Scopus İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.12573/395
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Article High Carbohydrate Diet Decreases Microbial Diversity and Increases Il-1β Levels in Mice Colon(Korean Society Food Science & Technology-kosfost, 2024-05-04) Ulutas, Mehmet Sefa; Aydin, Erkin; Cebeci, AysunWestern diet is known to contribute to intestinal dysbiosis and the progression of inflammation. Although the Turkish diet has different macronutrient contents, the intestinal inflammatory disease incidences in T & uuml;rkiye are comparable to Western countries. Thus, we hypothesized that high carbohydrate diets also contribute to inflammation of the colon. We compared diets with different macronutrient compositions and investigated their effects on colonic microbiota, cytokine, histology, and tight junction protein levels. High carbohydrate diet caused the lowest microbial diversity and is accompanied by the highest expression of interleukin-1 beta and claudin-1. A low carbohydrate diet with zero fiber resulted in the lowest inflammatory markers as well as the lowest occludin and claudin levels. Overall, our results indicate that carbohydrate and fiber contents of the diets are important contributors to colon health.Article Citation - WoS: 35Citation - Scopus: 37Glucose-Dependent Anaplerosis in Cancer Cells Is Required for Cellular Redox Balance in the Absence of Glutamine(Nature Portfolio, 2016-09-08) Cetinbas, Naniye Malli; Sudderth, Jessica; Harris, Robert C.; Cebeci, Aysun; Negri, Gian L.; Yilmaz, Oemer H.; Sorensen, Poul H.; Yllmaz, Ömer H.Cancer cells have altered metabolism compared to normal cells, including dependence on glutamine (GLN) for survival, known as GLN addiction. However, some cancer cell lines do not require GLN for survival and the basis for this discrepancy is not well understood. GLN is a precursor for antioxidants such as glutathione (GSH) and NADPH, and GLN deprivation is therefore predicted to deplete antioxidants and increase reactive oxygen species (ROS). Using diverse human cancer cell lines we show that this occurs only in cells that rely on GLN for survival. Thus, the preference for GLN as a dominant antioxidant source defines GLN addiction. We show that despite increased glucose uptake, GLN addicted cells do not metabolize glucose via the TCA cycle when GLN is depleted, as revealed by C-13-glucose labeling. In contrast, GLN independent cells can compensate by diverting glucose-derived pyruvate into the TCA cycle. GLN addicted cells exhibit reduced PDH activity, increased PDK1 expression, and PDK inhibition partially rescues GLN starvation-induced ROS and cell death. Finally, we show that combining GLN starvation with pro-oxidants selectively kills GLN addicted cells. These data highlight a major role for GLN in maintaining redox balance in cancer cells that lack glucose-dependent anaplerosis.