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Damage to enteric neurons occurs in mice that develop fatty liver disease but not diabetes in response to a high-fat diet

Rivera, L.R., Leung, C., Pustovit, R.V., Hunne, B.L., Andrikopoulos, S., Herath, C., Testro, A., Angus, P.W. and Furness, J.B. 2014, Damage to enteric neurons occurs in mice that develop fatty liver disease but not diabetes in response to a high-fat diet, Neurogastroenterology & motility, vol. 26, no. 8, pp. 1188-1199, doi: 10.1111/nmo.12385.

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Title Damage to enteric neurons occurs in mice that develop fatty liver disease but not diabetes in response to a high-fat diet
Author(s) Rivera, L.R.
Leung, C.
Pustovit, R.V.
Hunne, B.L.
Andrikopoulos, S.
Herath, C.
Testro, A.
Angus, P.W.
Furness, J.B.
Journal name Neurogastroenterology & motility
Volume number 26
Issue number 8
Start page 1188
End page 1199
Total pages 12
Publisher Wiley-Blackwell
Place of publication Chichester, Eng.
Publication date 2014-08
ISSN 1350-1925
Keyword(s) diabetes
enteric nervous system
fatty liver disease
neuropathy
Summary Background Disorders of gastrointestinal functionsthat are controlled by enteric neurons commonlyaccompany fatty liver disease. Established fatty liverdisease is associated with diabetes, which itselfinduces enteric neuron damage. Here, we investigatethe relationship between fatty liver disease andenteric neuropathy, in animals fed a high-fat, highcholesteroldiet in the absence of diabetes. MethodsMice were fed a high-fat, high-cholesterol diet (21%fat, 2% cholesterol) or normal chow for 33 weeks.Liver injury was assessed by hematoxylin and eosin,picrosirius red staining, and measurement ofplasma alanine aminotransaminase (ALT). Quantitative immunohistochemistry was performed for differenttypes of enteric neurons. Key Results The micedeveloped steatosis, steatohepatitis, fibrosis, and a 10-fold increase in plasma ALT, indicative of liverdisease. Oral glucose tolerance was unchanged. Lossand damage to enteric neurons occurred in the myentericplexus of ileum, cecum, and colon. Total numbersof neurons were reduced by 15–30% and neuronsexpressing nitric oxide synthase were reduced by20–40%. The RNA regulating protein, Hu, becamemore concentrated in the nuclei of enteric neuronsafter high-fat feeding, which is an indication of stresson the enteric nervous system. There was also disruptionof the neuronal cytoskeletal protein, neurofilamentmedium. Conclusions & Inferences Entericneuron loss and damage occurs in animals with fattyliver disease in the absence of glucose intolerance. Theenteric neuron damage may contribute to the gastrointestinalcomplications of fatty liver disease.
Language eng
DOI 10.1111/nmo.12385
Field of Research 110399 Clinical Sciences not elsewhere classified
1103 Clinical Sciences
1109 Neurosciences
Socio Economic Objective 920105 Digestive System Disorders
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, John Wiley & Sons
Persistent URL http://hdl.handle.net/10536/DRO/DU:30079262

Document type: Journal Article
Collection: School of Medicine
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