Short- and long-term insulin-like effects of monoamine oxidases and semicarbazide-sensitive amine oxidase substrates in cultured adipocytes
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- 作者：Christian Carpé ; né ; Daniè ; le Daviaud ; Jeremie Boucher ; S ; y Bour ; Virgile Visentin ; S ; ra Grè ; s ; Carine Duffaut ; Emi Fontana ; Xavier Testar ; Jean-Sé ; bastien Saulnier-Blache ; Philip
- 关键词：peanut ; Δ ; 12 fatty acid desaturase ; prokaryotical expression ; function identification
- 刊名：Metabolism
- 出版年：2006
- 出版时间：October 2006
- 年：2006
- 卷：55
- 期：10
- 页码：1397-1405
- 全文大小：448 K
文摘
Semicarbazide-sensitive amine oxidase (SSAO) is known to increase during in vitro adipogenesis and to be one of the most highly expressed membrane proteins of white adipocytes. Although less well documented, mitochondrial monoamine oxidases (MAOs) are also present in adipocytes and share with SSAO the capacity to generate hydrogen peroxide. This work therefore aimed to compare several biologic effects of MAO and SSAO substrates in 3T3-F442A adipocytes. In differentiated cells, tyramine oxidation was predominantly MAO dependent, whereas benzylamine oxidation was SSAO dependent. Both amines partially mimicked insulin actions, including stimulation of Akt phosphorylation and glucose uptake. In addition, tyramine and benzylamine impaired tumor necrosis factor α–dependent nitric oxide formation in a pargyline- and semicarbazide-sensitive manner, respectively. Various biogenic amines were tested in competition for tyramine or benzylamine oxidation and classified as MAO-preferring (methoxytyramine, tryptamine) or SSAO-preferring substrates (methylamine, octopamine). Short-term incubation with 1 mmol/L of all amines except histamine stimulated glucose uptake up to 20 % to 50 % of maximal insulin activation. One-week treatment with either MAO or SSAO substrates alone allowed postconfluent cells to differentiate into adipocytes, reproducing 60 % of insulin-promoted lipid accumulation. All amines also exerted a slight improvement in the adipogenic action of insulin. Therefore, like SSAO, substrate activation of MAO can interact with adipocyte metabolism by mimicking diverse effects of insulin in addition to preventing tumor necrosis factor α–dependent responses.