PMID- 25572340
OWN - NLM
STAT- MEDLINE
DCOM- 20160527
LR  - 20181202
IS  - 1877-8755 (Electronic)
IS  - 1138-7548 (Linking)
VI  - 71
IP  - 3
DP  - 2015 Sep
TI  - Glitazones inhibit human monoamine oxidase but their anti-inflammatory actions 
      are not mediated by VAP-1/semicarbazide-sensitive amine oxidase inhibition.
PG  - 487-96
LID - 10.1007/s13105-014-0379-3 [doi]
AB  - Glitazones are peroxisome proliferator-activated receptor gamma (PPARgamma) agonists 
      widely used as antidiabetic drugs also known as thiazolidinediones. Most of them 
      exert other effects such as anti-inflammatory actions via mechanisms supposed to 
      be independent from PPARgamma activation (e.g., decreased plasma monocyte 
      chemoattractant protein-1 (MCP-1) levels). Recently, pioglitazone has been shown 
      to inhibit the B form of monoamine oxidase (MAO) in mouse, while rosiglitazone 
      and troglitazone were described as non-covalent inhibitors of both human MAO A 
      and MAO B. Since molecules interacting with MAO might also inhibit 
      semicarbazide-sensitive amine oxidase (SSAO), known as vascular adhesion 
      protein-1 (VAP-1), and since VAP-1/SSAO inhibitors exhibit anti-inflammatory 
      activity, our aim was to elucidate whether VAP-1/SSAO inhibition could be a 
      mechanism involved in the anti-inflammatory behaviour of glitazones. To this aim, 
      MAO and SSAO activities were measured in human subcutaneous adipose tissue 
      biopsies obtained from overweight women undergoing plastic surgery. The 
      production of hydrogen peroxide, an end-product of amine oxidase activity, was 
      determined in tissue homogenates using a fluorometric method. The oxidation of 
      1 mM tyramine was inhibited by pargyline and almost resistant to semicarbazide, 
      therefore predominantly MAO-dependent. Rosiglitazone was more potent than 
      pioglitazone in inhibiting tyramine oxidation. By contrast, benzylamine oxidation 
      was only abolished by semicarbazide: hence SSAO-mediated. Pioglitazone hampered 
      SSAO activity only when tested at 1 mM while rosiglitazone was inefficient. 
      However, rosiglitazone exhibited anti-inflammatory activity in human adipocytes 
      by limiting MCP-1 expression. Our observations rule out any involvement of 
      VAP-1/SSAO inhibition and subsequent limitation of leukocyte extravasation in the 
      anti-inflammatory action of glitazones.
FAU - Carpene, Christian
AU  - Carpene C
AD  - Institut des Maladies Metaboliques et Cardiovasculaires, Institut National de la 
      Sante et de la Recherche Medicale (INSERM U1048), Toulouse, France, 
      christian.carpene@inserm.fr.
FAU - Bizou, Mathilde
AU  - Bizou M
FAU - Treguer, Karine
AU  - Treguer K
FAU - Hasnaoui, Mounia
AU  - Hasnaoui M
FAU - Gres, Sandra
AU  - Gres S
LA  - eng
PT  - Journal Article
DEP - 20150109
PL  - Spain
TA  - J Physiol Biochem
JT  - Journal of physiology and biochemistry
JID - 9812509
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Benzylamines)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Monoamine Oxidase Inhibitors)
RN  - 0 (Thiazolidinediones)
RN  - 05V02F2KDG (Rosiglitazone)
RN  - A1O31ROR09 (benzylamine)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.4.3.21 (AOC3 protein, human)
RN  - EC 1.4.3.21 (Amine Oxidase (Copper-Containing))
RN  - X4OV71U42S (Pioglitazone)
RN  - X8ZC7V0OX3 (Tyramine)
SB  - IM
MH  - Adipocytes/drug effects/enzymology
MH  - Adult
MH  - Amine Oxidase (Copper-Containing)/antagonists & inhibitors/metabolism
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Benzylamines/metabolism
MH  - Cell Adhesion Molecules/antagonists & inhibitors/metabolism
MH  - Drug Evaluation, Preclinical
MH  - Female
MH  - Humans
MH  - Hydrogen Peroxide/metabolism
MH  - Middle Aged
MH  - Monoamine Oxidase Inhibitors/*pharmacology
MH  - Pioglitazone
MH  - Rosiglitazone
MH  - Subcutaneous Fat/drug effects/enzymology/pathology
MH  - Thiazolidinediones/*pharmacology
MH  - Tyramine/metabolism
EDAT- 2015/01/13 06:00
MHDA- 2016/05/28 06:00
CRDT- 2015/01/10 06:00
PHST- 2014/10/17 00:00 [received]
PHST- 2014/12/26 00:00 [accepted]
PHST- 2015/01/10 06:00 [entrez]
PHST- 2015/01/13 06:00 [pubmed]
PHST- 2016/05/28 06:00 [medline]
AID - 10.1007/s13105-014-0379-3 [doi]
PST - ppublish
SO  - J Physiol Biochem. 2015 Sep;71(3):487-96. doi: 10.1007/s13105-014-0379-3. Epub 
      2015 Jan 9.