Food-grade titanium dioxide (E171) is a widely used food additive and the toxicity after oral consumption is still under research, although it has been already banned in some countries. The consumption of this additive occurs mainly through ultra-processed food products which also contain high amounts of fat. High fat diets (HFD) impair the physiological system controlling satiation and satiety, which are responsible for control of food intake and energy status. The impact of E171 on animal behavior has been poorly explored and here we hypothesize that E171 could worsen the effects on feeding behavior induced by HFD. Therefore, we aimed to evaluate the effects of E171 on the feeding pattern and the behavioral satiety sequence (BSS) of mice fed with a regular diet (RD) or a HFD after 1 and 16 weeks of exposure. The results showed that RD + E171 increased food intake and feeding time, but the prototypical structure of the BSS pattern (feeding→ grooming-activity → resting), was preserved. Conversely, food consumption was not altered in HFD + E171, but the BSS pattern was disrupted as the animals prolonged resting time and spent less time being active. Our findings suggest that E171 delayed the onset of satiation in mice fed with RD but induced the opposite effect in mice fed with HFD.
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http://dx.doi.org/10.1016/j.fct.2023.113610 | DOI Listing |
Nutrients
December 2024
Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
High sugar intake, particularly fructose, is implicated in obesity and metabolic complications. On the other hand, fructose from fruits and vegetables has undisputed benefits for metabolic health. This raises a paradoxical question-how the same fructose molecule can be associated with detrimental health effects in some studies and beneficial in others.
View Article and Find Full Text PDFNutrients
December 2024
IFF, Health & Biosciences, Sokeritehtaantie 20, 02460 Kantvik, Finland.
Background/objectives: Ergothioneine (EGT) is an effective antioxidant that animals cannot produce and has an important anti-inflammatory role in cell protection, which can help lower the risk of various diseases. In this study, we investigated the potential role of gut microbiota in the production of EGT, which was found to increase in the mouse liver after dietary supplementation with betaine (BET) or polydextrose (PDX).
Methods: The effects of BET and PDX on the gut microbiota and tissue EGT content were investigated using a diet-induced obese mouse model and simulated fermentation in the human colon.
Nutrients
December 2024
Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou 510080, China.
Background: Atherosclerotic calcification (AC) is a common feature of atherosclerotic cardiovascular disease. β-Hydroxybutyrate (BHB) has been identified as a molecule that influences cardiovascular disease. However, whether BHB can influence AC is still unknown.
View Article and Find Full Text PDFNutrients
December 2024
Department of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Background/objectives: This study builds on previous findings from mouse models, which showed that maternal overnutrition induced by a high-fat diet (HFD) promotes metabolic-associated fatty liver disease (MAFLD) in offspring, linked to global DNA hypermethylation. We explored whether epigenetic modulation with 5-Aza-CdR, a DNA methylation inhibitor, could prevent MAFLD in offspring exposed to maternal overnutrition.
Methods: The offspring mice from dams of maternal overnutrition were fed either a chow diet or a high-fat diet (HFD) for 10 weeks.
Nutrients
December 2024
Departments of Human Genetics and Pediatrics, McGill University, Montreal, QC H3A 0C7, Canada.
Background/objectives: The gene variant results in a thermolabile MTHFR enzyme associated with elevated plasma homocysteine in TT individuals. Health risks associated with the TT genotype may be modified by dietary and supplemental folate intake. Supplementation with methyltetrahydrofolate (methylTHF) may be preferable to folic acid because it is the MTHFR product, and does not require reduction by DHFR to enter one-carbon folate metabolism.
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