Open AccessNigella Sativa and Ginger Increase GLUT4 and PPARγ in Metabolic Syndrome‐Induced Rats
Author(s) -
Eman Adel Zayed,
Afaf A. Ain-Shoka,
Kamal A. El Shazly,
Aliaa E. M. K. El-Mosallamy,
Hekma A. Abd El Latif
Publication year - 2021
Publication title -
letters in applied nanobioscience
Language(s) - English
Resource type - Journals
ISSN - 2284-6808
DOI - 10.33263/lianbs111.32613269
Subject(s) - glut4 , insulin resistance , nigella sativa , adiponectin , medicine , endocrinology , fructose , metabolic syndrome , irs1 , glucose transporter , insulin , hyperlipidemia , diabetes mellitus , insulin receptor , pharmacology , biology , traditional medicine , biochemistry
Increased fructose intake has been linked to the epidemiology of insulin resistance, type 2 diabetes mellitus, renal damage, and metabolic syndrome (MS). As oxidative stress plays a pivotal role in the pathology of insulin resistance, the present study was conducted to investigate the effects of Nigella Sativa (NS) and ginger as potent antioxidants on fructose-induced MS in rats. Male rats were fed with a high‐fructose high-fat-fed diet for 8 weeks. By the end of the 8th week, rats were divided into four groups; one was left untreated (normal control) and MS control group was treated with saline. MS groups were given Nigella sativa (4 ml/kg) and ginger (500 mg/kg) daily for 4 weeks. Markers chosen for assessment included the effect on body weight gain, glucose, insulin, adiponectin levels, and lipid profile. Also, protein expressions were estimated by glucose transporter 4 (GLUT4) content and peroxisome proliferator‐activated receptor‐gamma (PPARγ). Nigella sativa and ginger ameliorated some manifestations of MS, including an increase in body weight, glucose, insulin level, and resistance. Besides, both drugs lowered insulin resistance, induced hyperlipidemia and increased adiponectin level. Drugs also increased GLUT4 and PPARγ protein expression compared with MS control group. Nigella sativa and ginger ameliorated parameters of MS via increased GLUT4 and PPARγ expression.