(p-ClPhSe)2 stabilizes metabolic function in a rat model of neuroendocrine obesity induced by monosodium glutamate. (August 2018) - Quines, Caroline B.
Abstract: Obesity is a chronic and complex medical condition characterized by excessive fat accumulation and its complications include metabolic syndrome, diabetes and chronic inflammation. The aim of this study was to expand the knowledge about p -chloro-diphenyl diselenide ( p -ClPhSe)2 effects on enzymes and proteins involved in the metabolism of lipids and carbohydrates in a model of neuroendocrine obesity induced by MSG. Male Wistar rats were treated during the first ten postnatal days with MSG (4 g/kg, s.c.) and received ( p -ClPhSe)2 (10 mg/kg, i.g.) from 90 th to 97th postnatal day. The hypothalamic function, insulin resistance and other biochemical parameters were determined in the rat blood, liver and skeletal muscle. The MSG administration induced hypothalamic neurotoxicity accompanied by metabolic disorders, including obesity, a transient insulin resistance, and metabolic alterations, demonstrated in the blood, liver and skeletal muscle, and lipotoxicity, characterized in the liver and skeletal muscle. The metabolic disorders in the liver and skeletal muscle were accompanied by the decrease in AMPK phosphorylation and activation of Akt. ( p -ClPhSe)2 restored most of metabolic parameters altered by MSG administration in rats. The hypothalamic neurotoxicity induced by MSG was accompanied by metabolic disorders in rats, which were regulated by ( p -ClPhSe)2 . Graphical abstract: Highlights: Neonatal administration of MSG induced hypothalamic neurotoxicity accompanied by metabolic disorders in rats. ( p -ClPhSe)2 elicited a neuroprotective effect in MSG-treated rats. ( p -ClPhSe)2 treatment restored metabolic homeostasis in the blood, liver and skeletal muscle of MSG-treated rats.