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
Wonder how many of the following paths support the premis that Pollution ==> poor health
Pollution reduces UV which reduces Vitamin D
Pollution reduces desire to go outdoors, which reduces Vitamin D
Pollution is associated with high temperatures, which reduces desire to go outdoors, which reduces vitamin D
Diesel pollution reduces liver functionality which reduces Omega-3
Low 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
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.