Subacute mycotoxin exposure in food is commonly overlooked. As one of the most toxic trichothecene mycotoxins, the T-2 toxin severely pollutes human foods and animal feeds. In our study, we investigated the effects of low-dose T-2 toxin on glucose and lipid metabolic function and further investigated the protective effect of tannic acid (TA) in C57BL/6J mice. Results showed that low-dose T-2 toxin significantly impaired blood glucose and lipid homeostasis, promoted ferroptosis in the pancreas and subsequent repression of insulin secretion in β-cells, and impacted hepatic glucose and lipid metabolism by targeted inhibition of the insulin receptor substrate (IRS)/phosphatidylin-ositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, which induced insulin resistance and steatosis in the liver. TA treatment attenuated pancreatic function and hepatic metabolism by ameliorating oxidative stress and insulin resistance in mice. These findings provide new perspectives on the toxic mechanism and intervention of chronic subacute toxicity of foodborne mycotoxins.
Keyphrases
- blood glucose
- low dose
- escherichia coli
- high fat diet induced
- glycemic control
- insulin resistance
- induced apoptosis
- signaling pathway
- oxidative stress
- protein kinase
- high dose
- type diabetes
- fatty acid
- high fat diet
- diabetic rats
- endothelial cells
- randomized controlled trial
- adipose tissue
- drug induced
- metabolic syndrome
- endoplasmic reticulum stress
- epithelial mesenchymal transition
- blood pressure
- pi k akt
- polycystic ovary syndrome
- mouse model
- high resolution
- mass spectrometry
- dna damage
- risk assessment
- induced pluripotent stem cells
- drug delivery
- weight loss
- human health
- binding protein
- pluripotent stem cells
- tyrosine kinase
- stress induced