Diet-induced dysmotility and neuropathy in the gut precedes endotoxaemia and metabolic syndrome: the chicken and the egg revisited
| Autor: | Yvonne Nyavor, Onesmo B. Balemba |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Metabolic Syndrome medicine.medical_specialty Neuroscience ‐ neurobiology of disease Physiology Saturated fat Biology medicine.disease Diet High-Fat Endotoxemia 03 medical and health sciences 030104 developmental biology Endocrinology Neuronal damage Internal medicine medicine Animals Metabolic syndrome Chickens |
| Zdroj: | The Journal of physiology. 595(5) |
| ISSN: | 1469-7793 |
| Popis: | A high‐fat diet (60% kcal from fat) is associated with motility disorders inducing constipation and loss of nitrergic myenteric neurons in the proximal colon. Gut microbiota dysbiosis, which occurs in response to HFD, contributes to endotoxaemia. High levels of lipopolysaccharide lead to apoptosis in cultured myenteric neurons that express Toll‐like receptor 4 (TLR4).Consumption of a Western diet (WD) (35% kcal from fat) for 6 weeks leads to gut microbiota dysbiosis associated with altered bacterial metabolites and increased levels of plasma free fatty acids. These disorders precede the nitrergic myenteric cell loss observed in the proximal colon.Mice lacking TLR4 did not exhibit WD‐induced myenteric cell loss and dysmotility. Lipopolysaccharide‐induced in vitro enteric neurodegeneration requires the presence of palmitate and may be a result of enhanced NO production.The present study highlights the critical role of plasma saturated free fatty acids that are abundant in the WD with respect to driving enteric neuropathy and colonic dysmotility. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text