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SLC1A2 is a membrane-bound transporter mediating neuronal uptake of amino-acids, which, among other things, is responsible for clearing glutamate from the synaptic cleft (e.g., Arriza et al., 1994)

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Together with reninangiotensinaldosterone activation, endothelin-1 (ET-1) upregulation, and smooth-muscle hypertrophy in resistance vessels, these changes contribute to the hypertensive phenotype in MetS and T2DM [1001,1002,1003,1004,1005,1006]

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Activated B cells show a marked increase in de novo fatty acid synthesis