Molecular signaling pathways in the gut influence NAFLD

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder and affects approximately 1 billion people worldwide. It is not clear how this disease develops, but recent studies suggest that the bacterial population in the gut influences NAFLD. A new study in the Journal of Clinical Investigation provides a link between molecular signaling pathways in the gut, the intestinal microbiome, and development of NAFLD. Frank Gonzalez and colleagues at the National Cancer Institute found that disruption of the gut microflora prevented development of NAFLD in mice fed a high fat diet. Additionally, disruption of the microflora decreased intestinal farnesoid X receptor (FXR) signaling, which influences bile acid synthesis. Mice lacking FXR were also protected from developing NAFLD when fed a high fat diet. Together, these data indicate that activation of FXR by the gut microbiome promotes development of NAFLD. Moreover, the results of this study suggest that altering microbial populations in the gut or inhibiting FXR may protect against the development of NAFLD.

Source: Journal of Clinical Investigation

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
The real cost of processed foods: How Western diets are harming global health