Amine oxidase substrates mimic several of the insulin effects on adipocyte differentiation in 3T3 F442A cells

Fontana, E.; Boucher, Jérémie; Marti, Luc; Lizcano, José M.; Testar, Xavier; Zorzano, António; Carpéné, Christian

doi:10.1042/bj3560769

Cited by 39 publications

(45 citation statements)

References 27 publications

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“…As to the mechanisms involved, we have demonstrated that the combination of SSAO substrates and vanadate stimulates tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and -3 proteins and activates phosphatidylinositol 3-kinase (10), i.e., crucial components of insulin signal transduction. In addition, chronic incubation of 3T3 adipocytes with SSAO substrates caused an enhanced insulin sensitivity (14). In keeping with these in vitro insulinomimetic effects, chronic treatment with benzylamine and vanadate lower hyperglycemia in streptozotocin-induced diabetic rats (12).…”

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confidence: 55%

Semicarbazide-Sensitive Amine Oxidase/Vascular Adhesion Protein-1 Activity Exerts an Antidiabetic Action in Goto-Kakizaki Rats

et al. 2003

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In this study we have explored whether the bifunctional protein semicarbazide-sensitive amine oxidase (SSAO)/ vascular adhesion protein-1 (VAP-1) represents a novel target for type 2 diabetes. To this end, Goto-Kakizaki (GK) diabetic rats were treated with the SSAO substrate benzylamine and with low ineffective doses of vanadate previously shown to have antidiabetic effects in streptozotocin-induced diabetic rats. The administration of benzylamine in combination with vanadate in type 2 diabetic rats acutely stimulated glucose tolerance, and the chronic treatment normalized hyperglycemia, stimulated glucose transport in adipocytes, and reversed muscle insulin resistance. Acute in vivo administration of benzylamine and vanadate stimulated skeletal muscle glucose transport, an effect that was also observed in incubated muscle preparations coincubated with adipose tissue explants or with human recombinant SSAO. Acute administration of benzylamine/vanadate also ameliorated insulin secretion in diabetic GK rats, and this effect was also observed in incubated pancreatic islets. In keeping with these observations, we also demonstrate that pancreatic islets express SSAO/ VAP-1. As far as mechanisms of action, we have found that benzylamine/vanadate causes enhanced tyrosine phosphorylation of proteins and reduced protein tyrosine phosphatase activity in adipocytes. In addition, incubation of human recombinant SSAO, benzylamine, and vanadate generates peroxovanadium compounds in vitro. Based on these data, we propose that benzylamine/vanadate administration generates peroxovanadium locally in pancreatic islets, which stimulates insulin secretion and also produces peroxovanadium in adipose tissue, activating glucose metabolism in adipocytes and in neighboring muscle. This opens the possibility of using the SSAO/VAP-1 activity as a local SSAO/VAP-1 is expressed in a variety of tissues, and under normal conditions expression is high in adipose cells. In isolated rat adipocytes, SSAO/VAP-1 is mainly at the plasma membrane, and nearly 17 ϫ 10 6 copies of this protein are present at the cell surface in a single adipocyte (5,6). In contrast, SSAO activity is very low or absent in other insulin-responsive tissues such as skeletal muscle or heart (7). In fact, it has been demonstrated that SSAO/ VAP-1 is not expressed in 3T3-L1 fibroblasts and that SSAO/VAP-1 gene expression is induced during adipogenesis (8). This finding is in complete agreement with the previous observation of an increase in the SSAO activity of stroma-vascular preadipocytes from rat adipose tissue during their conversion into adipocytes when cultured in vitro (9). This suggests that SSAO/VAP-1 is a member of the adipogenic gene program and, in addition, that SSAO/ VAP-1 may contribute to the acquisition of some final characteristics of fully differentiated adipose cells. Most of the SSAO/VAP-1 expressed in rat adipocytes is found in plasma membrane (5,6). Thus, subcellular fractionation of membranes from 3T3-L1 adipocytes or isolated rat adipocytes has demonstr...

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confidence: 55%

Semicarbazide-Sensitive Amine Oxidase/Vascular Adhesion Protein-1 Activity Exerts an Antidiabetic Action in Goto-Kakizaki Rats

et al. 2003

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“…The exact involvement of TNF-␣ in the pathophysiology of insulin resistance in obese humans and in noninsulin-dependent diabetes mellitus is still a matter of controversy, but it is reasonable to believe that TNF-␣, in addition to other cytokines and metabolic factors, could contribute to the balance of tissular insulin sensitivity. Several recent works have reported that SSAO substrates stimulate glucose transport in rodent Marti et al, 1998;Fontana et al, 2001) or human adipocytes (Morin et al, 2001). This amine-stimulated glucose transport may thus represent an original mechanism by which circulating or locally produced amines can regulate glucose homeostasis.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have reported that SSAO activation in response to its substrates can stimulate glucose transport in adipocytes Marti et al, 1998;Fontana et al, 2001;Morin et al, 2001). Otherwise, TNF-␣ is well known to inhibit insulin-stimulated glucose transport (Stephens and Pekala, 1991) and to be involved in the pathogenesis of obesity-associated insulin resistance (Hotamisligil, 2000;Moller, 2000).…”

Section: Tnf-␣ Modulation Of Ssao-mediated Glucose Uptake 1201mentioning

confidence: 99%

“…In fat cells, it has been recently documented that SSAO expression is strongly induced during preadipocyte differentiation (Moldes et al, 1999;Fontana et al, 2001) and that SSAO chronic activation promotes terminal adipocyte maturation Mercier et al, 2001). Furthermore, SSAO is not exclusively present at the plasma membrane of adipocytes, but is also detectable in vesicles containing the insulin-sensitive glucose transporter GLUT4 (Morris et al, 1997;Enrique-Tarancon et al, 1998).…”

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confidence: 99%

“…Furthermore, SSAO is not exclusively present at the plasma membrane of adipocytes, but is also detectable in vesicles containing the insulin-sensitive glucose transporter GLUT4 (Morris et al, 1997;Enrique-Tarancon et al, 1998). The acute effect of insulin on glucose transport can be mimicked by SSAO substrates Marti et al, 1998;Fontana et al, 2001;Morin et al, 2001) through the release of hydrogen peroxide (EnriqueTarancon et al, 1998;Marti et al, 1998). SSAO substrates can also promote IRS-1 and -3 tyrosine phosphorylation, and stimulate phosphatidylinositol 3-kinase activity and GLUT4 translocation to the plasma membrane (Enrique-Tarancon et al, 2000).…”

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confidence: 99%

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Regulation of Semicarbazide-Sensitive Amine Oxidase Expression by Tumor Necrosis Factor-α in Adipocytes: Functional Consequences on Glucose Transport

Mercier¹,

Moldes²,

Hadri³

et al. 2002

J Pharmacol Exp Ther

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Membrane-associated semicarbazide-sensitive amine oxidase (SSAO) is mainly present in the media of aorta and in adipose tissue. Recent works have reported that SSAO activation can stimulate glucose transport of fat cells and promote adipose conversion. In this study, the murine 3T3-L1 preadipose cell line was used to investigate SSAO regulation by tumor necrosis factor-␣ (TNF-␣), a cytokine that is synthesized in fat cells and known to be involved in obesity-linked insulin resistance. SSAO mRNA and protein levels, and enzyme activity were decreased by TNF-␣ in a dose-and time-dependent manner, without any change of SSAO affinity for substrates or inhibitors. SSAO inhibition caused by TNF-␣ was spontaneously reversed along the time after TNF-␣ removal. The decrease in SSAO expression also occurred in white adipose tissue of C57BL/6 mice treated with mTNF-␣. Overall, we demonstrated that reduction in SSAO expression induced by the cytokine had marked repercussions on amine-stimulated glucose transport, in a doseand time-dependent manner. This effect was more pronounced than the inhibiting effect of TNF-␣ on insulin-stimulated glucose transport. Moreover, the peroxisome proliferator-activated receptor ␥ agonists thiazolidinediones did not reverse either TNF-␣ effect on amine-sensitive glucose transport or the inhibition of SSAO activity, whereas they antagonized TNF-␣ effects on insulin-sensitive glucose transport. These results demonstrate that TNF-␣ can strongly down-regulate SSAO expression and activity, and through this mechanism can dramatically reduce amine-stimulated glucose transport. This suggests a potential role of this regulatory process in the pathogenesis of glucose homeostasis dysregulations observed during diseases accompanied by TNF-␣ overproduction, such as cachexia or obesity.

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Structure–Activity Relationships of SSAO/VAP‐1 Arylalkylamine‐Based Substrates

et al. 2009

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Semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 (SSAO/VAP-1) substrates show insulin-mimetic effects and are therefore potentially valuable molecules for the treatment of diabetes mellitus. Herein we review several structural and electronic aspects of SSAO arylalkylamine-based substrates. Two main modifications directly affect amine oxidase (AO) activity: 1) variation in ring substitution modulates the biological activity of the arylalkylamine ligand by converting a substrate into a substrate-like inhibitor, and 2) variation in the number of methylene units between the aromatic ring and the ammonium groups of the arylalkylamine substrates dramatically alters the oxidation rate between species. Furthermore, we review relevant information about mammalian SSAO/VAP-1 substrate selectivity and specificity over monoamine oxidases (MAOs).

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Amine oxidase substrates mimic several of the insulin effects on adipocyte differentiation in 3T3 F442A cells

Cited by 39 publications

References 27 publications

Semicarbazide-Sensitive Amine Oxidase/Vascular Adhesion Protein-1 Activity Exerts an Antidiabetic Action in Goto-Kakizaki Rats

Semicarbazide-Sensitive Amine Oxidase/Vascular Adhesion Protein-1 Activity Exerts an Antidiabetic Action in Goto-Kakizaki Rats

Regulation of Semicarbazide-Sensitive Amine Oxidase Expression by Tumor Necrosis Factor-α in Adipocytes: Functional Consequences on Glucose Transport

Structure–Activity Relationships of SSAO/VAP‐1 Arylalkylamine‐Based Substrates

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