Diesel air pollution causes liver problems (and low vitamin D) if low Omega-3 (mice)

Created November 2017

Impact of diesel exhaust exposure on the liver of mice fed on omega-3 polyunsaturated fatty acids-deficient diet

Food and Chemical Toxicology, Vol 111, Jan 2018, Pages 284–294, https://doi.org/10.1016/j.fct.2017.11.027

Masakazu Umezawaa, h, , , Masayuki Nakamurab, Ashraf A. El-Ghoneimya, c, Atsuto Onodaa, b, d, Hazem M. Shaheena, e, Hiroshi Horib, Yusuke Shinkaia, Yasser S. El-Sayedf, , , , Ali H. El-Farg,

* Air pollution associated with poor bone density (less vitamin D) – Nov 2017* Overview: Omega-3 many benefits include helping vitamin D* NAFLD in children nicely treated by combination of Vitamin D and Omega-3 – RCT Dec 2016* Non-Alcoholic Fatty Liver Disease treated by Omega-3 – three meta-analysis 2016-2017* Non-alcoholic Fatty Liver Disease (4 in 10 seniors) and Vitamin D* Pollution might be worse for Seniors with low vitamin D AND low Omega-3* Traffic pollution increases asthma unless supplement with Vitamin D (mice) June 2018--- 1. Wonder how many of the following paths support the premis that Pollution ==> poor healthPollution reduces UV which reduces Vitamin DPollution reduces desire to go outdoors, which reduces Vitamin DPollution is associated with high temperatures, which reduces desire to go outdoors, which reduces vitamin DDiesel pollution reduces liver functionality which reduces Omega-3Low Omega-3 reduces vitamin D getting to cells (way downstream from the blodd test indication of vitamin D level)Diesel pollution reduces liver functionality which reduces Vitamin D

image

Highlights

• Low-dose DE enhances impact of n-3 deficient diet intake on the liver.

• DE inhalation enhances up-regulation of genes for hepatic lipid synthesis.

• Combination of DE inhalation and n-3 deficient diet intake increases risk for incidence of fatty liver disease.

Exposure to diesel exhaust (DE) exacerbates non-alcoholic fatty liver disease , and may systemically affect lipid metabolism. Omega-3 polyunsaturated fatty acids (n-3 PUFA) have anti-inflammatory activity and suppresses hepatic triacylglycerol accumulation, but many daily diets are deficient in this nutrient. Therefore, the effect of DE exposure in mice fed n-3 PUFA–deficient diet was investigated. Mice were fed control chow or n-3 PUFA–deficient diet for 4 weeks, then exposed to clean air or DE by inhalation for further 4 weeks. Liver histology, plasma parameters, and expression of fatty acid synthesis-related genes were evaluated. N-3 PUFA–deficient diet increased hepatic lipid droplets accumulation and expression of genes promoting fatty acid synthesis: Acaca, Acacb, and Scd1. DE further increased the plasma leptin and the expression of fatty acid synthesis-related genes: Acacb, Fasn, and Scd1. N-3 PUFA–deficient diet and DE exposure potentially enhanced hepatic fatty acid synthesis and subsequently accumulation of lipid droplets. The combination of low-dose DE exposure and intake of n-3 PUFA–deficient diet may be an additional risk factor for the incidence of non-alcoholic fatty liver disease. The present study suggests an important mechanism for preventing toxicity of DE on the liver through the incorporation of n-3 PUFAs in the diet.

Tags: Liver Omega-3