Details of Metabolite

General Information of MET (ID: META00515)
Name D-Ornithine
Synonyms   Click to Show/Hide Synonyms of This Metabolite
(2R)-2,5-Diaminopentanoate; (2R)-2,5-Diaminopentanoic acid; (R)-Ornithine; Ornithine
Source Endogenous;Food
Structure Type   Amino acids, peptides, and analogues  (Click to Show/Hide the Complete Structure Type Hierarchy)
Organic acids and derivatives
Carboxylic acids and derivatives
Amino acids, peptides, and analogues
PubChem CID
71082
HMDB ID
HMDB0003374
Formula
C5H12N2O2
Structure
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3D MOL 2D MOL
  Click to Show/Hide the Molecular/Functional Data (External Links/Property/Function) of This Metabolite
KEGG ID
C00515
ChEBI ID
16176
FooDB ID
FDB023157
ChemSpider ID
64236
METLIN ID
6910
Physicochemical Properties Molecular Weight 132.16 Topological Polar Surface Area 89.3
XlogP -4.4 Complexity 95
Heavy Atom Count 9 Rotatable Bond Count 4
Hydrogen Bond Donor Count 3 Hydrogen Bond Acceptor Count 4
Function
D-Ornithine is an amino acid produced in the urea cycle by the splitting off of urea from arginine. Ornithine is one of the products of the action of the enzyme arginase on L-arginine, creating urea. Therefore, ornithine is a central part of the urea cycle, which allows for the disposal of excess nitrogen. D-Ornithine has been identified in the human placenta.
Regulatory Network
Full List of Protein(s) Regulating This Metabolite
      GPCR secretin (GPCR-2)
            Glucagon receptor (GCGR) Click to Show/Hide the Full List of Regulating Pair(s):   1 Pair(s)
               Detailed Information Protein   Info click to show the details of this protein
               Regulating Pair Experim Info click to show the details of experiment for validating this pair [1]
                      Introduced Variation Knockout of Gcgr
                      Induced Change D-Ornithine concentration: increase (FC = 5.4)
                      Summary Introduced Variation         Induced Change 
                      Disease Status Type 2 diabetes mellitus [ICD-11: 5A11]
                      Details It is reported that knockout of GCGR leads to the increase of D-Ornithine levels compared with control group.
      Hydrolases (EC 3)
            Sulfatase sulf-1 (SULF1) Click to Show/Hide the Full List of Regulating Pair(s):   1 Pair(s)
               Detailed Information Protein   Info click to show the details of this protein
               Regulating Pair Experim Info click to show the details of experiment for validating this pair [2]
                      Introduced Variation Knockdown (shRNA) of SULF1
                      Induced Change D-Ornithine concentration: decrease (FC = 0.36 / 0.52)
                      Summary Introduced Variation         Induced Change 
                      Disease Status Ovarian cancer [ICD-11: 2C73]
                      Details It is reported that knockdown of SULF1 leads to the decrease of D-Ornithine levels compared with control group.
      Pore-forming PNC peptide (PNC)
            Cellular tumor antigen p53 (TP53) Click to Show/Hide the Full List of Regulating Pair(s):   1 Pair(s)
               Detailed Information Protein   Info click to show the details of this protein
               Regulating Pair Experim Info click to show the details of experiment for validating this pair [3]
                      Introduced Variation Knockout of TP53
                      Induced Change D-Ornithine concentration: decrease (Log2 FC=0.68)
                      Summary Introduced Variation         Induced Change 
                      Disease Status Colon cancer [ICD-11: 2B90]
                      Details It is reported that knockout of TP53 leads to the decrease of D-Ornithine levels compared with control group.
References
1 Polyomic profiling reveals significant hepatic metabolic alterations in glucagon-receptor (GCGR) knockout mice: implications on anti-glucagon therapies for diabetes. BMC Genomics. 2011 Jun 1;12:281.
2 Erratum to: Loss of HSulf-1 promotes altered lipid metabolism in ovarian cancer. Cancer Metab. 2014 Nov 4;2:24.
3 Integrative omics analysis of p53-dependent regulation of metabolism. FEBS Lett. 2018 Feb;592(3):380-393.

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