Dysregulation of any step implicated in iron (Fe) metabolism in obesity may cause Fe overload. Excess Fe may cause toxic oxygen damage by generating oxygen-free radicals through the Fenton reaction. Furthermore, the three Fe chelating drugs deferiprone, deferoxamine, and deferasirox have many side effects which may limit their use. Therefore, this study intended to treat obesity-induced Fe overload with methanolic extract of goldenberry (GB) fruit with husk on obese rats. Overall, obese rats fed the GB extract showed lower levels of cholesterol, triacylglycerol, total low-density lipoprotein cholesterol, and higher levels of high-density lipoprotein cholesterol than obese rats, along with an improvement in anthropometric characteristics of obese rats. In addition, GB supplementation improved all parameters of Fe status in blood plasma and the trace elements homeostasis in adipose tissues, proving that the GB has a substantial ferric reducing property. GB enhanced the increase in hepcidin concentration in blood plasma and hepcidin gene expression in adipose tissues. In conclusion, there is an ascendant assessment of the role of GB as a natural Fe chelator that inhibits oxidative stress, which plays an essential role in recovering the conformational structure of hemoglobin as a macromolecule.
Key words: Goldenberry, Obesity, iron overload, hemoglobin, hepcidin, adipose tissues
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