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Abstract
In this study, the diabetogenic effects of long term Ochratoxin A (OTA) administration in rats were investigated, and its role in the etiology of diabetes mellitus (DM) was examined utilizing 42 female Wistar rats for these purposes. The rats were divided into three different study and control groups according to the duration of the OTA administration. The rats received 45 μg OTA daily in their feed for 6, 9 and 24 weeks, respectively. Three control groups were also used for the same time periods. Blood and pancreatic tissue samples were collected during the necropsy at the end of the 6, 9 and 24 weeks. The plasma values of insulin, glucagon and glucose were determined for the study and control groups. Pancreatic lesions were evaluated via histopathological examination and insulin and glucagon expression in these lesions was subsequently determined using immunohistochemical methods. Statistically significant decreases in insulin levels were observed, in contrast to increases in blood glucagon and glucose levels. Histopathological examinations revealed slight to moderate degeneration in Langerhans islet cells in all OTA-treated groups. Immunohistochemistry of pancreatic tissue revealed decreased insulin and increased glucagon expression. This study demonstrated that OTA may cause pancreatic damage in the Langerhans islet and predispose rats to DM.
Highlights
Ochratoxin A (OTA) is a mycotoxin that naturally occurs as a fungal metabolite and is the most toxic product of Aspergillus ochraceus and Penicillium verrucosum [1]
This study showed that OTA causes damage in endocrine pancreatic function, even groups
This study showed that OTA causes damage in endocrine pancreatic function, even during a during a six-week exposure period
Summary
Ochratoxin A (OTA) is a mycotoxin that naturally occurs as a fungal metabolite and is the most toxic product of Aspergillus ochraceus and Penicillium verrucosum [1]. Its widespread occurrence in human and animal food in conjunction with some preliminary cytotoxic and carcinogenic data suggest a possible role for dietary OTA in the development of various organ damage and the occurrence of different tumors [2,3,4,5]. Mutagenic and cytotoxic effects, OTA is known to lead to a decrease in food intake and body weight gain [6]. OTA has been shown to be nephrotoxic, immunotoxic and teratogenic to a variety of animal species [7]. It is a ubiquitous mycotoxin produced by fungi in improperly stored food products. The highest amounts of OTA in food of plant origin were found mainly in Eastern Europe [8,9,10,11,12]
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