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Background And Aim: The prevalence of hepatic steatosis continues to increase worldwide. Hepatic steatosis is increasingly recognized as an independent risk factor for cardiovascular mortality. However, there are limited options for the treatment of fatty liver. In this study, we evaluated the effect of semaglutide on liver fat as measured by non-contrast cardiac CT scans.
Methods And Results: STOP is a randomized controlled trial that evaluated the semaglutide treatment effect on coronary atherosclerosis progression (STOP) in type 2 diabetes. We utilized unenhanced cardiac CT scans to quantify liver fat based on the CT Hounsfield attenuation method. Of the 140 subjects who were originally randomized, a total of 114 individuals qualified for this study. 59 participants were in the semaglutide group and 55 were in the placebo group, and these subjects were followed for 12 months. The secondary outcome (liver fat attenuation) was quantified using non-contrast cardiac computed tomography (CT) images at both the baseline and 12-month follow-up time points. Multivariate regression models were then used to evaluate the change in liver fat content overtime. One hundred and fourteen subjects were included in the study: 61 % male, mean age of 57.8 ± 8.1 years, and mean BMI of 32.0 ± 6.7. The average of three liver measures over 12 months showed an improvement in the semaglutide group of 1.4 ± 9.0 mean HU, versus a worsening in the placebo group of 1.9 ± 9.5 mean HU. The multivariable linear regression models (after adjusting for age, gender, BMI, hypertension, hyperlipidemia, past smoking and baseline liver attenuation) showed that average liver attenuation measures improved by 4.4 HU in the semaglutide group when compared to the placebo group (p = 0.002). This result demonstrated improvement in the liver fat content within the treatment group.
Conclusion: In type 2 diabetes patients with hepatic steatosis, treatment with semaglutide resulted in a significant improvement in fatty liver reduction when compared to placebo.
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http://dx.doi.org/10.1016/j.numecd.2025.104036 | DOI Listing |
Life Sci
September 2025
Department of Experimental Medical Science, Faculty of Medicine, Lund University, 221 84, Lund, Sweden; Wallenberg Center for Molecular Medicine, Faculty of Medicine, Lund University, 221 84, Lund, Sweden. Electronic address:
Aims: Experimental evidence suggests an important role for sphingosine-1-phosphate (S1P) and its generating enzymes sphingosine kinase 1/2 (SphK1/2) in obesity. We and others have shown that plasma S1P levels are elevated in obese mice and humans. Preclinical studies suggest that genetic SphK2 ablation in mice protects from age- and diet-induced obesity and metabolic dysfunction.
View Article and Find Full Text PDFJ Hepatol
September 2025
National Research Council (CNR), Institute of Clinical Physiology (IFC), Pisa, Italy. Electronic address:
Biochem Pharmacol
September 2025
Department of Endocrinology, First Hospital of Shanxi Medical University, Shanxi Medical University, Taiyuan 030001, China. Electronic address:
Metabolic dysfunction-associated steatohepatitis (MASH) affects a large proportion of the global population and is widely regarded as the fastest growing cause of hepatocellular carcinoma. Currently, approved therapeutic strategies for MASH are limited. Therefore, this study used the Connectivity Map (CMap) database to identify a candidate compound for MASH, evaluate its efficacy in experimental models, and explore its mechanism of action.
View Article and Find Full Text PDFMagn Reson Med
September 2025
Institute for Diagnostic and Interventional Radiology, School of Medicine and Health, TUM University Hospital, Technical University of Munich, Munich, Germany.
Purpose: To develop a method for abdominal simultaneous 3D water ( ) and ( ) mapping with isotropic resolution using a free-breathing Cartesian acquisition with spiral profile ordering (CASPR) at 3 T.
Methods: The proposed data acquisition combines a Look-Locker scheme with the modified BIR-4 adiabatic preparation pulse for simultaneous and mapping. CASPR is employed for efficient and flexible k-space sampling at isotropic resolution during free breathing.
Cell Mol Gastroenterol Hepatol
September 2025
Department of Biological Sciences, The University of Texas at Dallas, Richardson, Texas. Electronic address:
Background & Aims: Binge drinking causes fat accumulation in the liver and is a known risk factor for more severe forms of alcohol-associated liver disease (ALD). Although adipocyte-released free fatty acids (FFA) have been shown to contribute to alcohol-induced liver damage, the signaling pathways that trigger lipolytic activity in adipose tissues following acute alcohol overconsumption is largely unknown. Notably, activation of sympathetic nerve-β3 adrenergic receptor (Adrb3) plays a central role in sustained adipocyte lipolysis.
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