Ignite Creation Date:
2024-05-05 @ 12:09 PM
Last Modification Date:
2024-10-26 @ 9:21 AM
Study NCT ID:
NCT00253760
Status:
COMPLETED
Last Update Posted:
2010-03-18
First Post:
2005-11-14
Brief Title:
Metabolic Analysis in Human Sulfur Amino Acid Deficiency
Sponsor:
National Institute of Diabetes and Digestive and Kidney Diseases NIDDK
Organization:
National Institute of Diabetes and Digestive and Kidney Diseases NIDDK
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2010-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Varied food intake disease and genetic differences result in complex diet-health interactions In principle information-rich metabolic analyses combined with bioinformatic tools provide an approach to explore these interactions This project is a feasibility study of the use of high-resolution 1H-nuclear magnetic resonance NMR to study metabolic perturbations induced by a deficiency in sulfur amino acids SAA The investigators will 1 test the hypothesis that deficient dietary intake of SAA in humans results in oxidation of reduced glutathione GSHoxidized glutathione GSSG redox and 2 determine whether 1H-NMR of blood and urine detects metabolic changes due to SAA deficiency
Detailed Description:
Varied food intake disease and genetic differences result in complex diet-health interactions In principle information-rich metabolic analyses combined with bioinformatic tools provide an approach to explore these interactions This project is a feasibility study of the use of high-resolution 1H-NMR to study metabolic perturbations induced by deficiency in sulfur amino acids SAA In cell culture sulfur amino acid SAA deficiency results in substantial oxidation of glutathione GSH redox state Because GSH redox affects central homeostatic and cell defense mechanisms redox changes in vivo due to SAA deficiency could induce complex physiologic effects that are not easily predictable by more traditional metabolic analyses We will 1 test the hypothesis that deficient dietary intake of SAA in humans results in oxidation of GSHGSSG redox and 2 determine whether 1H-NMR of blood and urine detects metabolic changes due to SAA deficiency Studies will be performed on 12 healthy individuals 6 males 6 females in the Emory General Clinical Research Center GCRC using a crossover design replete deficient replete Kinetic and balance studies will establish the time course and magnitude of changes in SAA and metabolites in blood and urine in response to SAA intake Plasma GSHGSSG and cysteinecystine redox will be measured to determine whether variation in intake of SAA affects steady-state thiol-disulfide redox state 1H-NMR spectra of blood and urine samples will be used to determine whether metabolic changes unrelated to the direct SAA metabolites can be detected in association with variation in SAA intake The results will show whether variation in SAA intake is likely to affect health risks associated with thiol-disulfide redox and oxidative stress Furthermore because NMR analysis of biofluids can be performed with a high throughput eg 300 samplesday with a flow cell results will show whether this approach could be useful for nutritional assessment of complex metabolic effects of SAA intake
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None