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| In biochemistry, medicine, and related sciences, inositol generally refers to myo-inositol (formerly meso-inositol), the most important stereoisomer of the chemical compound cyclohexane-1,2,3,4,5,6-hexol. Its formula is C6H12O6; the molecule has a ring of six carbon atoms, each with an hydrogen atom and a hydroxyl group (–OH). In myo-inositol, two of the hydroxyls, neither adjacent nor opposite, lie above the respective hydrogens relative to the mean plane of the ring.
The compound is a carbohydrate, specifically a sugar alcohol (as distinct from aldoses like glucose) with half the sweetness of sucrose (table sugar). It is one of the most ancient components of living beings with multiple functions in eukaryotes, including structural lipids and secondary messengers. A human kidney makes about two grams per day from glucose, but other tissues synthesize it too. The highest concentration is in the brain, where it plays an important role in making other neurotransmitters and some steroid hormones bind to their receptors. In other tissues, it mediates cell signal transduction in response to a variety of hormones, neurotransmitters, and growth factors and participates in osmoregulation. In most mammalian cells the concentrations of myo-inositol are 5 to 500 times greater inside cells than outside them.
A 2023 meta-analysis found that inositol is a safe and effective treatment in the management of polycystic ovary syndrome (PCOS). However, there is only evidence of very low quality for its efficacy in increasing fertility for IVF in women with PCOS.
The other naturally occurring stereoisomers of cyclohexane-1,2,3,4,5,6-hexol are scyllo-, muco-, D-chiro-, L-chiro-, and neo-inositol, although they occur in minimal quantities compared to myo-inositol. The other possible isomers are allo-, epi-, and cis-inositol. |
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Read full article at Wikipedia
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| InChI=1S/C6H12O6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-12H/t1-,2-,3-,4+,5-,6- |
| CDAISMWEOUEBRE-GPIVLXJGSA-N |
| O[C@H]1[C@H](O)[C@@H](O)[C@H](O)[C@H](O)[C@@H]1O |
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Daphnia magna
(NCBI:txid35525)
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See:
Mixtures of similarly acting compounds in Daphnia magna: From gene to metabolite and beyondTine Vandenbrouck, Oliver A.H. Jones, Nathalie Dom, Julian L. Griffin, Wim De CoenEnvironment International 36 (2010) 254-268
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Saccharomyces cerevisiae
(NCBI:txid4932)
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Source: yeast.sf.net
See:
PubMed
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
Saccharomyces cerevisiae metabolite
Any fungal metabolite produced during a metabolic reaction in Baker's yeast (Saccharomyces cerevisiae ).
compatible osmolytes
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
nutrient
A nutrient is a food component that an organism uses to survive and grow.
EC 3.1.4.11 (phosphoinositide phospholipase C) inhibitor
An EC 3.1.4.* (phosphoric diester hydrolase) inhibitor that interferes with the action of phosphatidylinositol-specific phospholipase C (EC 3.1.4.11).
Daphnia magna metabolite
A Daphnia metabolite produced by the species Daphnia magna.
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View more via ChEBI Ontology
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Outgoing
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myo-inositol
(CHEBI:17268)
has role
Daphnia magna metabolite
(CHEBI:83056)
myo-inositol
(CHEBI:17268)
has role
Escherichia coli metabolite
(CHEBI:76971)
myo-inositol
(CHEBI:17268)
has role
Saccharomyces cerevisiae metabolite
(CHEBI:75772)
myo-inositol
(CHEBI:17268)
has role
compatible osmolytes
(CHEBI:23366)
myo-inositol
(CHEBI:17268)
has role
EC 3.1.4.11 (phosphoinositide phospholipase C) inhibitor
(CHEBI:64763)
myo-inositol
(CHEBI:17268)
has role
human metabolite
(CHEBI:77746)
myo-inositol
(CHEBI:17268)
has role
mouse metabolite
(CHEBI:75771)
myo-inositol
(CHEBI:17268)
has role
nutrient
(CHEBI:33284)
myo-inositol
(CHEBI:17268)
is a
inositol
(CHEBI:24848)
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|
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Incoming
|
α-D-Galp-(1→3)-β-D-Galf-(1→3)-α-D-Manp-(1→3)-α-D-Manp-(1→4)-α-D-GlcpN-(1→6)-1D-myo-inositol
(CHEBI:61825)
has functional parent
myo-inositol
(CHEBI:17268)
α-D-Galp-(1→6)-α-D-Galp-(1→3)-β-D-Galf-(1→3)-α-D-Manp-(1→3)-α-D-Manp-(1→4)-α-D-GlcpN-(1→6)-myo-inositol
(CHEBI:61830)
has functional parent
myo-inositol
(CHEBI:17268)
α-D-galactosyl-(1→3)-1D-myo-inositol
(CHEBI:17505)
has functional parent
myo-inositol
(CHEBI:17268)
α-D-Manp-(1→2)-α-D-Manp-(1→2)-α-D-Manp-(1→6)-α-D-Manp-(1→6)-α-D-Manp-(1→6)-[α-D-Manp-(1→2)]-Ins
(CHEBI:140998)
has functional parent
myo-inositol
(CHEBI:17268)
(α-D-Man)-(1→4)-(α-D-GlcN)-(1→6)-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:61585)
has functional parent
myo-inositol
(CHEBI:17268)
(indol-3-ylacetyl)-myo-inositol 3-L-arabinoside
(CHEBI:28071)
has functional parent
myo-inositol
(CHEBI:17268)
1,3-bis(diphospho)-myo-inositol 2,4,5,6-tetrakisphosphate
(CHEBI:62925)
has functional parent
myo-inositol
(CHEBI:17268)
1,3-bis(diphospho)-myo-inositol 4,5,6-trisphosphate
(CHEBI:62929)
has functional parent
myo-inositol
(CHEBI:17268)
1,5-bis(diphospho)-1D-myo-inositol 2,3,4,6-tetrakisphosphate
(CHEBI:62923)
has functional parent
myo-inositol
(CHEBI:17268)
1,5-bis(diphospho)-1D-myo-inositol 3,4,6-trisphosphate
(CHEBI:62931)
has functional parent
myo-inositol
(CHEBI:17268)
1-acyl-sn-glycero-3-phospho-D-myo-inositol
(CHEBI:28914)
has functional parent
myo-inositol
(CHEBI:17268)
1-diphospho-1D-myo-inositol 2,3,4,5,6-pentakisphosphate
(CHEBI:62919)
has functional parent
myo-inositol
(CHEBI:17268)
1-diphospho-1D-myo-inositol 3,4,5,6-tetrakisphosphate
(CHEBI:62926)
has functional parent
myo-inositol
(CHEBI:17268)
1D-1-O-(indol-3-yl)acetyl-myo-inositol
(CHEBI:15711)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,2,3,4,5-pentakisphosphate
(CHEBI:18345)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,2,3,5,6-pentakisphosphate
(CHEBI:48405)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,2,4,5,6-pentakisphosphate
(CHEBI:16507)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,2,5,6-tetrakisphosphate
(CHEBI:133328)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,2-cyclic phosphate
(CHEBI:18426)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,3,4,5-tetrakisphosphate
(CHEBI:16783)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,3,4-trisphosphate
(CHEBI:18228)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,4,5,6-tetrakisphosphate
(CHEBI:16067)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1,4-bisphosphate
(CHEBI:17816)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 1-phosphate
(CHEBI:18297)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 2,4-bisphosphate
(CHEBI:133416)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 2-(L-cysteinylamino)-2-deoxy-α-D-glucopyranoside
(CHEBI:52285)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 2-acetamido-2-deoxy-α-D-glucopyranoside
(CHEBI:52442)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 2-acetamido-2-deoxy-α-D-glucopyranoside 3-phosphate
(CHEBI:52443)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 2-amino-2-deoxy-α-D-glucopyranoside
(CHEBI:52283)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 3,4,5,6-tetrakisphosphate
(CHEBI:15844)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 3,4,6-trisphosphate
(CHEBI:62918)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 3-phosphate
(CHEBI:18169)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 4,5-bisphosphate
(CHEBI:18156)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 4-phosphate
(CHEBI:18384)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 5-phosphate
(CHEBI:37493)
has functional parent
myo-inositol
(CHEBI:17268)
1D-myo-inositol 6-phosphate
(CHEBI:64838)
has functional parent
myo-inositol
(CHEBI:17268)
1L-1-O-(indol-3-yl)acetyl-myo-inositol
(CHEBI:52044)
has functional parent
myo-inositol
(CHEBI:17268)
1L-myo-inositol 1,2,3,4,6-pentakisphosphate
(CHEBI:11369)
has functional parent
myo-inositol
(CHEBI:17268)
2-O-(indol-3-ylacetyl)-myo-inositol galactoside
(CHEBI:19427)
has functional parent
myo-inositol
(CHEBI:17268)
3,5-bis(diphospho)-1D-myo-inositol 1,2,4,6-tetrakisphosphate
(CHEBI:62924)
has functional parent
myo-inositol
(CHEBI:17268)
3,5-bis(diphospho)-1D-myo-inositol 1,4,6-trisphosphate
(CHEBI:62930)
has functional parent
myo-inositol
(CHEBI:17268)
3-(α-D-galactosyl)ononitol
(CHEBI:133412)
has functional parent
myo-inositol
(CHEBI:17268)
3-diphospho-1D-myo-inositol 1,2,4,5,6-pentakisphosphate
(CHEBI:62922)
has functional parent
myo-inositol
(CHEBI:17268)
3-diphospho-1D-myo-inositol 1,4,5,6-tetrakisphosphate
(CHEBI:62927)
has functional parent
myo-inositol
(CHEBI:17268)
4-diphospho-1D-myo-inositol pentakisphosphate
(CHEBI:53064)
has functional parent
myo-inositol
(CHEBI:17268)
5-diphospho-1D-myo-inositol pentakisphosphate
(CHEBI:30164)
has functional parent
myo-inositol
(CHEBI:17268)
5-diphospho-myo-inositol 1,3,4,6-tetrakisphosphate
(CHEBI:62928)
has functional parent
myo-inositol
(CHEBI:17268)
5-triphospho-1D-myo-inositol 1,2,3,4,6-pentakisphosphate
(CHEBI:62985)
has functional parent
myo-inositol
(CHEBI:17268)
6-(α-D-glucosaminyl)-1D-myo-inositol
(CHEBI:44230)
has functional parent
myo-inositol
(CHEBI:17268)
6-O-(2-amino-2-deoxy-α-D-glucosyl)-1D-myo-inositol 1-(6-mercaptohexyl)phosphate
(CHEBI:61583)
has functional parent
myo-inositol
(CHEBI:17268)
6-diphospho-1D-myo-inositol pentakisphosphate
(CHEBI:53065)
has functional parent
myo-inositol
(CHEBI:17268)
myo-inositol 1,3,4,5,6-pentakisphosphate
(CHEBI:16322)
has functional parent
myo-inositol
(CHEBI:17268)
myo-inositol 1,3,4,6-tetrakisphosphate
(CHEBI:16155)
has functional parent
myo-inositol
(CHEBI:17268)
myo-inositol 1,3-bisphosphate
(CHEBI:18225)
has functional parent
myo-inositol
(CHEBI:17268)
myo-inositol hexanicotinate
(CHEBI:31699)
has functional parent
myo-inositol
(CHEBI:17268)
myo-inosose-5
(CHEBI:81197)
has functional parent
myo-inositol
(CHEBI:17268)
N-(2-hydroxyhexacosanoyl)phytosphingosine-1-phospho-(1D-myo-inositol)
(CHEBI:139522)
has functional parent
myo-inositol
(CHEBI:17268)
[α-D-Man-(1→2)-α-D-Man-(1→2)-α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)]-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:61591)
has functional parent
myo-inositol
(CHEBI:17268)
[α-D-Man-(1→2)-α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)]-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:61588)
has functional parent
myo-inositol
(CHEBI:17268)
[α-D-Man-(1→2)-6-PEA-α-D-Man-(1→2)-α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)]-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:61592)
has functional parent
myo-inositol
(CHEBI:17268)
[α-D-Man-(1→2)-6-PEA-α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)]-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:146150)
has functional parent
myo-inositol
(CHEBI:17268)
[α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)]-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:61587)
has functional parent
myo-inositol
(CHEBI:17268)
[6-O-(2-aminoethylphosphono)-α-D-Man-(1→2)-α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)]-1-O-(6-thiohexylphosphono)-D-myo-inositol
(CHEBI:61590)
has functional parent
myo-inositol
(CHEBI:17268)
CDP-1L-myo-inositol
(CHEBI:62566)
has functional parent
myo-inositol
(CHEBI:17268)
ethanolamine-P-6-α-Man-(1→2)-α-Man-(1→6)-[α-Gal-(1→2)-α-Gal-(1→6)-[α-Gal-(1→2)]-α-Gal-(1→3)]-α-Man-(1→4)-α-GlcN-(1→6)-inositol-1,2-cyclic phosphate
(CHEBI:62865)
has functional parent
myo-inositol
(CHEBI:17268)
inositol C20 phosphodihydroceramide(1−)
(CHEBI:72460)
has functional parent
myo-inositol
(CHEBI:17268)
inositol phosphosphingolipid
(CHEBI:53021)
has functional parent
myo-inositol
(CHEBI:17268)
Ins-1-P-6-Man-β1-3-Ins-1-P-Cer(t18:0/2-OH-26:0)
(CHEBI:53005)
has functional parent
myo-inositol
(CHEBI:17268)
Ins-1-P-Cer(t18:0/2-OH-26:0)
(CHEBI:53004)
has functional parent
myo-inositol
(CHEBI:17268)
Ins3P-(3P→5)-β-D-Araf-(1→2)-α-D-Araf-(1→5)-α-D-Araf-(1→5)-α-D-Araf
(CHEBI:140781)
has functional parent
myo-inositol
(CHEBI:17268)
methyl myo-inositols
(CHEBI:25270)
has functional parent
myo-inositol
(CHEBI:17268)
mycothiol
(CHEBI:16768)
has functional parent
myo-inositol
(CHEBI:17268)
6-O-(2-aminoethylphosphono)-α-D-Man-(1→2)-α-D-Man-(1→6)-α-D-Man-(1→4)-α-D-GlcN-(1→6)-D-myo-inositol
(CHEBI:133453)
is a
myo-inositol
(CHEBI:17268)
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(1r,2R,3S,4s,5R,6S)-cyclohexane-1,2,3,4,5,6-hexol
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IUPAC
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1,2,3,4,5,6-HEXAHYDROXY-CYCLOHEXANE
|
PDBeChem
|
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1,2,3,5/4,6-cyclohexanehexol
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IUPAC
|
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1D-myo-Inositol
|
KEGG COMPOUND
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1L-myo-Inositol
|
KEGG COMPOUND
|
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Bios I
|
KEGG COMPOUND
|
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cis-1,2,3,5-trans-4,6-cyclohexanehexol
|
ChemIDplus
|
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Cyclohexitol
|
KEGG COMPOUND
|
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D-myo-Inositol
|
KEGG COMPOUND
|
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Dambose
|
KEGG COMPOUND
|
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i-inositol
|
ChEBI
|
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inosite
|
ChEBI
|
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Inositol
|
KEGG COMPOUND
|
|
Ins
|
ChEBI
|
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L-myo-Inositol
|
KEGG COMPOUND
|
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Meat sugar
|
KEGG COMPOUND
|
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meso-Inositol
|
KEGG COMPOUND
|
|
myo-Inositol
|
KEGG COMPOUND
|
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myo-inositol
|
UniProt
|
|
Myoinositol
|
HMDB
|
|
1444
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DrugCentral
|
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C00001164
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KNApSAcK
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C00137
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KEGG COMPOUND
|
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D08079
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KEGG DRUG
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DB03106
|
DrugBank
|
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HMDB0000211
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HMDB
|
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Inositol
|
Wikipedia
|
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INS
|
PDBeChem
|
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MYO-INOSITOL
|
MetaCyc
|
| View more database links |
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1907329
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Reaxys Registry Number
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Reaxys
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82918
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Gmelin Registry Number
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Gmelin
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87-89-8
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CAS Registry Number
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NIST Chemistry WebBook
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87-89-8
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CAS Registry Number
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ChemIDplus
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Eagan DE, Gonzales MM, Tarumi T, Tanaka H, Stautberg S, Haley AP (2012)
Elevated serum C-reactive protein relates to increased cerebral myoinositol levels in middle-aged adults.
Cardiovascular psychiatry and neurology 2012, 120540 [PubMed:22461977]
[show Abstract]
C-reactive protein (CRP), a systemic marker of inflammation, is a risk factor for late life cognitive impairment and dementia, yet the mechanisms that link elevated CRP to cognitive decline are not fully understood. In this study we examined the relationship between CRP and markers of neuronal integrity and cerebral metabolism in middle-aged adults with intact cognitive function, using proton magnetic resonance spectrocospy. We hypothesized that increased levels of circulating CRP would correlate with changes in brain metabolites indicative of early brain vulnerability. Thirty-six individuals, aged 40 to 60, underwent neuropsychological assessment, a blood draw for CRP quantification, and (1)H MRS examining N-acetyl-aspartate, myo-inositol, creatine, choline, and glutamate concentrations in occipito-parietal grey matter. Independent of age, sex and education, serum CRP was significantly related to higher cerebral myo-inositol/creatine ratio (F(4,31) = 4.74, P = 0.004), a relationship which remained unchanged after adjustment for cardiovascular risk (F(5,30) = 4.356, CRP β = 0.322, P = 0.045). Because these biomarkers are detectable in midlife they may serve as useful indicators of brain vulnerability during the preclinical period when mitigating intervention is still possible. | Gheuens S, Smith DR, Wang X, Alsop DC, Lenkinski RE, Koralnik IJ (2012)
Simultaneous PML-IRIS after discontinuation of natalizumab in a patient with MS.
Neurology 78, 1390-1393 [PubMed:22517104]
[show Abstract]
ObjectiveProgressive multifocal leukoencephalopathy (PML) is a severe complication of natalizumab therapy in patients with multiple sclerosis (MS), which is often accompanied by an immune reconstitution inflammatory syndrome (IRIS) after removal of the drug. We describe a patient with MS who presented with simultaneous PML-IRIS 2 months after stopping natalizumab for other reasons.Case report and resultsThe patient had widespread PML and severe IRIS. He received corticosteroids and displayed a vigorous JC virus-specific cellular immune response. Elevated myoinositol and lipid/creatine peaks measured in PML lesions by proton magnetic resonance spectroscopy ((1)H-MRS) corresponded to episodes of contrast enhancement on MRI scans and persisted after the enhancement subsided. He demonstrated steady clinical improvement, but developed marked residual atrophy in areas affected by PML and inflammation, as well as seizures.ConclusionsNew enhancing white matter lesions, occurring after discontinuation of natalizumab, can be the manifestation of PML-IRIS rather than an MS exacerbation. Elevated myoinositol and lipid/creatine peaks appear to be more sensitive markers of inflammation in PML lesions than contrast enhancement. (1)H-MRS may become useful as a biomarker for PML-IRIS by helping clinicians determine the need for corticosteroid administration and anticipate continuing clinical recovery. | Mansouri MT, Naghizadeh B, López-Larrubia P, Cauli O (2012)
Gender-dependent behavioural impairment and brain metabolites in young adult rats after short term exposure to lead acetate.
Toxicology letters 210, 15-23 [PubMed:22285975]
[show Abstract]
We investigated the behavioural effects of short-term lead (Pb) exposure in adult rats producing blood Pb concentration (<10 μg/dL) below those associated with neurological impairment in occupationally exposed individuals. In order to assess gender differences, we performed parallel behavioural experiments in male and female rats. Exposure to Pb acetate (50 mg/L in drinking water) for 30-45 days induced behavioural alterations consisting in hyperactivity in a novel environment and impairment of spatial memory. These effects were observed only in male rats. Object recognition, motor coordination were unaffected by Pb exposure. Magnetic resonance spectroscopy allows in vivo assessment of main brain metabolites (glutamate/glutamine, creatine, myoinositol, N-acetylaspartate and choline) whose changes have been demonstrated in several central nervous system pathologies. Exposure to Pb did not affect metabolite profile in the striatum and increase myoinositol signal in the hippocampus of male rats. The increase in myoinositol in hippocampus suggests early Pb-induced alteration in glial metabolism in this brain region and may represent a potential marker of early brain dysfunction during Pb exposure. | Reynolds TB (2009)
Strategies for acquiring the phospholipid metabolite inositol in pathogenic bacteria, fungi and protozoa: making it and taking it.
Microbiology (Reading, England) 155, 1386-1396 [PubMed:19383710]
[show Abstract]
myo-Inositol (inositol) is an essential nutrient that is used for building phosphatidylinositol and its derivatives in eukaryotes and even in some eubacteria such as the mycobacteria. As a consequence, fungal, protozoan and mycobacterial pathogens must be able to acquire inositol in order to proliferate and cause infection in their hosts. There are two primary mechanisms for acquiring inositol. One is to synthesize inositol from glucose 6-phosphate using two sequentially acting enzymes: inositol-3-phosphate synthase (Ino1p) converts glucose 6-phosphate to inositol 3-phosphate, and then inositol monophosphatase (IMPase) dephosphorylates inositol 3-phosphate to generate inositol. The other mechanism is to import inositol from the environment via inositol transporters. Inositol is readily abundant in the bloodstream of mammalian hosts, providing a source from which many pathogens could potentially import inositol. However, despite this abundance of inositol in the host, some pathogens such as the bacterium Mycobacterium tuberculosis and the protist parasite Trypanosoma brucei must be able to make inositol de novo in order to cause disease (M. tuberculosis) or even grow (T. brucei). Other pathogens such as the fungus Candida albicans are equally adept at causing disease by importing inositol or by making it de novo. The role of inositol acquisition in the biology and pathogenesis of the parasite Leishmania and the fungus Cryptococcus are being explored as well. The specific strategies used by these pathogens to acquire inositol while in the host are discussed in relation to each pathogen's unique metabolic requirements. | Haroon E, Watari K, Thomas A, Ajilore O, Mintz J, Elderkin-Thompson V, Darwin C, Kumaran S, Kumar A (2009)
Prefrontal myo-inositol concentration and visuospatial functioning among diabetic depressed patients.
Psychiatry research 171, 10-19 [PubMed:19097871]
[show Abstract]
Patients with diabetes mellitus are reported to be at higher risk for developing neuropsychiatric disorders such as dementia and depression. Myo-inositol (mI), a neuronal/glial metabolite associated with multiple functions in the brain, has been shown to be increased in cognitive disorders, depression and diabetes. This study examined whether elevations in dorsolateral (DL) mI of diabetic patients with depression were associated with visuospatial deficits. Diabetic and depressed patients (n=18) were matched with patients with diabetes but without depression (n=20) and control subjects (n=19). Subjects were scored on both the recall and recognition tasks of the Rey-Osterreith Complex Figure (ROCF). Proton magnetic spectroscopy spectra from bilateral prefrontal white matter voxels were used to obtain concentrations of mI. Controls showed negative correlations between mI in right DL white matter and recall and recognition subtests. No correlation was observed for depressed diabetic patients. Correlations for diabetic controls fell midway between the comparison and depressed diabetic groups. The expected pattern of association between mI and visuospatial impairment in the right DL prefrontal region was seen among healthy controls. Progressive weakening of this association across both diabetic groups might be related to progressive changes in neural activity that underlies visuospatial function. | Bissonnette P, Lahjouji K, Coady MJ, Lapointe JY (2008)
Effects of hyperosmolarity on the Na+ -myo-inositol cotransporter SMIT2 stably transfected in the Madin-Darby canine kidney cell line.
American journal of physiology. Cell physiology 295, C791-9 [PubMed:18650262]
[show Abstract]
Myo-inositol (MI) is a compatible osmolyte used by cells to compensate for changes in the osmolarity of their surrounding milieu. In kidney, the basolateral Na(+)-MI cotransporter (SMIT1) and apical SMIT2 proteins are homologous cotransporters responsible for cellular uptake of MI. It has been shown in the Madin-Darby canine kidney (MDCK) cell line that SMIT1 expression was under the control of the tonicity-sensitive transcription factor, tonicity-responsive enhancer binding protein (TonEBP). We used an MDCK cell line stably transfected with SMIT2 to determine whether variations in external osmolarity could also affect SMIT2 function. Hyperosmotic conditions (+200 mosM raffinose or NaCl but not urea) generated an increase in SMIT2-specific MI uptake by three- to ninefold in a process that required protein synthesis. Using quantitative RT-PCR, we have determined that hyperosmotic conditions augment both the endogenous SMIT1 and the transfected SMIT2 mRNAs. Transport activities for both SMIT1 and SMIT2 exhibited differences in their respective induction profiles for both their sensitivities to raffinose, as well as in their time course of induction. Application of MG-132, which inhibits nuclear translocation of TonEBP, showed that the effect of osmolarity on transfected SMIT2 was unrelated to TonEBP, unlike the effect observed with SMIT1. Inhibition studies involving the hyperosmolarity-related MAPK suggested that p38 and JNK play a role in the induction of SMIT2. Further studies have shown that hyperosmolarity also upregulates another transfected transporter (Na(+)-glucose), as well as several endogenously expressed transport systems. This study shows that hyperosmolarity can stimulate transport in a TonEBP-independent manner by increasing the amount of mRNA derived from an exogenous DNA segment. | Mackenzie EA, Klig LS (2008)
Computational modeling and in silico analysis of differential regulation of myo-inositol catabolic enzymes in Cryptococcus neoformans.
BMC molecular biology 9, 88 [PubMed:18854045]
[show Abstract]
BackgroundInositol is a key cellular metabolite for many organisms. Cryptococcus neoformans is an opportunistic pathogen which primarily infects the central nervous system, a region of high inositol concentration, of immunocompromised individuals. Through the use of myo-inositol oxygenase C. neoformans can catabolize inositol as a sole carbon source to support growth and viability.ResultsThree myo-inositol oxygenase gene sequences were identified in the C. neoformans genome. Differential regulation was suggested by computational analyses of the three gene sequences. This included examination of the upstream regulatory regions, identifying ORE/TonE and UASINO sequences, conserved introns/exons, and in frame termination sequences. Homology modeling of the proteins encoded by these genes revealed key differences in the myo-inositol active site.ConclusionThe results suggest there are two functional copies of the myo-inositol oxygenase gene in the C. neoformans genome. The functional genes are differentially expressed in response to environmental inositol concentrations. Both the upstream regulatory regions of the genes and the structure of the specific proteins suggest that MIOX1 would function when inositol concentrations are low, whereas MIOX2 would function when inositol concentrations are high. | Castrillo JI, Zeef LA, Hoyle DC, Zhang N, Hayes A, Gardner DC, Cornell MJ, Petty J, Hakes L, Wardleworth L, Rash B, Brown M, Dunn WB, Broadhurst D, O'Donoghue K, Hester SS, Dunkley TP, Hart SR, Swainston N, Li P, Gaskell SJ, Paton NW, Lilley KS, Kell DB, Oliver SG (2007)
Growth control of the eukaryote cell: a systems biology study in yeast.
Journal of biology 6, 4 [PubMed:17439666]
[show Abstract]
BackgroundCell growth underlies many key cellular and developmental processes, yet a limited number of studies have been carried out on cell-growth regulation. Comprehensive studies at the transcriptional, proteomic and metabolic levels under defined controlled conditions are currently lacking.ResultsMetabolic control analysis is being exploited in a systems biology study of the eukaryotic cell. Using chemostat culture, we have measured the impact of changes in flux (growth rate) on the transcriptome, proteome, endometabolome and exometabolome of the yeast Saccharomyces cerevisiae. Each functional genomic level shows clear growth-rate-associated trends and discriminates between carbon-sufficient and carbon-limited conditions. Genes consistently and significantly upregulated with increasing growth rate are frequently essential and encode evolutionarily conserved proteins of known function that participate in many protein-protein interactions. In contrast, more unknown, and fewer essential, genes are downregulated with increasing growth rate; their protein products rarely interact with one another. A large proportion of yeast genes under positive growth-rate control share orthologs with other eukaryotes, including humans. Significantly, transcription of genes encoding components of the TOR complex (a major controller of eukaryotic cell growth) is not subject to growth-rate regulation. Moreover, integrative studies reveal the extent and importance of post-transcriptional control, patterns of control of metabolic fluxes at the level of enzyme synthesis, and the relevance of specific enzymatic reactions in the control of metabolic fluxes during cell growth.ConclusionThis work constitutes a first comprehensive systems biology study on growth-rate control in the eukaryotic cell. The results have direct implications for advanced studies on cell growth, in vivo regulation of metabolic fluxes for comprehensive metabolic engineering, and for the design of genome-scale systems biology models of the eukaryotic cell. | Zwingmann C (2007)
Nuclear magnetic resonance studies of energy metabolism and glutamine shunt in hepatic encephalopathy and hyperammonemia.
Journal of neuroscience research 85, 3429-3442 [PubMed:17722064]
[show Abstract]
Hepatic encephalopathy (HE) in both acute and chronic liver failure is more likely a reversible functional disease rather than an irreversible pathological lesion of brain cells. Metabolic alterations underlie many of the mechanisms leading to HE. This paper summarizes in vivo and ex vivo (1)H-, (13)C-, and (15)N-nuclear magnetic resonance (NMR) spectroscopy data on patients and experimental models of HE. In vivo NMR spectroscopy provides a unique opportunity to study metabolic changes noninvasively in the brain in vivo, and to quantify various metabolites in localized brain areas, and ex vivo NMR permits the high-resolution measurement of metabolites and the identification of different metabolic pathways. In vivo and ex vivo (1)H-NMR investigations consistently reveal severalfold increases in brain glutamine and concomitant decreases in myo-inositol, an important osmolyte in astrocytes. An osmotic disturbance in these cells has long been suggested to be responsible for astrocyte swelling and brain edema. However, ex vivo (13)C-NMR studies have challenged the convention that glutamine accumulation is the major cause of brain edema in acute HE. They rather indicate a limited anaplerotic flux and capacity of astrocytes to detoxify ammonia by glutamine synthesis and emphasize distortions of energy and neurotransmitter metabolism. However, recent (15)N-NMR investigations have demonstrated that glutamine fluxes between neurons and astrocytes are affected by ammonia. Further NMR studies may provide novel insights into the relationship between brain edema and/or astrocyte pathology and changes in inter- and intracellular glutamine homeostasis, which may secondarily alter brain energy metabolism. | Silver SM, Schroeder BM, Sterns RH, Rojiani AM (2006)
Myoinositol administration improves survival and reduces myelinolysis after rapid correction of chronic hyponatremia in rats.
Journal of neuropathology and experimental neurology 65, 37-44 [PubMed:16410747]
[show Abstract]
When chronic hyponatremia is rapidly corrected, reaccumulation of brain organic osmolytes is delayed and brain cell shrinkage occurs, leading to the osmotic demyelination syndrome (ODS). We hypothesized that treatment with myoinositol, a major organic osmolyte, could prevent ODS. Severe hyponatremia was induced in adult male rats by administration of arginine vasopressin and intravenous infusion of dextrose and water. Sixty-four hours after induction of hyponatremia, all animals underwent rapid correction of hyponatremia with infusion of hypertonic saline over 4 hours, increasing the serum sodium from 105 to 135 mM; half of the animals were also given myoinositol intravenously beginning 20 minutes before correction and continuing for 28 hours. Serum sodium concentrations were equivalent in both groups at all time points. At 7 days, 7 of 8 animals that received myoinositol survived compared with one of the 9 control animals (p < 0.01). In a second study, sodium was reduced to 106 mM over 64 hours in 24 animals and then corrected by 20 mM over 4 hours with concomitant loading and infusion of either mannitol (control) or myoinositol. Animals were killed 96 hours after correction of hyponatremia was begun. Myoinositol-treated animals had significantly fewer demyelinating lesions than mannitol (2.25 +/- 1.1 versus 6.42 +/- 1.4 lesions/brain, p < 0.03). We conclude that myoinositol administration improves survival and reduces myelinolysis after rapid correction of chronic hyponatremia in rats. | Harwood AJ (2005)
Lithium and bipolar mood disorder: the inositol-depletion hypothesis revisited.
Molecular psychiatry 10, 117-126 [PubMed:15558078]
[show Abstract]
Inositol, a simple six-carbon sugar, forms the basis of a number of important intracellular signaling molecules. Over the last 35 years, a series of biochemical and cell biological experiments have shown that lithium (Li(+)) reduces the cellular concentration of myo-inositol and as a consequence attenuates signaling within the cell. Based on these observations, inositol-depletion was proposed as a therapeutic mechanism in the treatment of bipolar mood disorder. Recent results have added significant new dimensions to the original hypothesis. However, despite a number of clinical studies, this hypothesis still remains to be either proven or refuted. In this review of our current knowledge, I will consider where the inositol-depletion hypothesis stands today and how it may be further investigated in the future. | Ashwal S, Holshouser B, Tong K, Serna T, Osterdock R, Gross M, Kido D (2004)
Proton spectroscopy detected myoinositol in children with traumatic brain injury.
Pediatric research 56, 630-638 [PubMed:15295080]
[show Abstract]
Previous studies have shown that proton magnetic resonance spectroscopy (MRS) is useful in predicting neurologic prognosis in children with traumatic brain injury (TBI). Reductions in N-acetyl derived metabolites and presence of lactate have been predictive of poor outcomes. We examined another spectroscopy metabolite, myoinositol (mI), to determine whether it is altered after TBI. Found primarily in astrocytes, mI functions as an osmolyte and is involved in hormone response pathways and protein-kinase C activation. Myoinositol is elevated in the newborn brain and is increased in a variety of diseases. We studied 38 children (mean age 11 y; range 1.6-17 y) with TBI using quantitative short echo time occipital gray and parietal white matter proton MRS at a mean of 7 d (range 1-17 d) after injury. We found that occipital gray matter mI levels were increased in children with TBI (4.30 +/- 0.73) compared with controls (3.53 +/- 0.48; p = 0.003). We also found that patients with poor outcomes 6-12 mo after injury had higher mI levels (4.78 +/- 0.68) than patients with good outcomes (4.15 +/- 0.69; p < 0.05). Myoinositol is elevated after pediatric TBI and is associated with a poor neurologic outcome. The reasons for its elevation remain unclear but may be due to astrogliosis or to a disturbance in osmotic function. | Bissonnette P, Coady MJ, Lapointe JY (2004)
Expression of the sodium-myo-inositol cotransporter SMIT2 at the apical membrane of Madin-Darby canine kidney cells.
The Journal of physiology 558, 759-768 [PubMed:15181167]
[show Abstract]
Myo-inositol is a compatible osmolyte used by cells which are challenged by variations in extracellular osmolarity, as in the renal medulla. In order to accumulate large quantities of this polyol, cells rely on Na(+)-dependent transporters such as SMIT1. We have recently identified a second Na(+)-myo-inositol cotransporter, SMIT2, which presents transport characteristics corresponding to those recently described for the apical membrane of renal proximal tubules. In order to further characterize this transport system, we transfected Madin-Darby canine kidney (MDCK) cells with rabbit SMIT2 cDNA and selected a stable clone with a high expression level. The accumulation of radiolabelled myo-inositol by this cell line is 20-fold larger than that seen in native MDCK cells. The affinity for myo-inositol of MDCK cells transfected with SMIT2 is slightly lower (K(m)= 334 microm) than that found in voltage-clamped Xenopus laevis oocytes expressing SMIT2 (K(m)= 120 microm). Transport studies performed using semipermeable filters showed complete apical targeting of the SMIT2 transporter. This apical localization of SMIT2 was confirmed by transport studies on purified rabbit renal brush border membrane vesicles (BBMVs). Using a purified antibody against SMIT2, we were also able to detect the SMIT2 protein (molecular mass = 66 kDa) in Western blots of BBMVs purified from SMIT2-transfected MDCK cells. SMIT2 activity was also shown to be stimulated 5-fold when submitted to 24 h hypertonic treatment (+200 mosmol l(-1)). The SMIT2-MDCK cell line thus appears to be a promising model for studying SMIT2 biochemistry and regulation. | Vanholder RC, Glorieux G, De Smet R, De Deyn PP (2003)
Low water-soluble uremic toxins.
Advances in renal replacement therapy 10, 257-269 [PubMed:14681857]
[show Abstract]
The uremic syndrome is the result of the retention of solutes, which under normal conditions are cleared by the healthy kidneys. Uremic retention products are arbitrarily subdivided according to their molecular weight. Low-molecular-weight molecules are characterized by a molecular weight below 500 D. The purpose of the present publication is to review the main water soluble, nonprotein bound uremic retention solutes, together with their main toxic effects. We will consecutively discuss creatinine, glomerulopressin, the guanidines, the methylamines, myo-inositol, oxalate, phenylacetyl-glutamine, phosphate, the polyamines, pseudouridine, the purines, the trihalomethanes, and urea per se. | Wehbi H, Feng J, Roberts MF (2003)
Water-miscible organic cosolvents enhance phosphatidylinositol-specific phospholipase C phosphotransferase as well as phosphodiesterase activity.
Biochimica et biophysica acta 1613, 15-27 [PubMed:12832083]
[show Abstract]
Phosphatidylinositol-specific phospholipase C (PI-PLC) from Bacillus thuringiensis catalyzes the hydrolysis of phosphatidylinositol (PI) in a Ca(2+)-independent two-step mechanism: (i) an intramolecular phosphotransferase reaction to form inositol 1,2-(cyclic)-phosphate (cIP), followed by (ii) a cyclic phosphodiesterase activity that converts cIP to inositol 1-phosphate (I-1-P). Moderate amounts of water-miscible organic solvents have previously been shown to dramatically enhance the cyclic phosphodiesterase activity, that is, hydrolysis of cIP. Cosolvents [isopropanol (iPrOH), dimethylsufoxide (DMSO), and dimethylformamide (DMF)] also enhance the phosphotransferase activity of PI-PLC toward PI initially presented in vesicles, monomers, or micelles. Although these water-miscible organic cosolvents caused large changes in PI particle size and distribution (monitored with pyrene-labeled PI fluorescence, 31P NMR spectroscopy, gel filtration, and electron microscopy) that differed with the activating solvent, the change in PI substrate structure in different cosolvents was not correlated with the enhanced catalytic efficiency of PI-PLC toward its substrates. PI-PLC stability was decreased in water/organic cosolvent mixtures (e.g., the T(m) for PI-PLC thermal denaturation decreased linearly with added iPrOH). However, the addition of myo-inositol, a water-soluble inhibitor of PI-PLC, helped stabilize the protein. At 30% iPrOH and 4 degrees C (well below the T(m) for PI-PLC in the presence of iPrOH), cosolvent-induced changes in protein secondary structure were minimal. iPrOH and diheptanoylphosphatidylcholine, each of which activates PI-PLC for cIP hydrolysis, exhibited a synergistic effect for cIP hydrolysis that was not observed with PI as substrate. This behavior is consistent with a mechanism for cosolvent activation that involves changes in active site polarity along with small conformational changes involving the barrel rim tryptophan side chains that have little effect on protein secondary structure. | Howlett A, Ohlsson A (2003)
Inositol for respiratory distress syndrome in preterm infants.
The Cochrane database of systematic reviewsCD000366 [PubMed:14583919]
[show Abstract]
BackgroundInositol is an essential nutrient required by human cells in culture for growth and survival. Inositol promotes maturation of several components of surfactant and may play a critical role in fetal and early neonatal life.ObjectivesTo assess the effectiveness/safety of supplementary inositol in preterm infants with RDS in reducing adverse neonatal outcomes.Search strategyMEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched in July, 2003 using key words: inositol and infant-newborn and random allocation or controlled trial or randomized trial (RCT). The reference lists of identified RCTs, personal files and Science Citation Index were searched. Unpublished additional information was obtained from the authors of one RCT published in abstract form.Selection criteriaAll randomized controlled trials of inositol supplementation to preterm infants with a control group that received a placebo or no intervention were included. Outcomes of interest were bronchopulmonary dysplasia (BPD), death, BPD or death, retinopathy of prematurity (ROP), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), and sepsis.Data collection and analysisData on neonatal outcomes were abstracted independently by the two researchers and any discrepancy was resolved through consensus. Revman was used for analysis of the data.Main resultsFive reports of three RCTs were identified. One report was a duplicate publication. One new report included both randomized and non-randomized patients and data could not be extracted for the randomized neonates only and the study was excluded. An interim report of this study previously published as an abstract was included in the previous version of this review. The outcome of death or bronchopulmonary dysplasia was reported in two trials, and was found to be significantly reduced (RR 0.56, 95% CI 0.42, 0.77; RD -0.215, 95% CI -0.323, -0.107). The outcome of death was reported in two trials and was found to be significantly reduced (RR 0.48, 95% CI 0.28, 0.80; RD -0.131, 95% CI -0.218, -0.043). Retinopathy of prematurity, stage 4 or needing therapy, was reported in two trials, and was found to be significantly reduced (RR 0.09, 95% CI 0.01, 0.67; RD -0.078, 95% CI -0.128, -0.027). Intraventricular hemorrhage, grade III-IV, was significantly decreased (RR 0.55, 95% CI 0.32, 0.95; RD -0.090, 95% CI -0.170, -0.010). Neither sepsis nor necrotizing enterocolitis outcomes were increased. When a secondary analysis was done excluding a study published in abstract form, the results differed only in that there was a significant reduction in retinopathy of prematurity, any stage (RR 0.53, 95% CI 0.29, 0.97; RD -0.082, 95% CI -0.159,-0.005).Reviewer's conclusionsInositol supplementation results in statistically significant and clinically important reductions in important short-term adverse neonatal outcomes. A multi-center RCT of appropriate size is justified to confirm these findings. | Nigou J, Besra GS (2002)
Characterization and regulation of inositol monophosphatase activity in Mycobacterium smegmatis.
The Biochemical journal 361, 385-390 [PubMed:11772411]
[show Abstract]
Mycobacterium tuberculosis and related members of the genus Mycobacterium contain a number of inositol-based lipids, such as phosphatidylinositol mannosides, lipomannan and lipoarabinomannan. The synthesis of phosphatidylinositol in M. smegmatis is essential for growth and myo-inositol is a key metabolite for mycobacteria. Little is known about the biosynthesis of inositol in mycobacteria and the only known de novo pathway for myo-inositol biosynthesis involves a two-step process. First, cyclization of glucose 6-phosphate to afford myo-inositol 1-phosphate via inositol-1-phosphate synthase and, secondly, dephosphorylation of myo-inositol 1-phosphate by inositol monophosphatase (IMP) to afford myo-inositol. The following report examines IMP activity in M. smegmatis extracts, with regard to pH dependence, bivalent cation requirement, univalent cation inhibition, regulation by growth and carbon source. We show that IMP activity, which is optimal at the end of the exponential growth phase in Sauton's medium, is Mg(2+)-dependent. Moreover, IMP activity is inhibited by Li(+) and Na(+), with Li(+) also being able to inhibit growth of M. smegmatis in vivo. This study represents a first step in the delineation of myo-inositol biosynthesis in mycobacteria. | Nemets B, Talesnick B, Belmaker RH, Levine J (2002)
Myo-inositol has no beneficial effect on premenstrual dysphoric disorder.
The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry 3, 147-149 [PubMed:12478879]
[show Abstract]
Inositol, a simple isomer of glucose, which serves as a precursor in the phosphatidyl-inositol (PI) second messenger cycle, was shown to be effective in double-blind, placebo-controlled studies of depression, panic and obsessive compulsive disorders as well as in bulimia. The following study was designed to investigate whether inositol has beneficial effects in another disorder shown to be responsive to SSRIs: premenstrual dysphoric disorder (PMDD). Eleven female patients with PMDD diagnosed according to DSM-IV participated in a cross-over, double-blind, placebo-controlled trial. The active drug was myo-inositol, 12 g daily, whereas placebo was d-glucose administered at the same dose. Each drug was given during the luteal phase only (14 days prior to menses). For each patient treatment alternated between these two drugs for six menstrual cycles. No beneficial effect was demonstrated for inositol over placebo. | Hecht SS, Kenney PM, Wang M, Upadhyaya P (2001)
Dose-response study of myo-inositol as an inhibitor of lung tumorigenesis induced in A/J mice by benzo.
Cancer letters 167, 1-6 [PubMed:11323092]
[show Abstract]
Dietary myo-inositol is an effective inhibitor of lung tumor induction in mice, but no dose-response studies have been reported. We assessed the ability of various doses of dietary myo-inositol to inhibit lung tumor induction in female A/J mice treated with eight weekly doses of benzo[a]pyrene (BaP) plus 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (3 micromol of each by gavage), then killed 18 weeks later. In Expt. 1, groups of 20 mice each were treated with myo-inositol at concentrations of 1, 0.5, 0.25, 0.125, 0.0625, 0.03125, and 0% in AIN-93 diet for 1 week prior to, during, and for 1 week after the carcinogen administration period. In Expt. 2, groups of 20 mice each were treated with the same concentrations of myo-inositol in the diet as in Expt. 1, except this diet was administered from 1 week after carcinogen administration until termination. There were no effects of myo-inositol on lung tumor incidence, which was 100% in all groups treated with BaP plus NNK. However, myo-inositol significantly decreased lung tumor multiplicity in both experiments. In Expt. 1, significant reductions of 28.9 and 33.0% were observed at the 1 and 0.5% doses of myo-inositol, but not at the lower doses. In Expt. 2, a significant reduction of 48.4% was observed at the 1% dose. In both Expts. 1 and 2, there was a significant dose trend for inhibition (P<0.0001). No toxicity was observed at any dose. These results firmly establish myo-inositol as a chemopreventive agent against lung tumor induction in A/J mice, at doses that can be envisioned for human use. | Handler JS, Kwon HM (2001)
Cell and molecular biology of organic osmolyte accumulation in hypertonic renal cells.
Nephron 87, 106-110 [PubMed:11244303]
[show Abstract]
When the renal medulla becomes hypertonic in association with the formation of concentrated urine, the cells of the medulla avoid the stress of high intracellular salts by accumulating small non-perturbing organic osmolytes. The response has been studied in most detail in cultured kidney-derived cells, and confirmed in studies of the intact kidney. The non-perturbing osmolytes, myo-inositol, betaine, and sorbitol, are accumulated because of stimulation of the transcription of the genes for the proteins that catalyze their accumulation by transport or synthesis. The genes involved have all been cloned and sequenced and contain tonicity responsive regulatory elements (TonEs) in their 5' region. During hypertonicity, the elements are occupied by TonE-binding protein, a transacting factor that has been cloned and characterized. Current efforts focus on identifying the mechanism by which cells sense hypertonicity and how that leads to activation of TonE-binding protein. | Howlett A, Ohlsson A (2000)
Inositol for respiratory distress syndrome in preterm infants.
The Cochrane database of systematic reviewsCD000366 [PubMed:11034685]
[show Abstract]
BackgroundInositol is an essential nutrient required by human cells in culture for growth and survival. Inositol promotes maturation of several components of surfactant and may play a critical role in fetal and early neonatal life.ObjectivesTo assess the effectiveness/safety of supplementary inositol in preterm infants with RDS in reducing adverse neonatal outcomes.Search strategyMedline, Embase, and Reference Update Databases were searched in August 1997 using key words: inositol and infant-newborn and random allocation or controlled trial or randomized trial (RCT). The reference lists of identified RCTs, personal files and Science Citation Index were searched. Unpublished additional information was obtained from the authors of one RCT published in abstract form.Selection criteriaAll randomized controlled trials of inositol supplementation to preterm infants with a control group that received a placebo or no intervention were included. Outcomes of interest were bronchopulmonary dysplasia (BPD), death, BPD or death, retinopathy of prematurity (ROP), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), and sepsis.Data collection and analysisData on neonatal outcomes were abstracted independently by the two researchers and any discrepancy was resolved through consensus. Revman was used for analysis of the data.Main resultsFour reports of three RCTs were identified. One report was a duplicate publication. The outcome of death or bronchopulmonary dysplasia was reported in two trials, and was found to be significantly reduced (RR 0.56, 95% CI 0.42, 0.77; RD -0.215, 95% CI -0.323, -0.107). The outcome of death was reported in two trials and was found to be significantly reduced (RR 0.48, 95% CI 0.28, 0.80; RD -0.131, 95% CI -0.218, -0.043). Retinopathy of prematurity, stage 4 or needing therapy, was reported in two trials, and was found to be significantly reduced (RR 0.09, 95% CI 0.01, 0.67; RD -0.078, 95% CI -0.128, -0.027). Intraventricular hemorrhage, grade III-IV, was significantly decreased (RR 0.55, 95% CI 0.32, 0.95; RD -0.090, 95% CI -0.170, -0.010). Neither sepsis nor necrotizing enterocolitis outcomes were increased. When a secondary analysis was done excluding a study published in abstract form, the results differed only in that there was a significant reduction in retinopathy of prematurity, any stage (RR 0.53, 95% CI 0.29, 0.97; RD -0.082, 95% CI -0.159,-0.005).Reviewer's conclusionsInositol supplementation results in statistically significant and clinically important reductions in important short-term adverse neonatal outcomes. A multi-center RCT of appropriate size is justified to confirm these findings. | Levy RA, Gharavi AE, Sammaritano LR, Habina L, Lockshin MD (1990)
Fatty acid chain is a critical epitope for antiphospholipid antibody.
Journal of clinical immunology 10, 141-145 [PubMed:1694860]
[show Abstract]
To explore the role of phospholipid fatty acids in binding of antiphospholipid antibody (aPL) in ELISA, we tested aPL binding to phospholipids containing fatty acids of varying chain length and degree of saturation using direct ELISA and inhibition methods. Polyclonal IgG and IgM human aPL's bind to C18:1 phosphatidylglycerol (PG) better than to C18:0 PG or C18:2 PG. Binding is greater to C18 than to C14:0 or C16:0 PGs; aPL's do not bind to C12:0 PG. aPL binding is not inhibited by C18:1 diacylglycerol, glycerol-3-phosphate, myoinositol, or myoinositol phosphate. The fatty acid chains are critical determinants for antigen recognition and, by projection, biological activity of aPL. | Clements RS, Reynertson R (1977)
Myoinositol metabolism in diabetes mellitus. Effect of insulin treatment.
Diabetes 26, 215-221 [PubMed:838172]
[show Abstract]
The metabolism of myoinositol has been studied in 10 nondiabetic subjects and in six patients with diabetes mellitus before and after insulin therapy. While dietary myoinositol intake and fecal myoinositol excretion were similar in both groups, urinary myoinositol excretion was increased 10-fold in the untreated diabetic and accounted for a significant fraction of his dietary myoinositol intake. Insulin treatment restored the urinary myoinositol excretion toward normal. Despite increased myoinositol excretion, plasma myoinositol concentrations were significantly higher in the diabetics following the ingestion of a standard diet or of a 3.0-gm. myoinositol load. This abnormality in oral myoinositol tolerance was also corrected by insulin treatment. The size of the rapidly equilibrating myoinositol pool was significantly decreased in the untreated diabetic and returned to normal following a brief period of insulin treatment. The elevated plasma myoinositol concentrations observed following myoinositol ingestion in the uncontrolled diabetic presumably represents a combination of enhanced gastrointestinal absorption and impaired intracellular transport of myoinositol. The decreased space of distribution of myoinositol also suggests an impairment of intracellular myoinositol transport in the untreated diabetic. These observations are consistent with the speculation that hyperglycemia may condition a widespread relative intracellular myoinositol deficiency in man and suggest that restoration of normal intracellular myoinositol concentrations might prove to be of benefit in the prevention and treatment of certain of the complications associated with human diabetes mellitus. |
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