Background: Gallbladder polyps (GBPs) are known to be associated with obesity and metabolic diseases. However, to date, the relationship between GBPs and abnormal body fat distribution, such as fatty liver, visceral obesity, or sarcopenia, has not yet been established.
Aim: To evaluate whether GBPs are associated with fatty liver, visceral obesity, or sarcopenia.
Methods: We retrospectively reviewed the medical records of subjects who underwent various laboratory tests, body composition measurement with a non-invasive body composition analyzer, and abdominal ultrasonography during health checkups. A total of 1405 subjects with GBPs were compared with 2810 age- and sex-matched controls.
Results: The mean age of the subjects was 46.8 ± 11.7 years, and 63.8% were male. According to multiple logistic regression analysis, the presence of fatty liver [odds ratio (OR) 1.413; 95% confidence interval (CI) 1.218-1.638; < 0.001] was an independent risk factor for GBP, together with low levels of alanine aminotransferase (OR 0.993; 95%CI 0.989-0.996; < 0.001). Additionally, fatty liver showed both independent (OR 1.629; 95%CI, 1.335-1.988; < 0.001) and dose-dependent (moderate to severe fatty liver; OR 2.137; 95%CI, 1.662-2.749; < 0.001) relationship with large GBPs (≥ 5 mm). The presence of sarcopenia and high visceral fat area were not significantly associated with GBPs.
Conclusion: Fatty liver was found to be closely associated with GBPs irrespective of sarcopenia and visceral obesity.
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http://dx.doi.org/10.3748/wjg.v26.i44.6979 | DOI Listing |
Environ Sci Technol
January 2025
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China.
Perfluorooctanoic acid (PFOA) is a persistent pollutant that has gained worldwide attention, owing to its widespread presence in the environment. Previous studies have reported that PFOA upregulates lipid metabolism and is associated with liver injury in humans. However, when the fatty acid degradation pathway is activated, lipid accumulation still occurs, suggesting the presence of unknown pathways and mechanisms that remain to be elucidated.
View Article and Find Full Text PDFCell Rep
January 2025
Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, Zhejiang, China; Key Laboratory of Growth Regulation and Translational Research of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China; Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou, Zhejiang, China; Research Center for Industries of the Future, Westlake University, Hangzhou, Zhejiang, China. Electronic address:
Glucagon has recently been found to modulate liver fat content, in addition to its role in regulating gluconeogenesis. However, the precise mechanisms by which glucagon signaling synchronizes glucose and lipid metabolism in the liver remain poorly understood. By employing chemical and genetic approaches, we demonstrate that inhibiting the androgen receptor (AR) impairs the ability of glucagon to stimulate gluconeogenesis and lipid catabolism in primary hepatocytes and female mice.
View Article and Find Full Text PDFJ Proteome Res
January 2025
Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Metabolic reprogramming is important in primary biliary cholangitis (PBC) development. However, studies investigating the metabolic signature within the liver of PBC patients are limited. In this study, liver biopsies from 31 PBC patients and 15 healthy controls were collected, and comprehensive metabolomics, lipidomics, and proteomics analysis were conducted to characterize the metabolic landscape in PBC.
View Article and Find Full Text PDFJ Family Med Prim Care
December 2024
Department of HIV and Blood Borne Viruses, Milton Keynes University Hospital, NHS Foundation Trust, Milton Keynes, UK.
We report a case of a 49-year-old female with a history of HIV infection for 12 years. The patient had excellent compliance with antiretroviral medications, raltegravir 400 mg twice daily and truvada once daily for HIV. Over the years, she maintained an undetectable viral load with a CD4+ count >200 cells/μL.
View Article and Find Full Text PDFObjectives: To identify cuproptosis- and ferroptosis-related genes involved in nonalcoholic fatty liver disease and to determine the diagnostic value of hub genes.
Methods: The gene expression dataset GSE89632 was retrieved from the Gene Expression Omnibus database to identify differentially expressed genes (DEGs) between the non-alcoholic steatohepatitis (NASH) group and the healthy group using the 'limma' package in R software and weighted gene co-expression network analysis. Gene ontology, kyoto encyclopedia of genes and genomes pathway, and single-sample gene set enrichment analyses were performed to identify functional enrichment of DEGs.
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