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Objectives: The aim of this study was to explore the relationship between the consumption of a high-fat diet and aging-dependent formation of maxillary incisor grooves in C57BL/6 mice, and to identify putative maxillary incisor groove-related genes.
Methods: We fed 2-month-old and 16-month-old C57BL/6 mice on either a chow diet or a high-fat diet for three months and observed changes in maxillary incisor grooves. We examined tissue sections of the maxillary incisors with grooves and carried out transcriptome analysis of the apical tissue fragments of maxillary incisors with/without grooves.
Results: Consumption of a high-fat diet for three months resulted in significant increases in both body weight and the number of incisor grooves. Both the number and frequency of incisor grooves increased in an age-dependent manner from 26 to 28 months, during which time an additional groove appeared. There was abnormal differentiation and apoptosis of ameloblasts on the labial surface at the grooves of the maxillary incisors. Transcriptome analysis identified 23 genes as being specific to 24-month-old mice; these included several genes related to apoptosis and cell differentiation.
Conclusions: The study findings indicate that, in C57BL/6 mice, consumption of a high-fat diet increases labial groove formation in maxillary incisors, which is related to aging of the tissue stem cells in the apical root end of the teeth.
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http://dx.doi.org/10.1016/j.job.2019.12.003 | DOI Listing |
Kaohsiung J Med Sci
September 2025
Hepatitis Research Center, College of Medicine; Center for Metabolic Disorders and Obesity; Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical University, Kaohsiung, Taiwan.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent chronic liver condition that can progress to severe complications such as metabolic dysfunction-associated steatohepatitis (MASH). Despite its growing burden, there are no reliable non-invasive biomarkers for tracking disease progression. In this study, we established a murine MASLD/MASH model using a high-fat diet and chemical (CCl) induction.
View Article and Find Full Text PDFKaohsiung J Med Sci
September 2025
Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
Rosuvastatin (RVS) is an HMG-CoA reductase inhibitor with lipid-lowering properties. This study aims to investigate the role of RVS in plaque formation in atherosclerosis (AS) and its functional mechanism. ApoE mice were fed a high-fat diet to generate a mouse model of AS.
View Article and Find Full Text PDFGen Physiol Biophys
September 2025
Department of Endocrinology and Metabolism, Central People's Hospital of Zhanjiang, Zhanjiang City, Guangdong Province, China.
This study explores how human antigen R (HuR) stabilizes fibroblast growth factor 19 (FGF19) mRNA, inhibiting Kupffer cell (KC) activation to reduce inflammation and fibrosis in non-alcoholic fatty liver disease (NAFLD). An animal model of NAFLD was established in mice by administering a high-fat diet (HFD). In vitro study utilized a lipopolysaccharide-induced immortalized mouse KC model.
View Article and Find Full Text PDFScand J Med Sci Sports
September 2025
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Dietary intake has an important influence on rates of fuel use during exercise, but the extent to which short-term diet changes affect peak fat oxidation (PFO) and the intensity at which this occurs (Fat) is unknown. This study examined the impact of diet-induced changes in substrate availability on PFO and Fat and the expression of key lipid-regulatory genes and proteins in skeletal muscle. Forty moderately to well-trained males (27 ± 5 years, V̇O 56.
View Article and Find Full Text PDFAutophagy
September 2025
Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Patients with metastatic colorectal cancer (mCRC) to the liver exhibit poor survival rates. Chemotherapy combined with anti-vascular therapy has emerged as the standard treatment, but resistance to anti-VEGFA therapy inevitably develops. The metabolic reprogramming of tumor vascular endothelial cells (TECs) plays a crucial, yet still poorly understood, role in the development of therapeutic resistance.
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