scholarly journals Psyllium and fat in diets differentially affect the activities and expressions of colonic sphingomyelinases and caspase in mice

2004 ◽  
Vol 91 (5) ◽  
pp. 715-723 ◽  
Author(s):  
Yajun Cheng ◽  
Lena Ohlsson ◽  
Rui-Dong Duan
Keyword(s):  
Ulcerative Colitis ◽  
Alkaline Phosphatase ◽  
High Fat Diet ◽  
Colonic Mucosa ◽  
Caspase 3 ◽  
High Fat ◽  
Acid And Alkaline Phosphatase ◽  
Alkaline Sphingomyelinase ◽  
Opposite Manner ◽  
Colonic Tumours

Dietary fibre and fat affect colonic tumourigenesis and inflammation. Sphingomyelin metabolism may have implications for the pathogenesis of colonic tumours and ulcerative colitis. The present study examined the effects of psyllium and fat on the enzymes responsible for sphingomyelin metabolism and apoptosis in the colon. Mice were fed control, psyllium-containing (100 g/kg), high-fat (313 g/kg, 53 % energy as fat) or high-fat plus psyllium diets for 4 weeks. The activities of acid, neutral and alkaline sphingomyelinase (SMase), neutral ceramidase, and caspase 3, 8 and 9 in colonic mucosa were determined. The expressions of alkaline SMase and caspase 3 were examined. The psyllium-containing diet was found to increase significantly the activities of alkaline SMase and caspase 3 and decreased those of acid SMase and neutral ceramidase. The high-fat diet had opposite effects on these enzymes and attenuated the effects of psyllium. Western blotting showed that psyllium increased and high-fat decreased the levels of alkaline SMase and caspase 3 in colonic mucosa. The change in caspase 3 activity was positively correlated with that of alkaline SMase and negatively with acid SMase. No similar changes of acid and alkaline phosphatase activities in the colon or acid and neutral SMase activity in the liver were identified. In conclusion, colonic sphingomyelin metabolism and apoptosis were affected by psyllium and fat in an opposite manner. The results may have implications for colorectal tumourigenesis and inflammation.

scholarly journals Gene expression profiles of the colonic mucosa associated with phenotypic changes in mice fed high‐fat diet

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Yun Jung Bae ◽  
Youn-Kyung Bak ◽  
Taesun Park ◽  
Myung-Sook Choi ◽  
Jeongseon Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Colonic Mucosa ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
High Fat ◽  
Phenotypic Changes

scholarly journals Probiotics and dietary intervention modulate the colonic mucosa-associated microbiota in high-fat diet populations

2020 ◽  
Vol 31 (4) ◽  
pp. 295-304
Author(s):  
Leimin Qian ◽  
◽  
Jianming Huang ◽  
Huanlong Qin ◽  
◽  
...  
Keyword(s):  
High Fat Diet ◽  
Colonic Mucosa ◽  
Dietary Intervention ◽  
High Fat

scholarly journals Guanxinkang Decoction Attenuates the Inflammation in Atherosclerosis by Regulating Efferocytosis and MAPKs Signaling Pathway in LDLR−/− Mice and RAW264.7 Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Yifan Zhang ◽  
Jie Ding ◽  
Yiru Wang ◽  
Xiaoteng Feng ◽  
Min Du ◽  
...  
Keyword(s):  
Western Blot ◽  
High Fat Diet ◽  
Caspase 3 ◽  
Density Lipoprotein ◽  
Treated Group ◽  
Raw264.7 Cells ◽  
Raw 264.7 Cells ◽  
High Fat ◽  
Phagocytic Ability ◽  
Tnf Α

Guanxinkang decoction (GXK), a traditional Chinese medicinal drug, is used to treat cardiovascular disease. The aim of the study was to investigate the effects of GXK on inflammation in LDLR−/− mice and RAW264.7 cells. Fed with high fat diet for 12 weeks, the mice were randomly divided into six groups, then administered with oral 0.9% saline or GXK (7.24, 14.48, and 28.96 g/kg) or Atorvastatin (1.3 mg/kg) for 12 weeks. RAW 264.7 cells were induced with ox-LDL or ox-LDL plus different concentrations of GXK (1.25, 2.5, and 5 μg/ml), or ox-LDL plus GXK plus MAPKs activators. Serum lipid profiles and inflammatory cytokines were detected by ELISA, gene expression by RT-qPCR, plaque sizes by Oil Red O, α-SMA, caspase 3, NF-κB p65 and TNF-α production by immunofluorescence staining, and protein expression by Western Blot. The phagocytic ability of cells was determined by neutral red uptake assay. Efferocytosis-related proteins (AML, MERTK, TYRO3 and MFGE8) and MAPKs pathways were detected by Western Blot. Compared to mice fed with high fat diet, the mice with GXK showed lower cholesterol, triglyceride, low-density lipoprotein cholesterol, IL-1β, IL-6, and TNF-α, smaller plaque sizes, higher α-SMA, and lower caspase 3 and NF-κB p65 in aortic roots. RAW264.7 cells treated with ox-LDL plus GXK had lower IL-1β, IL-6, and TNF-α. GXK also increased the phagocytic ability of cells. High levels of AML, MERTK, TYRO3 and MFGE8, and decreased levels of iNOS, VCAM-1, LOX-1 and MCP-1, and phosphorylation of ERK1/2, JNK, p38, and NF-κB were detected in GXK-treated group. MAPKs activators reversed the effects of GXK in repressing inflammation and promoting phagocytosis. These results suggested that GXK could attenuate atherosclerosis and resolve inflammation via efferocytosis and MAPKs signaling pathways in LDLR−/− mice and RAW264.7 cells.

scholarly journals EFFECT OF SILYMARIN ON INTESTINAL ALKALINE PHOSPHATASE LEVEL IN A RAT MODEL OF TYPE 2 DIABETES MELLITUS: STREPTOZOTOCIN AND HIGH-FAT DIET TREATED WISTAR RATS

2018 ◽  
Vol 11 (11) ◽  
pp. 304
Author(s):  
Lalitha V ◽  
Sivakumar T
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Alkaline Phosphatase ◽  
Lipid Profile ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Diabetic Rats ◽  
High Fat ◽  
Intestinal Alkaline Phosphatase

Objective: This research elucidated the role of silymarin on intestinal alkaline phosphatase (IAP) level in type 2 diabetic rats.Methods: The type 2 diabetes mellitus was induced by a high-fat diet (HFD - 58% calories fat) for 2 weeks, and rats were intraperitoneally injected with streptozotocin (STZ) 35 mg/kg. Wistar rats were divided into four groups. Group I served as a non-diabetic (normal), Group II served as diabetic, Group III diabetic animals treated glibenclamide 600 μg/kg for 14 days, and Group IV diabetic animal treated with glibenclamide and silymarin 50 mg/kg/twice/d for 14 days. At the end of the study, blood glucose, lipid profile, and IAP level were measured.Results: A significant decrease in IAP, elevated levels of blood glucose, and lipid profile was seen in diabetic rats when compared with normal. The silymarin treatment showed a significant increase in IAP level, a significant reduction in glucose and lipid profile than diabetic rats.Conclusion: The present study concludes that silymarin treatment enhances the IAP levels which protect against hyperglycemia, hyperlipidemia, and vascular complications in diabetic rats.

scholarly journals High-Fat Diet Promotes DSS-Induced Ulcerative Colitis by Downregulated FXR Expression through the TGFB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Di Zhao ◽  
Chenwen Cai ◽  
Qiyi Chen ◽  
Shuang Jin ◽  
Bo Yang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
High Fat Diet ◽  
Target Genes ◽  
Intestinal Inflammation ◽  
Farnesoid X Receptor ◽  
Mucosal Barrier ◽  
High Fat ◽  
Colon Rectal Cancer ◽  
Chronic Intestinal Inflammation

Ulcerative colitis is one of the IBD which cause a chronic intestinal inflammation and dysfunctional of the mucosal barrier. For now, the incident of UC was steadily increased all over the world. It has become a novel independent risk factor of several severe diseases especially colon-rectal cancer. However, the etiology of UC was still obscure. Previous studies show that high-fat diet contributed to the pathogenesis of immune system dysregulation, and farnesoid X receptor (FXR) was also implicated in the pathogenesis of various inflammatory symptoms. Yet, their inner roles in the pathogenesis of UC have not been mentioned. In this study, we aim to investigate the role of FXR in UC. High-fat diet (HFD) promotes the progression of DSS-induced UC, shows an increasing secretion of bile acid in serum, and leads to a downregulation of FXR target genes (FXRα, Shp, and lbabp). Adding FXR agonist FexD rescues the phenotype induced by high-fat diet, whereas TGFBRI inhibitor SB431542 abrogates the restoration by FexD in DSS-induced UC mice. To further verify the relationship between the FXR and TGFB signaling pathway, we made a UC-HFD model in the Caco2 cell line. Results shows the same conclusion that FXR mitigate UC inflammation through a TGFB-dependent pathway. These results expand the role of FXR in ulcerative colitis and suggest that FXR activation may be considered a therapeutic strategy for UC.

Effects of swim training on liver carcinogenesis in male Wistar rats fed a low-fat or high-fat diet

2012 ◽  
Vol 37 (6) ◽  
pp. 1101-1109 ◽  
Author(s):  
Marco Aurélio Aguiar e Silva ◽  
Ivan José Vechetti-Junior ◽  
André Ferreira do Nascimento ◽  
Kelly Silva Furtado ◽  
Luciana Azevedo ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Wistar Rats ◽  
Caspase 3 ◽  
The Body ◽  
Nuclear Antigen ◽  
Liver Carcinogenesis ◽  
High Fat ◽  
Low Fat ◽  
Dietary Regimen ◽  
Male Wistar Rats

The present study aimed to investigate the beneficial effects of swim training on the promotion–progression stages of rat liver carcinogenesis. Male Wistar rats were submitted to chemically induced liver carcinogenesis and allocated into 4 major groups, according their dietary regimen (16 weeks) and swim training of 5 days per week (8 weeks): 2 groups were fed low-fat diet (LFD, 6% fat) and trained or not trained and 2 groups were fed high-fat diet (HFD, 21% fat) and trained or not trained. At week 20, the animals were killed and liver samples were processed for histological analyses; immunohistochemical detection of persistent or remodeling preneoplastic lesions (pPNL and rPNL) expressing placental glutathione S-transferase (GST-P) enzyme; or proliferating cell nuclear antigen (PCNA), cleaved caspase-3, and bcl-2 protein levels by Western blotting or malonaldehyde (MDA) and total glutathione detection by HPLC. Overall analysis indicated that swim training reduced the body weight and body fat in both LFD and HFD groups, normalized total cholesterol levels in the HFD group while decreased the MDA levels, increased glutathione levels and both number of GST-P-positive pPNL and hepatocellular adenomas in LFD group. Also, a favorable balance in PCNA, cleaved caspase-3, and bcl-2 levels was detected in the liver from the LFD-trained group in relation to LFD-untrained group. The findings of this study indicate that the swim training protocol as a result of exercise postconditioning may attenuate liver carcinogenesis under an adequate dietary regimen with lowered fat intake.

Unusually high alkaline phosphatase due to intestinal isoenzyme in a healthy adult

2005 ◽  
Vol 43 (11) ◽  
Author(s):  
Sung R. Cho ◽  
Young A. Lim ◽  
Wee G. Lee
Keyword(s):  
Alkaline Phosphatase ◽  
Blood Group ◽  
High Fat Diet ◽  
Healthy Adult ◽  
High Fat ◽  
Intestinal Alkaline Phosphatase ◽  
Before And After

AbstractIntestinal alkaline phosphatase (ALP) is more prevalent in individuals of blood group O or B, and increases after a meal, especially on a high-fat diet. We did not realize that clinicians could underestimate the importance of fasting for ALP measurement until one healthy adult showed a huge difference in ALP levels before and after a meal. We report a case of transient hyperphosphatasemia resulting in unnecessary workup due to intestinal ALP in a healthy adult of blood group O.

scholarly journals Glucagon-like peptide-2 and mouse intestinal adaptation to a high-fat diet

2013 ◽  
Vol 217 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Sara Baldassano ◽  
Antonella Amato ◽  
Francesco Cappello ◽  
Francesca Rappa ◽  
Flavia Mulè
Keyword(s):  
High Fat Diet ◽  
Caspase 3 ◽  
Potential Role ◽  
Intestinal Adaptation ◽  
Cell Number ◽  
Standard Diet ◽  
High Fat ◽  
Villus Height ◽  
Glucagon Like Peptide

Endogenous glucagon-like peptide-2 (GLP2) is a key mediator of refeeding-induced and resection-induced intestinal adaptive growth. This study investigated the potential role of GLP2 in mediating the mucosal responses to a chronic high-fat diet (HFD). In this view, the murine small intestine adaptive response to a HFD was analyzed and a possible involvement of endogenous GLP2 was verified using GLP2 (3–33) as GLP2 receptor (GLP2R) antagonist. In comparison with animals fed a standard diet, mice fed a HFD for 14 weeks exhibited an increase in crypt–villus mean height (duodenum, 27.5±3.0%; jejunum, 36.5±2.9%;P<0.01), in the cell number per villus (duodenum, 28.4±2.2%; jejunum, 32.0±2.9%;P<0.01), and in Ki67-positive cell number per crypt. No change in the percent of caspase-3-positive cell in the villus–crypt was observed. The chronic exposure to a HFD also caused a significant increase in GLP2 plasma levels and in GLP2R intestinal expression. Daily administration of GLP2 (3–33) (30–60 ng) for 4 weeks did not modify the crypt–villus height in control mice. In HFD-fed mice, chronic treatment with GLP2 (3–33) reduced the increase in crypt–villus height and in the cell number per villus through reduction of cell proliferation and increase in apoptosis. This study provides the first experimental evidence for a role of endogenous GLP2 in the intestinal adaptation to HFD in obese mice and for a dysregulation of the GLP2/GLP2R system after a prolonged HFD.

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