth weight and sex. The number of days with parenteral amino acids support independently predicted severe ROP. Further understanding and modulating amino acids may help improve nutritional intervention and prevent Phase I ROP
ORGANISM(S): Mouse Mus Musculus
TISSUE(S): Retina
DISEASE(S): Eye Disease
SUBMITTER: Zhongjie Fu
PROVIDER: ST002497 | MetabolomicsWorkbench | Thu Feb 16 00:00:00 GMT 2023
REPOSITORIES: MetabolomicsWorkbench
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