Green Coffee Bean Extract Potentially Ameliorates Liver Injury due to HFD/STZ-Induced Diabetes in Rats

Abstract

The goal of the current study was to examine the therapeutic potential of green coffee bean extract (GCBE) in the treatment of diabetic hepatic damage induced by high-fat diet (HFD) and streptozotocin (STZ) administration. The novelty of this study lies in constructing a newly stabilized in vivo obese diabetic animal model in rats using HFD/STZ for investigating the dose-dependent effect of two commonly used doses of GCBE in hepatoprotection against oxidative stress-induced hepatic damage by measuring many parameters that have not been carried out previously in other studies. GCBE that was used in this study was a hot water extract of green coffee beans with a concentration of 0.1 g ml−1. Male albino rats were given a single dose of STZ (35 mg kg−1), and HFD to induce diabetes mellitus (DM). For 28 days, two separate doses of GCBE 50 mg kg−1 and 100 mg kg−1 were administered orally to diabetic animals. Leptin, liver enzymes, oxidative stress parameters, inflammatory parameters, fasting plasma glucose (FPG), fasting plasma insulin (FPI), and lipid profile levels were examined. Real-time PCR and ELISA were used to quantitatively detect the mRNAs of the genes involved in the insulin signaling pathway, the genes involved in glucose metabolism, and the amounts of proteins. The levels of FPG, lipid profile, liver enzymes, inflammatory markers, and leptin in the HFD/STZ diabetic group revealed a considerable spike, while they considerably decreased after GCBE treatment in a dose-dependent manner. After GCBE treatment, the diabetic group showed a significant rise in the antioxidant markers glutathione, superoxide dismutase, and catalase, as well as a decrease in malondialdehyde and nitric oxide levels. The liver changes caused by HFD/STZ were entirely reversed by GCBE, and most intriguingly, in a dose-dependent manner. We concluded that GCBE can repair the hepatic oxidative damage caused by HFD and STZ by reversing all the previously measured parameters and improving the insulin signaling pathways. GCBE demonstrated strong antifree radical activity and significantly protected cells from oxidative damage caused by HFD/STZ.