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high-fat diet
Also known as: high-fat diets
Facts (30)
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Dietary interventions as regulators of stem cell behavior in ... genesdev.cshlp.org 26 facts
claimCaloric restriction, a high-fat diet, and fasting all converge on enhanced crypt proliferation and survival in both homeostasis and injury-based regenerative programs, though they may utilize different underlying mechanisms.
claimComparisons between caloric restriction/prolonged fasting, the ketogenic diet, and high-fat diets suggest the importance of the balance between glucose and fatty acid utilization as oxidative substrates in stem cells.
claimA high-fat diet and intermittent fasting can alter serum lipid composition, as a high-fat diet likely enriches for circulating lipids that differ from those released from adipose tissue breakdown during intermittent fasting.
claimBoth a high-fat diet and intermittent fasting lead to intestinal stem cell-autonomous activation of PPARδ signaling, which enhances self-renewal through partial activation of a Wnt signaling program and enhanced fatty acid oxidation.
claimHigh-fat diets enhance stemness through enforcing self-renewal via microbiota-derived butyrate, while ketogenesis enhances stemness via β-OHB accumulation.
claimA high-fat diet increases the number and proliferation of intestinal stem cells under conditions of normal intestinal homeostasis.
claimWhile metabolites from a high-fat diet can promote self-renewal in tissue stem cells, the diet is likely to alter stem cells in ways that skew their fates or exacerbate their response to inflammation in many contexts.
claimHigh-fat diets elevate circulating glucose despite increasing insulin levels, according to Winzell and Ahrén (2004).
referenceGeneral dysbiosis caused by a high-fat diet is associated with tumor progression due to a lack of secreted butyrate as a waste product by the microbiota.
claimA high-fat diet induces obesity in mice within months.
claimIn a model of oral squamous cell carcinoma, a high-fat diet promotes metastasis in a CD36-dependent fashion, as reported by Pascual et al. in 2017.
claimCaloric restriction, prolonged fasting, ketogenesis, and high-fat diets all diminish the levels of circulating glucose.
referenceFecal microbiota transfer from mice fed a high-fat diet to mice fed a control diet results in increased tumor formation.
claimA high-fat diet depletes Paneth cells in the intestine via activation of PPARδ signaling, which subsequently induces Wnt target genes in intestinal stem cells, as reported by Beyaz et al. (2016).
claimPharmacologic administration of a PPARδ agonist phenocopies the tumor-forming capacity induced by a high-fat diet in premalignant intestinal progenitors, suggesting that high-fat diets function at least in part through PPARδ signaling.
claimIn a model of ionizing radiation-induced intestinal injury, a high-fat diet increased the number of surviving, proliferating, and Olfm4/OLFM4-positive crypts without altering the numbers of enteroendocrine or goblet cells.
claimIn an esophageal carcinoma tumor initiation model, a high-fat diet increases Lgr5+ progenitor cells and promotes tumor growth in mice with premalignant esophageal lesions, acting as a second hit to initiate tumors in situ.
claimA high-fat diet endows progenitors in the intestinal crypt with stem cell properties, which may contribute to an enhanced propensity for tumorigenesis.
claimThe interplay between a high-fat diet and stem cell behavior may form a positive feedback loop that leads to a decline in organismal health.
claimHigh-fat or cholesterol-rich diets and intermittent fasting directly alter intestinal stem cell and progenitor function.
referenceIn an esophageal tumor initiation model, the high-fat diet-associated increase in Lgr5+ progenitors is dependent on the microbiota within the gastrointestinal tract.
claimA high-fat diet can bestow tumor-forming capacity in premalignant intestinal progenitors independent of the niche.
claimHigh-fat diets may enforce gene expression to enable carcinogenesis, which may explain why increased carcinogenesis is not observed under ketogenic conditions.
claimA high-fat diet increases glucose availability, increases circulating levels of unsaturated fatty acids that may act as signaling ligands, and results in insulin resistance.
claimTumor-initiating cells in squamous cell carcinoma normally up-regulate the fatty acid transporter CD36, suggesting that the uptake and oxidation of fatty acids are partially responsible for the increased metastasis observed after a high-fat diet.
claimIn a one-hit model of intestinal stem cells, a high-fat diet acts as a 'second hit' that enables tumor initiation, rather than an oncogenic mutation.
The role of Plant Foods in the evolution and Dispersal of early Humans kernsverlag.com Jul 30, 2022 1 fact
claimBen-Dor and colleagues hypothesize that Middle Pleistocene Homo species specialized in hunting large prey, such as elephants, to obtain the high-fat diet necessary to sustain a hyper-carnivorous lifestyle (Ben-Dor et al. 2011, 2021; Ben-Dor and Barkai 2021).
Research reveals devastating impact of Western diet on human health news-medical.net Jun 18, 2023 1 fact
claimHigh-fat diets, such as the Western diet, result in unfavorable lipid profiles characterized by increased low-density-lipoprotein (LDL) levels and decreased high-density lipoprotein (HDL) levels, which leads to endothelial dysfunction.
Origins and evolution of the Western diet: health implications for the ... academia.edu 1 fact
referenceNelson GJ, Schmidt PC, and Kelley DS found that low-fat diets do not lower plasma cholesterol levels in healthy men compared to high-fat diets when the fatty acid composition is similar and caloric intake remains constant, as published in Lipids in 1995.
Western diet – Knowledge and References - Taylor & Francis taylorandfrancis.com 1 fact
measurementA high-fat and high-carbohydrate diet consisting of 46.1% fat, 35.8% carbohydrate, and 18.1% protein by weight causes insulin resistance in rats, characterized by increased Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and fasting blood glucose (FBG) levels.