Background: L-Fucose (Fuc), a six-deoxy hexose monosaccharide, is present endogenously in humans and animals and has a wide range of biological functions. In the present study, we aimed to examine the effect of Fuc on obesity and hepatic steatosis in mice fed a high-fat diet (HFD).
Methods: C57BL/6 mice were fed a normal chow (NC) or HFD for 18 weeks to induce obesity and fatty liver. Fuc was administered intragastrically from the 8th week to the end of the experiment (18 weeks).
Results: Metagenomic analysis showed that HFD altered the genomic profile of gut microbiota in the mice; specifically, expression of alpha-L-fucosidase, the gene responsible for Fuc generation, was markedly reduced in the HFD group compared with that in the NC group. Fuc treatment decreased body weight gain, fat accumulation, and hepatic triglyceride elevation in HFD-fed mice. In addition, Fuc decreased the levels of endotoxin-producing bacteria of the Desulfovibrionaceae family and restored HFD-induced enteric dysbiosis at both compositional and functional levels.
Conclusion: Our findings suggest that Fuc might be a novel strategy to treat HFD-induced obesity and fatty liver.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286552 | PMC |
http://dx.doi.org/10.1186/s12967-018-1718-x | DOI Listing |
Curr Opin Gastroenterol
January 2025
Department of Nutrition Sciences.
Purpose Of Review: Metabolic dysfunction-associated steatotic liver disease (MASLD) is present in 25-35% of individuals in the United States. The purpose of this review is to provide the contextual framework for hepatic ketogenesis in MASLD and to spotlight recent advances that have improved our understanding of the mechanisms that drive its development and progression.
Recent Findings: Traditionally, hepatic ketogenesis has only been considered metabolically during prolonged fasting/starvation or with carbohydrate deplete ketogenic diets where ketones provide important alternative energy sources.
Gut Liver
January 2025
Department of Gastroenterology and Hepatology, Singapore General Hospital, Singapore.
Metabolic dysfunction-associated steatotic liver disease (MASLD), is the most common cause of liver disease, and its burden on health systems worldwide continues to rise at an alarming rate. MASLD is a complex disease in which the interactions between susceptible genes and the environment influence the disease phenotype and severity. Advances in human genetics over the past few decades have provided new opportunities to improve our understanding of the multiple pathways involved in the pathogenesis of MASLD.
View Article and Find Full Text PDFJ Biomed Sci
January 2025
Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Background: Obesity is becoming one of the major non-communicable diseases with increasing incidence and risks that cannot be ignored. However effective and safe clinical treatment strategies still need to be deeply explored. Increased number and volume of adipocytes lead to overweight and obesity.
View Article and Find Full Text PDFElife
January 2025
Division of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Together with obesity and type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing global epidemic. Activation of the complement system and infiltration of macrophages has been linked to progression of metabolic liver disease. The role of complement receptors in macrophage activation and recruitment in MASLD remains poorly understood.
View Article and Find Full Text PDFNutrients
December 2024
Departamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, CDMX, México 14080, Mexico.
Background/objective: In recent studies, it has been shown that dietary bioactive compounds can produce health benefits; however, it is not known whether an improvement in solubility can enhance their biological effects. Thus, the aim of this work was to study whether co-amorphous (CoA) naringenin or fisetin with enhanced solubility modify glucose and lipid metabolism, thermogenic capacity and gut microbiota in mice fed a high-fat, high-sucrose (HFSD) diet.
Methods: Mice were fed with an HFSD with or without CoA-naringenin or CoA-fisetin for 3 months.
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