Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. Fats and compounds known as advanced glycation end products (AGEs) exacerbate liver injury. AGEs are complexes of reducing sugars and proteins formed when proteins are overheated in the presence of fats and sugars (e.g., by deep frying). AGEs are low in traditional diets, but are common when diets include so‐called fast foods. Impaired gastrointestinal function has been implicated in the development of NAFLD, but there is very little known about the effects AGEs and fats on enteric neurons in the context of NAFLD. This study aimed to assess damage to myenteric neurons within the ileum, caecum, and colon of C57bl/6 mice with NAFLD induced by high fat high cholesterol (HFHC), and HFHC baked diets (which increases AGEs content fivefold) for 20 weeks. There was a significant decrease in the number of Hu and nitric oxide synthase (NOS) immunoreactive neurons, as well as a loss of neurofilament immunoreactive fibres in the HFHC and HFHC baked groups compared to control. In addition, there was a significant increase in Hu translocation to the nucleus, granular Hu deposits in the cytoplasm, and the presence of cytoplasmic vacuoles (indices of damage) in the HFHC and HFHC baked groups compared to control. This work indicates that HFHC and HFHC baked diets result in enteric neuropathy that may underlie impaired gastrointestinal function in NAFLD.Grant Funding Source: National Health and Medical Research Council

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call