Difference between revisions of "Burning Stored Fat"

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(Created page with " = Amlexanox = Old drug may point the way to new treatments for diabetes and obesity Published on Feb 10, 2013 ANN ARBOR—Researchers at the University of Michigan's Life...")
 
(Amlexanox)
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ANN ARBOR—Researchers at the University of Michigan's Life Sciences Institute have found that amlexanox, an off-patent drug currently prescribed for the treatment of asthma and other uses, also reverses obesity, diabetes and fatty liver in mice.
 
ANN ARBOR—Researchers at the University of Michigan's Life Sciences Institute have found that amlexanox, an off-patent drug currently prescribed for the treatment of asthma and other uses, also reverses obesity, diabetes and fatty liver in mice.
 
http://www.ns.umich.edu/new/releases/21179-old-drug-may-point-the-way-to-new-treatments-for-diabetes-and-obesity
 
http://www.ns.umich.edu/new/releases/21179-old-drug-may-point-the-way-to-new-treatments-for-diabetes-and-obesity
 +
 +
Could this be how Amlexanox works?
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Orphanet J Rare Dis. 2012 Aug 31;7:58.
 +
Rescue of nonsense mutations by amlexanox in human cells.
 +
Gonzalez-Hilarion S, Beghyn T, Jia J, Debreuck N, Berte G,
 +
Mamchaoui K, Mouly V, Gruenert DC, Déprez B, Lejeune F.
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Université Lille Nord de France, IFR142, Lille, France.
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http://www.ncbi.nlm.nih.gov/pubmed/22938201
 +
http://www.ojrd.com/content/7/1/58
 +
 +
ABSTRACT: BACKGROUND: Nonsense mutations are at the origin
 +
of many cancers and inherited genetic diseases. The
 +
consequence of nonsense mutations is often the absence of
 +
mutant gene expression due to the activation of an mRNA
 +
surveillance mechanism called nonsense-mediated mRNA decay
 +
(NMD). Strategies to rescue the expression of
 +
nonsense-containing mRNAs have been developed such as NMD
 +
inhibition or nonsense mutation readthrough. METHODS: Using
 +
a dedicated screening system, we sought molecules capable to
 +
block NMD. Additionally, 3 cell lines derived from patient
 +
cells and harboring a nonsense mutation were used to study
 +
the effect of the selected molecule on the level of
 +
nonsense-containing mRNAs and the synthesis of proteins from
 +
these mutant mRNAs. RESULTS: We demonstrate here that
 +
amlexanox, a drug used for decades, not only induces an
 +
increase in nonsense-containing mRNAs amount in treated
 +
cells, but also leads to the synthesis of the full-length
 +
protein in an efficient manner. We also demonstrated that
 +
these full length proteins are functional. CONCLUSIONS: As a
 +
result of this dual activity, amlexanox may be useful as a
 +
therapeutic approach for diseases caused by nonsense mutations.

Revision as of 18:24, 11 February 2013

Amlexanox

Old drug may point the way to new treatments for diabetes and obesity

Published on Feb 10, 2013 

ANN ARBOR—Researchers at the University of Michigan's Life Sciences Institute have found that amlexanox, an off-patent drug currently prescribed for the treatment of asthma and other uses, also reverses obesity, diabetes and fatty liver in mice. http://www.ns.umich.edu/new/releases/21179-old-drug-may-point-the-way-to-new-treatments-for-diabetes-and-obesity

Could this be how Amlexanox works? Orphanet J Rare Dis. 2012 Aug 31;7:58. Rescue of nonsense mutations by amlexanox in human cells. Gonzalez-Hilarion S, Beghyn T, Jia J, Debreuck N, Berte G, Mamchaoui K, Mouly V, Gruenert DC, Déprez B, Lejeune F. Université Lille Nord de France, IFR142, Lille, France. http://www.ncbi.nlm.nih.gov/pubmed/22938201 http://www.ojrd.com/content/7/1/58

ABSTRACT: BACKGROUND: Nonsense mutations are at the origin of many cancers and inherited genetic diseases. The consequence of nonsense mutations is often the absence of mutant gene expression due to the activation of an mRNA surveillance mechanism called nonsense-mediated mRNA decay (NMD). Strategies to rescue the expression of nonsense-containing mRNAs have been developed such as NMD inhibition or nonsense mutation readthrough. METHODS: Using a dedicated screening system, we sought molecules capable to block NMD. Additionally, 3 cell lines derived from patient cells and harboring a nonsense mutation were used to study the effect of the selected molecule on the level of nonsense-containing mRNAs and the synthesis of proteins from these mutant mRNAs. RESULTS: We demonstrate here that amlexanox, a drug used for decades, not only induces an increase in nonsense-containing mRNAs amount in treated cells, but also leads to the synthesis of the full-length protein in an efficient manner. We also demonstrated that these full length proteins are functional. CONCLUSIONS: As a result of this dual activity, amlexanox may be useful as a therapeutic approach for diseases caused by nonsense mutations.