Background & aims: Recent experimental models and epidemiological studies suggest that specific environmental contaminants (ECs) contribute to the initiation and pathology of non-alcoholic fatty liver disease (NAFLD). However, the underlying mechanisms linking EC exposure with NAFLD remain poorly understood and there is no data on their impact on the human liver metabolome. Herein, we hypothesized that exposure to ECs, particularly perfluorinated alkyl substances (PFAS), impacts liver metabolism, specifically bile acid metabolism.
Glucose-dependent Insulinotropic polypeptide (GIP) is a peptide hormone of the incretin family. It has growth factor properties and can re-activate energy utilization. In progressive neurodegenerative disorders such as Alzheimer's and Parkinson's disease, energy utilization is much reduced, and GIP has the potential to reverse this. Furthermore, GIP can reduce the inflammation response in the brain and reduce levels of pro-inflammatory cytokines. Tests in animal models of Alzheimer's and Parkinson's disease show good neuroprotective effects.
FINDINGS: We used data from 751 studies including 4,372,000 adults from 146 of the 200 countries we make estimates for. Global age-standardised diabetes prevalence increased from 4.3% (95% credible interval 2.4-7.0) in 1980 to 9.0% (7.2-11.1) in 2014 in men, and from 5.0% (2.9-7.9) to 7.9% (6.4-9.7) in women. The number of adults with diabetes in the world increased from 108 million in 1980 to 422 million in 2014 (28.5% due to the rise in prevalence, 39.7% due to population growth and ageing, and 31.8% due to interaction of these two factors).