Semicarbazide-sensitive amine oxidase activation promotes adipose conversion of 3T3-L1 cells

Mercier, Nathalie; Moldes, Marthe; Hadri, Khadija El; Fève, Bruno

doi:10.1042/bj3580335

Cited by 45 publications

(46 citation statements)

References 43 publications

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“…These insulin-like effects seem to be mediated, at least in part, by tyrosine phosphorylation of intracellular proteins (Heffetz et al, 1990). Other insulin-like effects, also dependent on hydrogen peroxide generation, have been reported for amine oxidase substrates: stimulation of adipose differentiation in 3T3 preadipocyte lineages Mercier et al, 2001) and inhibition of lipolysis in human fat cells ).…”

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confidence: 99%

Tyramine Stimulates Glucose Uptake in Insulin-Sensitive Tissues in Vitro and in Vivo via Its Oxidation by Amine Oxidases

Morin¹,

Visentin²,

Calise³

et al. 2002

J Pharmacol Exp Ther

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Tyramine and benzylamine have been described as stimulators of glucose transport in adipocytes. This effect is dependent on amine oxidation by monoamine oxidase (MAO) or semicarbazide-sensitive amine oxidase (SSAO) and on the subsequent hydrogen peroxide formation as already demonstrated by blockade with oxidase inhibitors or antioxidants and potentiation with vanadate. In this work, we extended these observations to skeletal muscle and cardiac myocytes using in vitro and in vivo approaches. Tissue distribution studies showed that substantial extrahepatic peripheral MAO activities exist in kidney and gut, but also in insulin-sensitive tissues: heart, adipose tissue, and skeletal muscles. SSAO activity is also widely distributed and present at a lower level than MAO, except in fat depots where both oxidases were equally involved in tyramine oxidation. When tested in vitro at millimolar doses, tyramine caused a large stimulation of glucose transport in rat adipocytes and in skeletal and cardiac muscles. In vivo administration of tyramine (4 mg/kg i.p.) lowered the hyperglycemic responses to a glucose challenge in control and in streptozotocin-treated rats. This positive effect on glucose disposal was obtained without vanadate and was abolished by SSAO and MAO inhibitors. Tyramine increased hexose uptake in vivo in insulin-sensitive tissues, whereas it induced only transient effects on plasma insulin or cardiovascular parameters. In conclusion, activation of the amine oxidases present in insulin-sensitive tissues induces insulin-like effects, readily detectable in vitro, and increasing peripheral glucose utilization in vivo.

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confidence: 99%

Tyramine Stimulates Glucose Uptake in Insulin-Sensitive Tissues in Vitro and in Vivo via Its Oxidation by Amine Oxidases

Morin¹,

Visentin²,

Calise³

et al. 2002

J Pharmacol Exp Ther

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“…It is now well established that in different species, SSAO expression and activity are largely induced during the adipose conversion process Mercier et al, 2001). SSAO activation by exogenous substrates activates glucose transport (Enrique-Tarancón et al, 1998), adipocyte differentiation , and inhibits lipolysis (Morin et al, 2001;Visentin et al, 2003;Amant et al, 2005).…”

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confidence: 99%

Antidepressant Phenelzine Alters Differentiation of Cultured Human and Mouse Preadipocytes

F¹,

Guillou²,

Chétrite³

et al. 2009

Molecular Pharmacology

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Change in body weight is a frequent side effect of antidepressants and is considered to be mediated by central effects on food intake and energy expenditure. The antidepressant phenelzine (Nardil) potently inhibits both monoamine oxidase and semicarbazide-sensitive amine oxidase activities, two enzymes that are highly expressed in adipose tissue, raising the possibility that it could directly alter adipocyte biology. Treatment with this compound is rather associated with weight gain. The aim of this work was to examine the effects of phenelzine on differentiation and metabolism of cultured human and mouse preadipocytes and to characterize the mechanisms involved in these effects. In all preadipocyte models, phenelzine induced a time-and dosedependent reduction in differentiation and triglyceride accumulation. Modulation of lipolysis or glucose transport was not involved in phenelzine action. This effect was supported by the reduced expression in the key adipogenic transcription factors peroxisome proliferator-activated receptor-␥ (PPAR-␥) and CCAAT/enhancer binding protein-␣, which was observed only at the highest drug concentrations (30 -100 M). The PPAR-␥ agonists thiazolidinediones did not reverse phenelzine effects. By contrast, the reduction in both cell triglycerides and sterol regulatory element-binding protein-1c (SREBP-1c) was detectable at lower phenelzine concentrations (1-10 M). Phenelzine effect on triglyceride content was prevented by providing free fatty acids to the cells and was partially reversed by overexpression of a dominant-positive form of SREBP-1c, showing the privileged targeting of the lipogenic pathway. When considered together, these findings demonstrate that an antidepressant directly and potently inhibits adipocyte lipid storage and differentiation, which could contribute to psychotropic drug side effects on energy homeostasis.

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“…Polyamine oxidase activity was also tested with the same procedure, using N 1 -acetyl spermidine as a substrate. G3PDH activity was assayed by recording the initial rate of oxidation of NADH at 340 nm at 25°C (Mercier et al, 2001). The standard mixture contained 50 mM triethanolamine-HCl buffer, pH 7.5, 1 mM EDTA, 0.13 mM ␤-NADH, 1 mM dihydroxyacetone phosphate, 1 mM 2-mercaptoethanol, and variable amounts of 10,000g cell supernatants.…”

Section: Methodsmentioning

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).…”

mentioning

confidence: 98%

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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Semicarbazide-sensitive amine oxidase activation promotes adipose conversion of 3T3-L1 cells

Cited by 45 publications

References 43 publications

Tyramine Stimulates Glucose Uptake in Insulin-Sensitive Tissues in Vitro and in Vivo via Its Oxidation by Amine Oxidases

Tyramine Stimulates Glucose Uptake in Insulin-Sensitive Tissues in Vitro and in Vivo via Its Oxidation by Amine Oxidases

Antidepressant Phenelzine Alters Differentiation of Cultured Human and Mouse Preadipocytes

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

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