Abstract

Introduction: Clinical and epidemiological studies suggest that patients who are overweight or obese are more at risk in developing glucose intolerance (G/I) and insulin resistance (I/R) leading to type 2 diabetes (T2DM) and cardiovascular disease. Aim of work: Assess the dynamic contribution of visfatin in the development of obesity and/or diabetes and demonstrate their possible molecular mechanism(s) from side and from another side, modulate role of Raspberry ketone (RK) as weight management supplement and illustrate their possible molecular mechanism(s). Materials and Methods: Eighty adult rats were divided into eight groups (10 rats for each group, G); G1: Normal Control Group (Normal diet); G2: Diabetic Control Group (received streptozotocin 35 mg/kg); G3: Obese Control Group (received high fat diet, HFD); G4: Obese Diabetic Control Group, G5: Raspberry ketone Control Group (received 500 mg/kg), G6: Diabetic rats treated with Raspberry ketone; G7: Obese rats treated with Raspberry ketone and G8: Obese Diabetic rats treated with Raspberry ketone to assess the study’s aims, their effect was determined on body weight, OGTT, glucose homeostasis (glucose, insulin, HOMA-IR), oxidative stress markers, cytoglobin, visfatin and liver histopathology. Results: RK caused weight loss, corrected the disturbed glucose and insulin homeostasis, Furthermore, RK increased hepatic content of glutathione (GSH), while decreased hepatic content of malonaldialdehyde (MDA). RK also up regulated hepatic protein expression of cytoglobin, while down regulated hepatic mRNA expression of visfatin. Conclusion: This study assessed the involvement of visfatin and cytoglobin in obese diabetic rats and modulated the role of RK through the efficient rebalance of glucose homeostasis, I/R, the redox status and liver histopathology.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.