Ultraviolet exposure of mice fed a high fat diet reduces weight gain and markers of liver disease progression

TL;DR

Exposing mice to low-dose UV light while on a high-fat diet may help reduce weight gain and liver disease, possibly through non-vitamin D pathways.

Contribution

This study explores UV effects in female mice and uses UV levels similar to natural sunlight, expanding prior research focused on males.

Findings

UV exposure reduced lipid droplet size in the liver of high-fat diet mice.

High-fat diets increased 25(OH)D levels more in female mice.

UV exposure caused minimal DNA damage in skin and cells.

Abstract

Research suggests that ultraviolet (UV) exposure of mice placed on a high fat diet can reduce incidence of metabolic disease. However, current research had primarily focused on male mice with UV outside level of terrestrial sunlight.

Here we attempt to address this imbalance, with a pilot study presented wherein female mice C57Bl6 mice are included, with UV exposure at level comparable to low dose (non-burning) sunlight exposure.

2% UV-B and 98% UV-At a dose of 1.83 J/cm2 with UV-A and 0.04 J/ cm2 UV-B were delivered over a 10-min timeframe twice weekly. Mice were placed on a low-fat diet or high fat diet, with the high fat diet cohort either exposed twice weekly to UV light or sham exposed.

Non-significant trends are observed for weight amelioration in UV exposed mice across both sexes at study endpoint, whereas in the liver, a reduction of lipid droplet size due to UV exposure is observed. Assessment of vitamin D status at study endpoint shows that the high fat diet increases 25(OH)D level in both sexes, more so in female mice, with further non-significant rises due to UV exposure.

This study supports previous evidence that non-vitamin D mediated pathways may be responsible for the outcomes reported in this study. The UV exposures used in this study also resulted in minimal damage to ex vivo skin or in vitro cells, as assessed by cyclobutene-pyrimidine dimers (CPD’s) (characteristic signature mutations induced by UV), and double stranded breaks, further demonstrating the potential benefit of such exposures. This study supports and builds on current evidence that non-vitamin D pathways mediated through UV exposure may be beneficial in slowing weight gain and liver disease progression.

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