Postnatal hyperglycemia alters amino acid profile in retinas (model of Phase I ROP)

Area of Science:

• Ophthalmology
• Neonatology
• Nutritional Science

Background:

• Nutritional deprivation in preterm infants can lead to hyperglycemia, a risk factor for retinopathy of prematurity (ROP).
• Phase I ROP involves suppressed physiological retinal vascularization, potentially leading to pathological neovascularization.
• The role of amino acids in Phase I ROP is not well understood.

Purpose of the Study:

• To investigate the contribution of amino acids to hyperglycemia-associated Phase I ROP in a mouse model.
• To examine the association between parenteral and enteral amino acid intake and severe ROP in premature infants.

Main Methods:

• A mouse model of hyperglycemia-associated Phase I ROP was used to analyze retinal amino acid profiles.
• The effect of parenteral L-isoleucine on retinal vascularization was assessed in mice.
• Retrospective analysis of amino acid intake (parenteral vs. enteral) in premature infants with and without severe ROP.

Main Results:

• Significant changes in retinal amino acids were observed in the mouse model, with notable decreases in L-leucine, L-isoleucine, and L-valine.
• Parenteral L-isoleucine administration suppressed physiological retinal vascularization in mice.
• In premature infants, higher parenteral amino acid intake correlated with severe ROP, and the duration of parenteral support independently predicted ROP severity.

Conclusions:

• Amino acid alterations are implicated in hyperglycemia-associated Phase I ROP.
• Modulating amino acid levels, particularly via parenteral nutrition, may influence ROP development.
• Further research into amino acid metabolism and targeted nutritional interventions could improve ROP prevention in preterm infants.