Constant Light Exposure Alters Gut Microbiota and Promotes the Progression of Steatohepatitis in High Fat Diet Rats

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) poses a significant health concern worldwide. With the progression of urbanization, light pollution may be a previously unrecognized risk factor for NAFLD/NASH development. However, the role of light pollution on NAFLD is insufficiently understood, and the underlying mechanism remains unclear. Interestingly, recent studies indicate the gut microbiota affects NAFLD/NASH development. Therefore, the present study explored effects of constant light exposure on NAFLD and its related microbiotic mechanisms. Materials and Methods: Twenty-eight SD male rats were divided into four groups (n = 7 each): rats fed a normal chow diet, and exposed to standard light-dark cycle (ND-LD); rats fed a normal chow diet, and exposed to constant light (ND-LL); rats fed a high fat diet, and exposed to standard light-dark cycle (HFD-LD); and rats on a high fat diet, and exposed to constant light (HFD-LL). Body weight, hepatic pathophysiology, gut microbiota, and short/medium chain fatty acids in colon contents, serum lipopolysaccharide (LPS), and liver LPS-binding protein (LBP) mRNA expression were documented post intervention and compared among groups. Result: In normal chow fed groups, rats exposed to constant light displayed glucose abnormalities and dyslipidemia. In HFD-fed rats, constant light exposure exacerbated glucose abnormalities, insulin resistance, inflammation, and liver steatohepatitis. Constant light exposure altered composition of gut microbiota in both normal chow and HFD fed rats. Compared with HFD-LD group, HFD-LL rats displayed less Butyricicoccus, Clostridium, and Turicibacter, butyrate levels in colon contents, decreased colon expression of occludin-1 and zonula occluden−1 (ZO-1), and increased serum LPS and liver LBP mRNA expression. Conclusion: Constant light exposure impacts gut microbiota and its metabolic products, impairs gut barrier function and gut-liver axis, promotes NAFLD/NASH progression in HFD rats.

High Fat Diet Dysbiotic Mechanism of Decreased Gingival Blood Flow

“…LPS, as the most important component of the Gram-negative bacteria membrane, binds to Toll-like receptor 4 (TLR4) and activates innate immune response. In our study, elevated level of this receptor expression was observed in the HFD group ( Figure 5A ; Wei et al, 2020 ). LPS transfer to the TLR4 is catalyzed by local and systemically LPS binding protein.…”

Standardized Astragalus Mongholicus Bunge-Curcuma Aromatica Salisb. Extract Efficiently Suppresses Colon Cancer Progression Through Gut Microbiota Modification in CT26-Bearing Mice

“…Studies have shown that the protein expressions of ZO-1 and occludin are reduced in adenocarcinoma of the digestive tract and that the intestinal barrier is impaired, followed by increased intestinal permeability ( Han X. et al, 2019 ). Simultaneously, butyrate in colon contents could decrease expressions of occludin-1 and ZO-1 in colon tissue ( Wei et al, 2020 ). In the present study, intestinal barrier was injured after colon cancer modelling, accompanied with infiltration of lymphocytes, monocytes in the intestinal mucosal layer, and a decreasing in intestinal tight junction proteins.…”

Leaky Gut: Effect of Dietary Fiber and Fats on Microbiome and Intestinal Barrier

“…Constant light exposure with HFD induces glucose abnormalities, insulin resistance, inflammation, and liver steatohepatitis in mice, which is associated with less abundance of Butyricicoccus , Clostridium , and Turicibacter , also known as butyrate producers. These changes correlate with decreased butyrate levels in colon contests, decreased colon expressions of occludin-1 and ZO-1, and increased serum LPS and mRNA expression of liver LPS-binding protein [ 139 ]. As described earlier, A. muciniphila exhibits protective effects on intestinal permeability.…”