sodium-acetate--anhydrous and carfentanil

A recent study has shown that acetate administration leads to a fourfold increase in the transcription of proopiomelanocortin (POMC) mRNA in the hypothalamus. POMC is cleaved to peptides, including β-endorphin, an endogenous opioid (EO) agonist that binds preferentially to the µ-opioid receptor (MOR). We hypothesised that an acetate challenge would increase the levels of EO in the human brain. We have previously demonstrated that increased EO release in the human brain can be detected using positron emission tomography (PET) with the selective MOR radioligand [. Seven volunteers each completed a baseline [. Following sodium acetate administration, 2.5-6.5% reductions in [. We have demonstrated that an acute acetate challenge has the potential to increase EO release in the human brain, providing a plausible mechanism of the central effects of acetate on appetite in humans.

Topics: Adult; Analgesics, Opioid; Brain; Carbon Radioisotopes; Fentanyl; Humans; Male; Middle Aged; Opioid Peptides; Positron-Emission Tomography; Receptors, Opioid; Sodium Acetate