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Thus, if in peripheral tissues adenosine mediates anti-inflammatory effects through A2A receptors, in the case of neuroinflammation, the activation of these receptors is responsible for neuronal degradation [89] through the influence exerted on glial cells, which involves the stimulation of cyclooxygenase type 2 (COX2), nitric oxide synthase (NOS), the release of prostaglandins, cytokines, and stimulation of Glu efflux from the presynaptic level [90,91,92]

Previously, we have shown that chemogenetic activation of GIPR-expressing cells in either the hypothalamus or the hindbrain supresses food intake 7,8 , and GIPR-expression in oligodendrocytes has recently been linked to enhanced access of co-administered GLP-1R agonists 23

4.1 Food allergy An additional study set out to determine the constituents of FAHF-2 and B-FAHF-2 that specifically reduce IgE

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