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Diabetes mellitus (DM) is a chronic endocrine disease characterized by persistent hyperglycemia. Oxidative damage, inflammatory cytokines, and apoptotic cell death play a major role in the induction and progression of male testicular damage. Plant-derived phytochemicals such as green coffee (Coffea arabica) can possess antidiabetic effects with little toxicity. The current study is aimed at investigating the therapeutic roles of green coffee in diabetic testicular injury stimulated by high-fat diet/streptozotocin administration. Diabetes mellitus was induced by a high-fat diet and a single dose of streptozotocin (STZ) (35 mg kg-1) in male albino rats. Diabetic animals were orally given two different concentrations of green coffee (50 mg kg-1 and 100 mg kg-1) for 28 days. The levels of testosterone, luteinizing hormone, and follicle-stimulating hormone and parameters of oxidative stress, inflammation, and apoptosis were measured. mRNAs and protein levels were detected quantitatively by real-time PCR and ELISA, respectively. In the diabetic group, the levels of testosterone, luteinizing hormone, and follicle-stimulating hormone showed a significant reduction while they increased significantly after green coffee treatment. A significant increase of antioxidant markers glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase along with decreased levels of lipid peroxides and nitric oxide was observed after green coffee treatment in the diabetic group. Finally, the levels of IL-1β, TNF-α, Bax, and caspase-3 were also decreased in both treated groups (metformin and green coffee) when compared to the diabetic group. We conclude that testicular oxidative impairment induced by a high-fat diet (HFD) and STZ can be reversed by green coffee. Administration of green coffee could represent a promising therapeutic agent which can help the treatment of type 2 DM-induced testicular dysfunction.

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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.