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Researchers at University of California, Los Angeles Health have discovered exposure to diesel exhaust causes substantial disruption to liver function in mice.
The investigation revealed altered activity in 658 genes and 118 metabolites following exposure, potentially shedding light on how air pollution contributes to metabolic disorders in humans.
The study found diesel exhaust exposure led to increased production of triglycerides, fatty acids, and sugars in the mice. These metabolic changes were largely attributed to mitochondrial dysfunction, as these cellular structures play a crucial role in energy production.
When researchers directly exposed liver cells to diesel particles, they observed activation of a gene called Pck1, which triggered increased glucose production. By subsequently inhibiting this gene, they were able to reduce glucose levels, confirming Pck1's role in the metabolic response to diesel exposure.
UCLA researchers noted this is the first study to demonstrate the ability of diesel exhaust exposure to induce mitochondrial dysfunction in living organisms. Previous work by the same team had established that diesel particles cause mitochondrial problems in liver tissue cells, but this new research extends those findings to whole organisms.
Diesel emissions constitute a significant component of air pollution, which has been linked to various health conditions – including type 2 diabetes, fatty liver disease, cardiovascular diseases, and cancer. While the connection between air pollution and metabolic diseases has been observed, the specific mechanisms and genes involved have remained poorly understood.
Researchers suggest targeting the Pck1 gene could serve as an intervention against diesel-induced type 2 diabetes, though additional research is needed to explore this possibility.
