Mitochondrial uncoupling protein 2 (UCP2) in the nonhuman primate brain and pituitary

Energy dissipating mechanisms and their regulatory components represent key elements of metabolism and may offer novel targets in the treatment of met abolic disorders, such as obesity and diabetes. Recent studies have shown t hat a mitochondrial uncoupling protein (UCP2), which uncouples mitochondria l oxidation from phosphorylation, is expressed in the rodent brain by neuro ns that are known to regulate autonomic, metabolic, and endocrine processes . To help establish the relevance of these rodent data to primate physiolog y, we now examined UCP2 messenger RNA and peptide expressions in the brain and pituitary gland of nonhuman primates. In situ hybridization histochemis try showed that UCP2 messenger RNA is expressed in the paraventricular, sup raoptic, suprachiasmatic, and arcuate nuclei of the primate hypothalamus an d also in the anterior lobe of the pituitary gland. Immunocytochemistry rev ealed abundant UCP2 expression in cell bodies and axonal processes in the a forementioned nuclei as well as in other hypothalamic and brain stem region s and all parts of the pituitary gland. In the hypothalamus, UCP2 was coexp ressed with neuropeptide Y, CRH, oxytocin, and vasopressin. In the pituitar y, vasopressin and oxytocin-producing axonal processes in the posterior lob e and POMC cells in the intermediate and anterior lobes expressed UCP2. On the other hand, none of the GH-producing cells of the anterior pituitary wa s found to produce UCP2. The abundance and distribution pattern of UCP2 in the primate brain and pituitary suggest that this protein is evolutionary c onserved and may relate to central autonomic, endocrine and metabolic regul ation.