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Science Forum Index » Life Extension Forum » Osmotic stress and insulin resistance
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| kofi |
 Posted: Sun Jan 11, 2004 6:46 am |
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J Biol Chem. 2003 Jul 18;278(29):26550-7. Epub 2003 May 01. Related
Articles, Links
Click here to read
Hyperosmotic stress inhibits insulin receptor substrate-1 function
by distinct mechanisms in 3T3-L1 adipocytes.
Gual P, Gonzalez T, Gremeaux T, Barres R, Le Marchand-Brustel Y,
Tanti JF.
INSERM U 568 and l'Institut Federatif de Recherches 50, Faculte de
Medecine, Avenue de Valombrose, 06107 Nice Cedex 02, France.
In 3T3-L1 adipocytes, hyperosmotic stress was found to inhibit
insulin signaling, leading to an insulin-resistant state. We show here
that, despite normal activation of insulin receptor, hyperosmotic stress
inhibits both tyrosine phosphorylation of insulin receptor substrate-1
(IRS-1) and IRS-1-associated phosphoinositide 3 (PI 3)-kinase activity
in response to physiological insulin concentrations. Insulin-induced
membrane ruffling, which is dependent on PI 3-kinase activation, was
also markedly reduced. These inhibitory effects were associated with an
increase in IRS-1 Ser307 phosphorylation. Furthermore, the mammalian
target of rapamycin (mTOR) inhibitor rapamycin prevented the osmotic
shock-induced phosphorylation of IRS-1 on Ser307. The inhibition of mTOR
completely reversed the inhibitory effect of hyperosmotic stress on
insulin-induced IRS-1 tyrosine phosphorylation and PI 3-kinase
activation. In addition, prolonged osmotic stress enhanced the
degradation of IRS proteins through a rapamycin-insensitive pathway and
a proteasome-independent process. These data support evidence of new
mechanisms involved in osmotic stress-induced cellular insulin
resistance. Short-term osmotic stress induces the phosphorylation of
IRS-1 on Ser307 by an mTOR-dependent pathway. This, in turn, leads to a
decrease in early proximal signaling events induced by physiological
insulin concentrations. On the other hand, prolonged osmotic stress
alters IRS-1 function by inducing its degradation, which could
contribute to the down-regulation of insulin action.
PMID: 12730242 [PubMed - indexed for MEDLINE] |
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| Hua Kul |
| Posted: Sun Jan 11, 2004 9:05 pm |
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kofi <kofi@anon.un> wrote in message news:<kofi-15AE5B.05471311012004@news01.west.earthlink.net>...
Quote:
On the other hand, prolonged osmotic stress
alters IRS-1 function by inducing its degradation, which could
contribute to the down-regulation of insulin action.
PMID: 12730242 [PubMed - indexed for MEDLINE]
Please forgive my ignorance kofi, but could you give me a brief
explanation of osmotic stress in adipocytes? Do you know any causes
of prolonged osmotic stress? Thanks for any help.
--Hua Kul
huaREMOVEkul@hotmail.com |
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| anon |
| Posted: Mon Jan 12, 2004 12:14 am |
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In article <3da4c6e5.0401111805.763568f8@posting.google.com>,
gmp@adres.nl (Hua Kul) wrote:
Quote: kofi <kofi@anon.un> wrote in message
news:<kofi-15AE5B.05471311012004@news01.west.earthlink.net>...
On the other hand, prolonged osmotic stress
alters IRS-1 function by inducing its degradation, which could
contribute to the down-regulation of insulin action.
PMID: 12730242 [PubMed - indexed for MEDLINE]
Please forgive my ignorance kofi, but could you give me a brief
explanation of osmotic stress in adipocytes? Do you know any causes
of prolonged osmotic stress? Thanks for any help.
Fluid retention or something altering ions channels, maybe? Maybe
taurine uptake? |
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| kofi |
| Posted: Mon Jan 12, 2004 12:57 pm |
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Quote: Please forgive my ignorance kofi, but could you give me a brief
explanation of osmotic stress in adipocytes? Do you know any causes
of prolonged osmotic stress? Thanks for any help.
Hyperglycemia.
Biosci Biotechnol Biochem. 1997 Apr;61(4):651-4. Related Articles, Links
Inhibition of aldose reductase and sorbitol accumulation by astilbin
and taxifolin dihydroflavonols in Engelhardtia chrysolepis.
Haraguchi H, Ohmi I, Fukuda A, Tamura Y, Mizutani K, Tanaka O, Chou
WH.
Faculty of Engineering, Fukuyama University, Japan.
Dihydroflavonol taxifolin and its glycoside, astilbin, from
Engelhardtia chrysolepis inhibited rat lens and recombinant human aldose
reductase. Taxifolin also inhibited sorbitol accumulation in human red
blood cells. Furthermore, this dihydroflavonol aglycone maintained the
clarity of rat lens incubated with a high concentration of glucose.
These dihydroflavonols may be effective for preventing osmotic stress in
hyperglycemia.
PMID: 9145524 [PubMed - indexed for MEDLINE] |
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