Endogenous substrates of the semicarbazide-sensitive amine oxidase increased nitric oxide production in rat white adipocytes

In addition to the classical diamine oxidase (DAO; EC 1.4.3.6), other amine oxidases may scavenge histamine. For example, in rat white adipocytes which lack the DAO, the membrane-bound semicarbazide-sensitive amine oxidase which preferentially oxidizes benzylamine (Bz-SSAO; EC 1.4.3.6), is the only enzyme able to degrade histamine. Interestingly, the histamine degradation rate by Bz-SSAO is increased in buffer containing bicarbonate ions [1] and histamine derivatives, including receptor agonists and antagonists, may behave as substrates or inhibitors for this enzyme [2]. Methylamine (MET) is the simplest endogenous amine oxidised by Bz-SSAO [3]. White adipocytes possess a complete nitrergic system including the endothelial (NOS-III) and inducible (NOS-II) nitric oxide synthases. Different roles for each synthase in infl ammation, insulin resistance and adipocyte differentiation have been postulated [4]. Histamine-dependent production of nitric oxide (NO) has been shown in several experimental cell models [5] and a role for MET in raising NO in rat hypothalamus following potassium channel interaction has been described recently [6]. Moreover, metabolic roles for histamine and MET in rat white adipocytes have been also described [7, 8]. The aim of this work was to assess whether: 1) MET and histamine may stimulate NO production in rat white adipocytes; and 2) Bz-SSAO activity may have a role in regulating the effects of amines.