Abstract
In recent years, a wealth of factors are associated with increased risk of developing non-alcoholic fatty liver disease (NAFLD) and NAFLD is now thought to increase the risk of multiple extra-hepatic diseases. The aim of this review is first to focus on the role of ageing and sex as key, poorly understood risk factors in the development and progression of NAFLD. Secondly, we aim to discuss the roles of white adipose tissue (WAT) and intestinal dysfunction, as producers of extra-hepatic factors known to further contribute to the pathogenesis of NAFLD. Finally, we aim to summarise the role of NAFLD as a multi-system disease affecting other organ systems beyond the liver. Both increased age and male sex increase the risk of NAFLD and this may be partly driven by alterations in the distribution and function of WAT. Similarly, changes in gut microbiota composition and intestinal function with ageing and chronic overnutrition are likely to contribute to the development of NAFLD both directly (i.e. by affecting hepatic function) and indirectly via exacerbating WAT dysfunction. Consequently, the presence of NAFLD significantly increases the risk of various extra-hepatic diseases including CVD, type 2 diabetes mellitus, chronic kidney disease and certain extra-hepatic cancers. Thus changes in WAT and intestinal function with ageing and chronic overnutrition contribute to the development of NAFLD - a multi-system disease that subsequently contributes to the development of other chronic cardiometabolic diseases.
Highlights
Conference on Nutrition in a changing world Symposium four: Changing nutrition and non-alcoholic fatty liver disease (NAFLD)
Changes in white adipose tissue (WAT) and intestinal function with ageing and chronic overnutrition contribute to the development of NAFLD – a multi-system disease that subsequently contributes to the development of other chronic cardiometabolic diseases
Current estimates indicate that about 30 % of the global adult population are affected by non-alcoholic fatty liver disease (NAFLD) and the increasing prevalence of this disease has occurred in parallel with the global epidemic of obesity and type 2 diabetes mellitus (T2DM)(1,2)
Summary
The limited capacity of SAT to store TAG in men and with increasing age is likely to re-direct lipid accumulation ectopically in non-adipose tissues, including the liver, leading to lipotoxicity, a chronic local and systemic pro-inflammatory environment and eventually NAFLD development[46]. Findings indicate that changes in the production of adipokines and increased WAT inflammation may contribute to NAFLD via modulating local and hepatic function, inducing insulin resistance and modulating the local and systemic pro-inflammatory conditions Whether these changes in WAT function contribute to the increased risk of extra-hepatic diseases associated with NAFLD independently requires further investigation. Bacteroides abundance was found to be significantly increased in
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