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#Lipids

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egusphere.copernicus.orgUtilizing Probability Estimates from Machine Learning and Pollen to Understand the Depositional Influences on Branched GDGT in Wetlands, Peatlands, and LakesAbstract. Branched glycerol dialkyl glycerol tetraethers (brGDGTs) serve as critical molecular biomarkers for the quantitative reconstruction of past environments, ambient temperature and pH across various archives. Despite their success, numerous issues persist that limit their application. The distribution of brGDGTs varies significantly based on provenance, resulting in biases in environmental reconstructions that rely on fractional abundances and derived indices, such as the MBT’5ME. This issue is especially significant in shallow lakes, wetlands, and peatlands within semi-arid and arid regions, where ecosystems are sensitive to diverse environmental and climatic factors. Recent advancements, such as machine learning techniques, have been developed to identify changes in sources; however, these techniques are insufficient for detecting mixed source environments. The probability estimates derived from five machine learning algorithms are employed here to detect provenance changes in brGDGT downcore records and to identify periods of mixed provenance. A new global modern database (n=2301) was compiled to train, validate, test, and apply these algorithms to two sedimentary records. Our findings are corroborated by pollen and non-pollen palynomorphs obtained from the identical records. These microfossil proxies are utilized to discuss changes in provenance, hydrology, and ecology that influence the distribution of brGDGTs. Probability estimates derived from Random Forest with a sigmoid calibration are most effective in detecting changes in brGDGT distribution. Minor changes in the relative contributions of brGDGTs provenance can significantly influence the distribution of brGDGTs, especially regarding the MBT'5ME index. This study introduces a novel brGDGT wetland index aimed at monitoring potential biases arising from wetland development.

🧈 Dietary Lipids, Gut Microbiota, and Their Metabolites: Insights from Recent Studies

mdpi.com/2072-6643/17/4/639

MDPIDietary Lipids, Gut Microbiota, and Their Metabolites: Insights from Recent StudiesDietary lipid intake can influence the gut microbiota (GM) and their metabolites, such as short-chain fatty acids (SCFA) and bile acids, which are key mediators of health. The objective is to examine how dietary lipids’ quantity and quality influence the GM and metabolite profiles. A literature review of 33 studies in animals and humans was performed on the effects of saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs), trans-fatty acids (TFAs), and sterols on GM composition and gut-derived metabolites. The results show that diets rich in MUFAs, n-3 PUFAs, and short-chain FAs have the potential to enhance beneficial bacteria and metabolites. In addition, trans-palmitoleic acid, conjugated linoleic acid, and phytosterols may also have potentially beneficial effects on GM, but more research is needed. Medium-chain FAs and n-6 PUFAs have variable effects on the GM. Conversely, intakes of high-fat diets, long-chain SFAs, industrial TFAs, and cholesterol disrupt GM balance. In conclusion, animal studies clearly demonstrate that dietary fats influence the GM and related metabolites. Yet, human studies are limited. Therefore, well-designed human studies that consider the whole diet and baseline health status are needed to better understand the effects of dietary lipids on GM.

High #fructose dietary supplements can promote #cancer growth in mice. Fructose increases production of #lipids in #liver that then are taken up by tumors.
nature.com/articles/s41586-024

www.nature.comDietary fructose enhances tumour growth indirectly via interorgan lipid transfer | NatureFructose consumption has increased considerably over the past five decades, largely due to the widespread use of high-fructose corn syrup as a sweetener1. It has been proposed that fructose promotes the growth of some tumours directly by serving as a fuel2,3. Here we show that fructose supplementation enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer without causing weight gain or insulin resistance. The cancer cells themselves were unable to use fructose readily as a nutrient because they did not express ketohexokinase-C (KHK-C). Primary hepatocytes did express KHK-C, resulting in fructolysis and the excretion of a variety of lipid species, including lysophosphatidylcholines (LPCs). In co-culture experiments, hepatocyte-derived LPCs were consumed by cancer cells and used to generate phosphatidylcholines, the major phospholipid of cell membranes. In vivo, supplementation with high-fructose corn syrup increased several LPC species by more than sevenfold in the serum. Administration of LPCs to mice was sufficient to increase tumour growth. Pharmacological inhibition of ketohexokinase had no direct effect on cancer cells, but it decreased circulating LPC levels and prevented fructose-mediated tumour growth in vivo. These findings reveal that fructose supplementation increases circulating nutrients such as LPCs, which can enhance tumour growth through a cell non-autonomous mechanism. Dietary fructose enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer indirectly via metabolite transfer.

Mitochondrial fatty acid oxidation drives senescence
science.org/doi/10.1126/sciadv

* cellular senescence: stress-induced irreversible cell cycle arrest in tumor suppression/aging
* pharmacological activation of fatty acid oxidation induced senescence in vitro/in vivo
* mitochondrial energy metabolism: critical role in senescence induction
* potential intervention to control senescence