High-Fructose Corn Syrup Promotes Proinflammatory Macrophage Activation via ROS-Mediated NF-κB Signaling and Exacerbates Colitis in Mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA776868 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16678442_1.fastq.gz | Fastqsanger.gz | |||
| SRR16678442_2.fastq.gz | Fastqsanger.gz | |||
| SRR16678443_1.fastq.gz | Fastqsanger.gz | |||
| SRR16678443_2.fastq.gz | Fastqsanger.gz | |||
| SRR16678444_1.fastq.gz | Fastqsanger.gz |
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Project description:we focused on HFCS and found that HFCS aggravates colitis by altering the intestinal immune microenvironment. Our data demonstrate that short-term consumption of HFCS upregulates the proportion of macrophages in IBD mice but not in healthy mice. HFCS promotes proinflammatory cytokine production through reactive oxygen species (ROS)-mediated nuclear factor-κB (NF-κB) signaling. Our work unveils the important role of macrophages in HFCS-induced exacerbation of colitis and reveals the mechanism of how HFCS immunologically aggravates IBD.
2024-10-01 | GSE186953 | GEO
Project description:Excessive consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity and with an increased risk of colorectal cancer. Whether HFCS contributes directly to tumorigenesis is unclear. We investigated the effects of daily oral administration of HFCS in APC mutant mice, which are predisposed to develop intestinal tumors. The HFCS-treated mice showed a dramatic increase in tumor size and tumor grade in the absence of obesity or metabolic syndrome. HFCS increased the levels of fructose and glucose in the intestinal lumen and serum, respectively, and the tumors absorbed both sugars. Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysis and increased synthesis of fatty acids that support tumor growth. These mouse studies support the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis.
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Project description:High-Fructose Corn Syrup Enhances Intestinal Tumor Growth in Mice
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Project description:Th17 cells are quite heterogeneous, with pathogenic roles in autoimmunity and non-pathogenic roles in maintaining tissue homeostasis. Although efforts have been made to study genetic and cellular factors in regulating Th17 cell differentiation, little is known about the role of environmental factors and their underlying mechanisms. Here, we revealed that high-fructose intake selectively enhanced the differentiation and function of IL1b+IL-6+IL-23-induced pathogenic Th17 cells (pTh17), without affecting TGFb1+IL-6-induced non-pTh17 cells, and exacerbated autoimmune diseases models. Notably, fructose enhanced both aerobic glycolysis and OXPHOS activity in pTh17 cells, leading to increased ROS production and subsequently promoting their differentiation. N-acetyl cysteine (NAC), a ROS scavenger, specifically impaired pTh17 cell immunity and mitigated autoimmune disease under high-fructose consumption. Mechanistically, ROS accumulation resulted in higher EGFR expression and activation, which subsequently translocated in nucleus to bind with STAT3, enhancing its transcriptional activity of CNS6 and CNS9 regions of Rorc. Taking together, we illustrated a previously unrecognized mechanism underlying the adverse effects of high-fructose intake in pTh17 cell-related pathologies and diseases.
2025-09-29 | GSE285450 | GEO
Project description:High Fructose Corn Syrup (HFCS), a sweetener rich in glucose and fructose, is nowadays widely used in beverages and processed foods, and its consumption has been correlated to the emergence and progression of Non-Alcoholic Fatty Liver Disease (NAFLD). Nevertheless, the exact molecular mechanisms by which HFCS impacts hepatic metabolism are still unclear, especially in the context of obesity. In contrast, the vast majority of current studies in the field focus either on the detrimental role of fructose on NAFLD or compare the additive impact of fructose versus glucose in this process. Besides, studies elaborating on the role of fructose in NAFLD utilize molecular fructose, rather than HFCS, thus lacking simulation of human NAFLD in a more realistic way. Herein, by engaging combined omic approaches, we sought to characterize the additive impact of HFCS on NAFLD during obesity and recognize candidate pathways and molecules which could mediate the exaggeration of steatosis under these conditions. To achieve this goal, C57BL/6 male mice were fed a normal-fat (ND), a high-fat (HFD) or a HFD supplemented with HFCS (HFD-HFCS) and upon examination of their metabolic and NAFLD phenotype, proteomic and lipidomic analyses were conducted and utilized separately or in an integrated mode to identify HFCS-related molecular alterations of the hepatic metabolic landscape. Although HFD and HFD-HFCS mice displayed comparable obesity, HFD-HFCS mice showed greater aggravation of hepatic steatosis. Importantly, the HFD-HFCS hepatic proteome was characterized by an upregulation of the enzymes implicated in de novo lipogenesis (DNL), while palmitic-acid containing diglycerides were significantly increased in the HFD-HFCS hepatic lipidome, as compared to the HFD group. Integrated omic analysis further suggested that TCA cycle overstimulation, is likely contributing towards the intensification of steatosis in the HFD-HFCS dietary theme. Overall, our results imply that HFCS may significantly contribute to NAFLD aggravation during obesity, with its fructose-rich properties being the main suspect.
2023-08-03 | PXD033612 | Pride
Project description:Concerns are growing regarding the role of dietary sugars in the development of obesity and cardiometabolic diseases, including diabetes. High-fructose corn syrup (HFCS) and sucrose are the most important dietary sweeteners. Both HFCS and sucrose have overlapping metabolic actions with adverse effects attributed to their fructose moiety. Ecological studies have linked the rise in fructose availability with the increases in obesity and diabetes worldwide. This link has been largely underpinned by animal models and select human trials of fructose overfeeding at high levels of exposure. Although prospective cohort studies have shown significant associations comparing the highest with the lowest levels of intake sugar-sweetened beverages, these associations are small, do not hold at moderate levels of intake and are subject to collinearity effects from related dietary and lifestyle factors. Most systematic reviews and meta-analyses from controlled feeding trials have shown that fructose-containing sugars in isocaloric exchange for other carbohydrates do not show evidence of harm and, in the case of fructose, may even have advantages for glycaemic control, especially at small doses. Nevertheless, trials in which fructose-containing sugars supplement diets with excess energy have shown adverse effects, effects that appear more attributable to the excess energy than the sugar. There is no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects, although there is potentially cause for concern where fructose is provided at high doses or contributes excess energy to diets. Further investigation is warranted due to the significant knowledge gaps and weaknesses in existing research.
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Project description:Fructose specifically exacerbates pathogenic-Th17 cell differentiation and autoimmune diseases through ROS-EGFR signal
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Project description:Rats fed a 20%-maple syrup diet (maple syrup group) for 11 days showed significantly lower values of the hepatic function markers than those fed a 20%-sugar mix syrup diet (control) likewise. One reasons was suggested by DNA microarray analysis which revealed that the expression of genes for enzymes of ammonia production were down-regulated in the liver of maple syrup group. Rats were quarantined and conditioned by administration of the authentic AIN93G diet for 4 days. Rats had free access to the diet and drinking water during this preliminary feeding. For feeding tests, they were dichotomized (n = 7 and 8) for maple syrup and sugar mix syrup group, respectively, and then fed for 11 days on either the AIN93G diet containing 20% maple syrup or on the 20% sugar mix syrup with a similar sugar composition; the amount of maple syrup or the sugar mix syrup was arranged. Rats in both diet groups were fasted for 16 hours, prior to being anesthetically sacrificed for dissection.
2011-08-31 | E-GEOD-30532 | biostudies-arrayexpress
Project description:Rats fed a 20%-maple syrup diet (maple syrup group) for 11 days showed significantly lower values of the hepatic function markers than those fed a 20%-sugar mix syrup diet (control) likewise. One reasons was suggested by DNA microarray analysis which revealed that the expression of genes for enzymes of ammonia production were down-regulated in the liver of maple syrup group.
2011-09-01 | GSE30532 | GEO
Project description:Excessive consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity and with an increased risk of colorectal cancer. Whether HFCS contributes directly to tumorigenesis is unclear. We investigated the effects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are predisposed to develop intestinal tumors. The HFCS-treated mice showed a substantial increase in tumor size and tumor grade in the absence of obesity and metabolic syndrome. HFCS increased the concentrations of fructose and glucose in the intestinal lumen and serum, respectively, and the tumors transported both sugars. Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysis and increased synthesis of fatty acids that support tumor growth. These mouse studies support the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis.
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