Soybean Diacylglycerol Regulates Lipid Metabolism in D-galactose induced Aging Rats by Altering Gut Microbiota and Gene Expression of Colonic Epithelial Cells

2022 ◽  
Author(s):  
Lulu Han ◽  
Rongrong Sun ◽  
Yong Wang ◽  
Jianming Luo ◽  
Xichun Peng

Lipid metabolism is closely related to the health of aging bodies, and its disorder often leads to cardiovascular diseases and chronic diseases. Dietary fat is one of the important sources...

2018 ◽  
Vol 9 (5) ◽  
pp. 2962-2969 ◽  
Author(s):  
Jianming Luo ◽  
Lulu Han ◽  
Liu Liu ◽  
Lijuan Gao ◽  
Bin Xue ◽  
...  

The present study showed that catechin controlled rats’ body weights by altering gut microbiota and gene expression of colonic epithelial cells when supplemented into a high-fructo-oligosaccharide (FOS) diet.


2020 ◽  
Author(s):  
Xiaohong Lin ◽  
Jiamei Qi ◽  
Guangwen Zhang ◽  
Xichun Peng

Abstract BackgroundObesity is one of the most serious public health challenges. Recently, we found that flaxseed polysaccharide (FP) had an anti-obesity effect through promoting lipid metabolism, inducing satiety and regulating gut microbiota, but how FP promote lipid metabolism through altering the colonic epithelial cells remains to be elucidated. In this study, a transcriptome study was performed to investigate the effect of FP altering the gene expression of colonic epithelial cells in an obese rat model. ResultsThe transcriptome analysis showed that 3,785 genes were differentially expressed after FP intervention in colonic epithelial cells, including 374 down-regulated and 3,411 up-regulated genes. Through KEGG analysis, we found out three classical pathways related to lipid metabolism and energy metabolism, including PPAR signaling pathway, nitrogen metabolism and oxidative phosphorylation (OXPHOS). Moreover, qRT-PCR results showed consistent expression trends of differential genes with transcriptome analysis. ConclusionsThe anti-obesity effect of FP may be achieved by regulating the expression of lipid metabolism- and energy metabolism-related proteins acting on the PPAR (peroxisome proliferator-activated receptor) signaling pathway, nitrogen metabolism and OXPHOS pathway in vivo.


2020 ◽  
Vol 4 (4) ◽  
pp. 178-190 ◽  
Author(s):  
Kyoko Takahashi ◽  
Yutaka Sugi ◽  
Kou Nakano ◽  
Tetsuro Kobayakawa ◽  
Yusuke Nakanishi ◽  
...  

PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0212850 ◽  
Author(s):  
Stephen M. Matthews ◽  
Melanie A. Eshelman ◽  
Arthur S. Berg ◽  
Walter A. Koltun ◽  
Gregory S. Yochum

2020 ◽  
Vol 150 (7) ◽  
pp. 1790-1798 ◽  
Author(s):  
Tao Zhao ◽  
Shui-Bo Yang ◽  
Guang-Hui Chen ◽  
Yi-Huan Xu ◽  
Yi-Chuang Xu ◽  
...  

ABSTRACT Background Dietary carbohydrate affects intestinal glucose absorption and lipid deposition, but the underlying mechanisms are unknown. Objectives We used yellow catfish and their isolated intestinal epithelial cells (IECs) to test the hypothesis that sodium/glucose cotransporters (SGLTs) 1/2 and acetylated carbohydrate response element binding protein (ChREBP) mediated glucose-induced changes in glucose absorption and lipid metabolism. Methods Yellow catfish (mean ± SEM weight: 4.68 ± 0.02 g, 3 mo old, mixed sex) were fed diets containing 250 g carbohydrates/kg from glucose (G, control), corn starch (CS), sucrose (S), potato starch (PS), or dextrin (D) for 10 wk. IECs were isolated from different yellow catfish and incubated for 24 h in a control or glucose (15 mM) solution with or without a 2-h pretreatment with an inhibitor [sotagliflozin (LX-4211) or tubastatin A (TBSA)]. Human embryonic kidney cells (HEK293T cells) were transfected with a Flag-ChREBP plasmid to explore ChREBP acetylation. Triglyceride (TG) and glucose concentrations and enzymatic activities were measured in the intestine and IECs of yellow catfish. They also were subjected to immunofluorescence, immunoprecipitation, qPCR, and immunoblotting. Immunoblotting and immunoprecipitation were performed with HEK293T cells. Results The G group had greater intestine TGs (0.99- to 2.30-fold); activities of glucose 6-phospate dehydrogenase, 6-phosphogluconate dehydrogenase, and isocitrate dehydrogenase (0.12- to 2.10-fold); and expression of lipogenic genes (0.32- to 2.34-fold) than the CS, PS, and D groups. The G group had greater intestine sglt1/2 mRNA and protein expression than the CS, S and D groups (0.35- to 1.12-fold and 0.40- to 4.67-fold, respectively), but lower mRNA amounts of lipolytic genes (48.6%–65.8%) than the CS and PS groups. LX-4211 alleviated the glucose-induced increase in sglt1/2 mRNA (38.2%–47.4%) and SGLT1 protein (48.0%) expression, TGs (29.3%), and lipogenic enzyme activities (27.7%–42.1%) and gene expression (38.0%–55.5%) in the IECs. TBSA promoted the glucose-induced increase in TGs (11.3%), fatty acid synthase activity (32.6%), and lipogenic gene expression (21.6%–34.4%) in the IECs and acetylated ChREBP (10.5%) in HEK293T cells. Conclusions SGLT1/2 signaling and acetylated ChREBP mediated glucose-induced changes in glucose absorption and lipid metabolism in the intestine and IECs of yellow catfish.


Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2287 ◽  
Author(s):  
Zumin Shi

A Western diet characterised by high intake of energy-dense and processed food is a risk factor for many chronic diseases including diabetes, obesity and cardiovascular diseases [...]


2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S40-S41
Author(s):  
Peder Lund ◽  
Sarah Smith ◽  
Johayra Simithy ◽  
Lillian Chau ◽  
Elliot Friedman ◽  
...  

Abstract Inflammatory bowel disease (IBD) is often associated with a disruption in the composition and activity of the gut microbiota, referred to as dysbiosis. Since the microbiota has the potential to interact with host epithelial cells through small molecules generated from microbial metabolism, knowledge of how inflammation alters the microbial metabolome and how epithelial cells react is important for a better understanding of how IBD develops and persists. Butyrate, a short chain fatty acid produced through fermentation of dietary polysaccharides, has long been known to inhibit histone deacetylases (HDACs), which represent one of the many types of enzymes responsible for the epigenetic control of gene expression through the post-translational modification of histone proteins. We and others have observed that colonic epithelial cells from germ-free mice have reduced levels of acetylation on histone H4, which appears to be distributed throughout the genome based on sequencing analysis. The decreased levels of H4 acetylation may stem from a lack of butyrate, and therefore uninhibited HDAC activity, in germ-free mice. However, since colonic epithelial cells utilize short chain fatty acids as an energy source, an alternative explanation is that the germ-free condition results in less oxidation of butyrate to acetyl-CoA, which is the donor substrate for histone acetylation reactions. Isotope tracing experiments, in which cultured cells were incubated with labeled butyrate, demonstrated that the acetyl groups of histones contained carbon derived from butyrate. We have also performed isotope tracing experiments in mice using labeled inulin, a plant polysaccharide that presumably undergoes fermentation into short chain fatty acids. In this more physiologically relevant model, we detected isotope incorporation into the acetylated histones of colonic epithelial cells at rates of 5–20%, which appears dependent on the microbiota since labeling is sensitive to antibiotic treatment. To identify the metabolic pathways that link inulin to histone acetylation, we are investigating which metabolites become isotopically labeled using untargeted metabolomics. We will apply the same approach to the DSS-induced model of colitis to investigate how inflammation modulates the gut metabolome as well as the metabolic connections between the microbiota and the host. Our studies may uncover metabolic pathways that become dysregulated during inflammation, which may contribute to the pathogenesis of diseases such as IBD.


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