Homeostatic effect of p-chloro-diphenyl diselenide on glucose metabolism and mitochondrial function alterations induced by monosodium glutamate administration to rats

Abstract

The metabolic syndrome is a group of metabolic alterations considered a worldwide public health problem. Organic selenium compounds have been reported to have many different pharmacological actions, such as anti-hypercholesterolemic and anti-hyperglycemic. The aim of this study was to evaluate the effect of p-chloro-diphenyl diselenide (p-ClPhSe)2, an organic selenium compound, in a model of obesity induced by monosodium glutamate (MSG) administration in rats. The rats were treated during the first ten postnatal days with MSG and received (p-ClPhSe)2 (10 mg/kg, intragastrically) from 45th to 51 th postnatal day. Glucose, lipid and lactate levels were determined in plasma of rats. Glycogen levels and activities of tyrosine aminotransferase, hexokinase, citrate synthase and glucose-6-phosphatase (G-6-Pase) were determined in livers of rats. Renal G-6-Pase activity was also determined. The purine content [Adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate] and mitochondrial functionality in the liver were also investigated. p-(ClPhSe)2 did not alter the reduction in growth performance and in the body weight caused by MSG but reduced epididymal fat deposition of rats. p-(ClPhSe)2 restored glycemia, triglycerides, cholesterol and lactate levels as well as the glucose metabolism altered in rats treated with MSG. p-(ClPhSe)2 restored hepatic mitochondrial dysfunction and the decrease in citrate synthase activity and ATP and ADP levels caused by MSG in rats. In summary, (p-ClPhSe)2 had homeostatic effects on glucose metabolism and mitochondrial function alterations induced by MSG administration to rats.

(p-ClPhSe)2Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

“…In fact, hyperglycemia is a characteristic symptom of rats treated with MSG [Shen et al, ; Miranda et al, ]. In animal models, subcutaneous neonatal MSG administration induces neuroendocrine obesity through hypothalamic lesion: resulting in fat tissue accumulation, glucose intolerance, hyperinsulinemia, and insulin resistance [Shen et al, ; Miranda et al, ; Quines et al, ]. Furthermore, it has been demonstrated that hyperglycemia is associated with systemic insulin resistance and mitochondrial dysfunction in animal models of obesity induced by MSG administration [Shen et al, ; Miranda et al, ].…”

“…route for 7 days. The dose of 10 mg/kg of ( p ‐ClPhSe) 2 was chosen based on our previous study group [Quines et al, ].…”

“…Indeed, it has been reported that treatment with p ‐chloro‐diphenyl diselenide ( p ‐ClPhSe) 2 elicits an anorectic‐like action in rats mediated by the serotonergic system with an early behavioral satiety and without causing major toxic effects [Bortolatto et al, ]. Moreover, our research group recently demonstrated that ( p ‐ClPhSe) 2 was effective against the first signs of obesity, regulating the glucose metabolism and the hepatic function in 45‐days old rats treated with monosodium glutamate (MSG) [Quines et al, ].…”

Combined Therapy With Swimming Exercise and a Diet Supplemented With Diphenyl Diselenide Is Effective Against Age‐Related Changes in the Hepatic Metabolism of Rats

“…panel B). Accordingly, our previous data demonstrated the effectiveness of another organoselenium compound in normalizing the activities of hepatic enzymes in a model of metabolic disorder induced by glutamate monosodium in rats [Quines et al, ].…”

Resistance exercise reduces memory impairment induced by monosodium glutamate in male and female rats

“…In general, the induction of glutamate neurotoxicity involves the development of intracellular changes and subsequent events resulting in neuronal disintegration (Choi, 1994). Furthermore, it has been demonstrated that the MSG model, which consists of MSG administration to newborn rats, induces functional and behavioural alterations in adulthood, including obesity, hyperexcitability, pain sensitivity, anxiogenic-like and depressive-like behaviours, as well as impairment of memory (Quines et al 2014;Rosa et al 2015;Quines et al 2016).…”