Summary of Study ST002497

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001612. The data can be accessed directly via it's Project DOI: 10.21228/M8BB1T This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

Study ID	ST002497
Study Title	Postnatal hyperglycemia alters amino acid profile in retinas
Study Summary	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
Institute	Boston Childrens Hospital
Last Name	Fu
First Name	Zhongjie
Address	1 Blackfan Circle, Boston, MA 02114
Email	Zhongjie.Fu@childrens.harvard.edu
Phone	617-919-2534
Submit Date	2023-02-16
Raw Data Available	Yes
Raw Data File Type(s)	mzXML
Analysis Type Detail	LC-MS
Release Date	2023-03-22
Release Version	1

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Treatment:

Treatment ID:	TR002606
Treatment Summary:	To study the metabolic alterations occurring in hyperglycemia-associated Phase I ROP, we applied quantitative metabolomics and proteomics on mouse retinas from HAR and normal control mice. C57BL/6J (Jackson Laboratory, Bar Harbor, ME) mice, of each sex, aged 10-12 weeks, were purchased, housed and bred in the institutional vivarium and maintained on a 12hour/12hour light/dark cycle with mouse chow provided ad libitum. Neonatal mice were randomly assigned to experimental groups. Induction of hyperglycemia was accomplished as previously described 1. Neonatal mice were intraperitoneally injected with 50mg/kg/day STZ consecutively from P1 to P9 using a 34-G needle (Hamilton syringe) (Fig. 1B). Vehicle control animals received equal volumes of vehicle phosphate-buffered saline (PBS, Gibco, Waltham, MA). Hyperglycemia is induced around P8 and delayed retinal vascularization is found at P10 1. Mice with weight range 4 to 5 grams were used for further metabolomics and proteomics analysis. Mouse litters were randomly assigned to HAR or control groups, both sexes were used. The cages were located at close spots to minimize the potential housing influences. All procedures were approved by our Institutional Animal Care and Use Committee and adhered to ARRIVE guidelines and the NIH Guide for the Care and Use of Laboratory Animals. With conditions tested with β=0.8 and α=0.05, at least n=6 per group will be needed for the analysis. Control was re-named as group 1 and HAR was re-named as group 2 for analysis.

Treatment ID:

TR002606

Treatment Summary:

To study the metabolic alterations occurring in hyperglycemia-associated Phase I ROP, we applied quantitative metabolomics and proteomics on mouse retinas from HAR and normal control mice. C57BL/6J (Jackson Laboratory, Bar Harbor, ME) mice, of each sex, aged 10-12 weeks, were purchased, housed and bred in the institutional vivarium and maintained on a 12hour/12hour light/dark cycle with mouse chow provided ad libitum. Neonatal mice were randomly assigned to experimental groups. Induction of hyperglycemia was accomplished as previously described 1. Neonatal mice were intraperitoneally injected with 50mg/kg/day STZ consecutively from P1 to P9 using a 34-G needle (Hamilton syringe) (Fig. 1B). Vehicle control animals received equal volumes of vehicle phosphate-buffered saline (PBS, Gibco, Waltham, MA). Hyperglycemia is induced around P8 and delayed retinal vascularization is found at P10 1. Mice with weight range 4 to 5 grams were used for further metabolomics and proteomics analysis. Mouse litters were randomly assigned to HAR or control groups, both sexes were used. The cages were located at close spots to minimize the potential housing influences. All procedures were approved by our Institutional Animal Care and Use Committee and adhered to ARRIVE guidelines and the NIH Guide for the Care and Use of Laboratory Animals. With conditions tested with β=0.8 and α=0.05, at least n=6 per group will be needed for the analysis. Control was re-named as group 1 and HAR was re-named as group 2 for analysis.