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Impact of aflatoxin B1 on hypothalamic neuropeptides regulating feeding behavior. | LitMetric

Impact of aflatoxin B1 on hypothalamic neuropeptides regulating feeding behavior.

Neurotoxicology

Laboratory of Neuroendocrinology & Nutritional and climatic Environment, University Sidi Mohamed Ben Abdellah, Faculty of Sciences DM, Fez, Morocco.

Published: July 2015

AI Article Synopsis

  • Mycotoxins in food, particularly aflatoxins (AF) like AFB1, pose significant health risks, causing immunosuppression, liver toxicity, and potential cancer, and their effects on neuroendocrine functions are not well understood.
  • A study on rats showed that AFB1 exposure resulted in significant weight loss and altered expression of critical hypothalamic neuropeptides that regulate appetite, impacting both orexigenic (hunger-promoting) and anorexigenic (satiation-promoting) signals.
  • The research also highlighted a reduction in neurons producing EM66, a peptide linked to food intake control, indicating that AFB1 may disrupt neuropeptide regulation related to feeding behavior and

Article Abstract

The presence of mycotoxins in food is a major problem of public health as they produce immunosuppressive, hepatotoxic and neurotoxic effects. Mycotoxins also induce mutagenic and carcinogenic effects after long exposure. Among mycotoxins that contaminate food are aflatoxins (AF) such as AFB1, which is the most powerful natural carcinogen. The AF poisoning results in symptoms of depression, anorexia, diarrhea, jaundice or anemia that can lead to death, but very few studies have explored the impact of AF on neuroendocrine regulations. To better understand the neurotoxic effects of AF related to anorexia, we explored in rat the impact of AFB1 on the major hypothalamic neuropeptides regulating feeding behavior, either orexigenic (NPY, Orexin, AgRP, MCH) or anorexigenic (α-MSH, CART, TRH). We also studied the effect of AFB1 on a novel neuropeptide, the secretogranin II (SgII)-derived peptide EM66, which has recently been linked to the control of food intake. For this, adult male rats were orally treated twice a week for 5 weeks with a low dose (150 μg/kg) or a high dose (300 μg/kg) of AFB1 dissolved in corn oil. Repeated exposure to AFB1 resulted in reduced body weight gain, which was highly significant for the high dose of AF. Immunocytochemical and quantitative PCR experiments revealed a dose-related decrease in the expression of all the hypothalamic neuropeptides studied in response to AFB1. Such orexigenic and anorexigenic alterations may underlie appetite disorders as they are correlated to a dose-dependent decrease in body weight gain of treated rats as compared to controls. We also found a decrease in the number of EM66-containing neurons in the arcuate nucleus of AFB1-treated animals, which was associated with a lower expression of its precursor SgII. These findings show for the first time that repeated consumption of AFB1 disrupts the hypothalamic regulation of neuropeptides involved in feeding behavior, which may contribute to the lower body weight gain associated to AF exposure.

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Source
http://dx.doi.org/10.1016/j.neuro.2015.06.008DOI Listing

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