Aims: An increased amount of submucosal (SM) fat in the colon on imaging is considered to be characteristic of inflammatory bowel disease (IBD); however, a recent study in patients without IBD reported a correlation between colonic SM fat deposition and body weight (BW). The aim of this study was to perform a morphometric investigation of SM thickness in areas of fat deposition in the terminal ileum (TI), ileocaecal valve (ICV), and colonic sections, to determine whether there are variations by site, and whether it shows a correlation with BW, body mass index (BMI), or age.
Methods And Results: Representative samples of TI, ICV and colonic sections were collected prospectively from 115 autopsy cases without IBD. All of the study subjects were male (Veterans Hospital). SM thickness was measured in areas of fat deposition. Correlation analysis was performed between SM thickness and BW, BMI, and age. Fat deposition was common; however, with the exception of the ICV, it was neither consistent nor prominent, and it did not show a statistical correlation with BW, BMI, or age.
Conclusions: SM fat deposition is common but not uniform or conspicuous in the TI or colon. In contrast to extravisceral intra-abdominal fat, it does not show a correlation with BW or BMI, and is not associated with ageing. As all study subjects were male, gender-dependent variability cannot be excluded.
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http://dx.doi.org/10.1111/his.12683 | DOI Listing |
Exp Cell Res
January 2025
Department of Internal Medicine, Hebei Medical University, Shijiazhuang 050017, Hebei, China; Department of Cardiology, Hebei General Hospital, Shijiazhuang 050051, Hebei, China. Electronic address:
SRY-Box Transcription Factor-11 (SOX11) is a transcriptional regulatory factor that plays a crucial role in inflammatory responses. However, its involvement in atherosclerosis (AS), a cardiovascular disease driven by endothelial cell inflammation, remains unknown. This study aims to elucidate the role of SOX11 in AS.
View Article and Find Full Text PDFWhile fructose is a key dietary component, concerns have been raised about its potential risks to the liver. This study aimed to assess quercetin's protective effects against fructose-induced mouse hepatic steatosis. Thirty-two male C57BL/6J mice were randomly allocated into four groups: control, high fructose diet (HFrD), HFrD supplemented with low-dose quercetin (HFrD+LQ), and HFrD supplemented with high-dose quercetin (HFrD+HQ).
View Article and Find Full Text PDFFood Sci Nutr
January 2025
Laboratory of Biotechnology and Natural Resources Valorization, Faculty of Sciences Ibn Zohr University Agadir Morocco.
Hepatic steatosis/non-alcoholic fatty liver disease is a major public health delinquent caused by the excess deposition of lipid into lipid droplets (LDs) as well as metabolic dysregulation. Hepatic cells buildup with more fat molecules when a person takes high fat diet that is excessive than the body can handle. At present, millions of people in the world are affected by this problem.
View Article and Find Full Text PDFDiabetes Metab Syndr Obes
January 2025
Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Purpose: Mitochondrial dysfunction mediated by c-Jun N-terminal kinase (JNK) plays an important role in lipotoxic liver injury in nonalcoholic steatohepatitis (NASH). This study aims to investigate the pharmacological mechanism of Jiangzhi Granule (JZG), a Chinese herbal formula against NASH, with a focus on its regulation of JNK signaling-mediated mitochondrial function.
Methods: Hepatocytes were induced by palmitic acid (PA) for 24 h to establish an in vitro lipotoxic model, which was simultaneously treated with either JZG or vehicle control.
Nat Commun
January 2025
Department of Cardiology, Tangdu Hospital, Airforce Medical University, Xi'an, China.
Physical exercise is a cornerstone for preventing diet-induced obesity, while it is unclear whether physical exercise could offset high-fat, high-calories diet (HFCD)-induced cardiac dysfunction. Here, mice were fed with HFCD and simultaneously subjected to physical exercise. As expected, physical exercise prevented HFCD-induced whole-body fat deposition.
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