AUTHOR=Elnagar Asmaa , El-Dawy Khalifa , El-Belbasi Hussein I. , Rehan Ibrahim F. , Embark Hamdy , Al-Amgad Zeinab , Shanab Obeid , Mickdam Elsayed , Batiha Gaber E. , Alamery Salman , Fouad Samer S. , Cavalu Simona , Youssef Mohammed 

TITLE=Ameliorative Effect of Oxytocin on FBN1 and PEPCK Gene Expression, and Behavioral Patterns in Rats' Obesity-Induced Diabetes

JOURNAL=Frontiers in Public Health

VOLUME=10

YEAR=2022

URL=https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2022.777129

DOI=10.3389/fpubh.2022.777129

ISSN=2296-2565

ABSTRACT=<p>Amelioration of hyperinsulinemia and insulin resistance associated with obesity is a cardinal target for therapeutics. Therefore, we investigated the relation of <italic>Fibrilln-1</italic> (<italic>FBN1) mRNA</italic> expression and hepatic <italic>phosphoenolpyruvate caboxykinase</italic> (<italic>PEPCK</italic>) enzyme to the ameliorative impact of oxytocin on obesity-induced diabetes, suggesting glycogenolysis markers in diabetic models. Four groups of forty male Wistar rats were formed (<italic>n</italic> = 10): a control group fed basal diet and <italic>intra</italic>peritoneal injections of saline; an oxytocin-injected group; a diet-induced obese group fed a high-fat/high-sugar diet and injected with saline; a diet-induced obese group injected with oxytocin. Depending on blood glucose levels, obese groups were further sub-grouped into prediabetic, and diabetic rats, with 5 rats each, at the ninth and the 16th week of the feeding period, respectively. <italic>FBN1</italic> expression and <italic>PEPCK</italic> activity were determined using the <italic>qPCR</italic> technique and some biochemical parameters (glycemic, lipid profile, kidney, and liver functions) were determined using kits. Obese groups showed an elevation of brain <italic>FBN1</italic> expression, high serum lipid profile, high glucose level, and a deleterious impact on liver and kidney functions. Obese groups showed the stimulator effect of the <italic>PEPCK</italic> enzyme and time-dependent pathological changes in renal and hepatic tissues. The motor activities were negatively correlated with <italic>FBN1</italic> gene expression in prediabetic and diabetic rats. In addition to our previous review of the crucial role of asprosin, here we showed that oxytocin could ameliorate obesity-induced diabetes and decrease <italic>FBN1</italic> gene expression centrally to block appetite. Oxytocin caused decreases in <italic>PEPCK</italic> enzyme activity as well as glycogenolysis in the liver. Therefore, oxytocin has a potential effect on <italic>FBN1</italic> expression and <italic>PEPCK</italic> enzyme activity in the obesity-induced diabetic-rat model.</p>