Objective: The objective of this study was to examine the relationship between iron deficiency and caries susceptibility in a mouse model.
Materials And Methods: Three-week-old C57BL/J6 mice were fed a cariogenic diet containing either standard iron (48 ppm Fe) or low iron (4 ppm Fe) levels. Concurrently, groups of mice with both diets were orally inoculated with Streptococcus mutans (1 × 10) cells on three consecutive days. At the end of the 5th week after infection, mice were sacrificed and jaws were collected for caries scoring, rating the number and severity of lesions using a modified Keyes method applicable to mice.
Results: Blood analysis by the end of the 5th week revealed marked reduction in the hemoglobin and hematocrit levels of the mice fed the iron deficient diet (IDA and IDA-S. mutans). Anemic mice in both groups lacked the incisor enamel pigmentation observed in mice fed an iron deficient diet. Anemic infected mice had the highest caries severity scores reflecting extensive deep lesions (P < 0.05). S. mutans infected mice fed a standard iron diet had similar numbers of lesions and severity scores as un-infected IDA animals (p < 0.05). IDA did not alter S. mutans CFU counts in infected animals (P < 0.05).
Conclusion: These results demonstrated that IDA mice are at a higher risk of developing deep dental caries compared to non-anemic mice; highlighting the protective role of iron against dental caries.
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http://dx.doi.org/10.1016/j.archoralbio.2019.05.002 | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University of Hospital Würzburg, 97080 Würzburg, Germany.
Background: The inheritance of the short allele, encoding the serotonin transporter (SERT) in humans, increases susceptibility to neuropsychiatric and metabolic disorders, with aging and female sex further exacerbating these conditions. Both central and peripheral mechanisms of the compromised serotonin (5-HT) system play crucial roles in this context. Previous studies on SERT-deficient (Sert) mice, which model human SERT deficiency, have demonstrated emotional and metabolic disturbances, exacerbated by exposure to a high-fat Western diet (WD).
View Article and Find Full Text PDFNutrients
January 2025
Department of Food & Nutrition, Kyung Hee University, Seoul 02447, Republic of Korea.
Background/objectives: The pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH) is closely associated with increased oxidative stress and lipid peroxidation. Coenzyme Q (CoQ) and selenium (Se) are well-established antioxidants with protective effects against oxidative damage. This study aimed to investigate the effects of CoQ and Se in ameliorating MASH induced by a methionine choline-deficient (MCD) diet in mice.
View Article and Find Full Text PDFNutrients
January 2025
Department of Food Science and Nutrition, Dankook University, Cheonan 31116, Republic of Korea.
Background/objectives: Obesity is a key factor in metabolic syndrome (MetS) development. Consumption of a high-fat diet (HFD) accelerates the onset of obesity and associated metabolic complications. (PB) has been traditionally utilized in Korean medicine for its antioxidant, anti-diabetic, anticancer, and hepatoprotective effects.
View Article and Find Full Text PDFLife (Basel)
January 2025
Department of Chemistry, College of Sciences, United Arab Emirates University, Al-Ain 15551, United Arab Emirates.
Microorganisms synthesize diverse types of exopolysaccharides (EPSs). EPSs with varying structural and physical properties can demonstrate unique health benefits, which allow for their tailored applications as functional foods such as prebiotics. Levan, a fructose-based EPS, is gaining considerable attention as an effective prebiotic to support the growth of beneficial gut bacteria.
View Article and Find Full Text PDFGenes (Basel)
December 2024
Zhejiang Key Laboratory of Medical Epigenetics, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Background/objectives: UFMylation, a newly identified ubiquitin-like modification, modulates a variety of physiological processes, including endoplasmic reticulum homeostasis maintenance, DNA damage response, embryonic development, and tumor progression. Recent reports showed that UFMylation plays a protective role in preventing liver steatosis and fibrosis, serving as a defender of liver homeostasis in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the regulation of UFMylation in MASLD remains unclear.
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