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The regulatory mechanism of chlorogenic acid on fatty acid metabolism in human embryonic stem cells

ABSTRACT: The regulatory mechanism of chlorogenic acid on fatty acid metabolism in human embryonic stem cells

PROVIDER: PRJNA1115124 | ENA |

REPOSITORIES: ENA

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The regulatory mechanism of chlorogenic acid on fatty acid metabolism in human embryonic stem cells

Project description:Chlorogenic acid (CGA) is a crucial bioactive dietary polyphenol found in plants and serves as the primary ingredient in numerous traditional Chinese medicine preparations. Due to its beneficial impact on treating metabolic syndrome, it has garnered significant attention in medical research. Previous studies have demonstrated that chlorogenic acid possesses antioxidative, antibacterial, antiviral, anti-tumor, lipid-lowering, glucose-lowering, and immunomodulatory properties, indicating its potential role in regulating metabolism. Human embryonic stem cells (hESCs) exhibit self-renewal and multi-directional differentiation capabilities. Any element within the culture system can alter the microenvironment and influence hESC metabolism. Therefore, hESCs provide a valuable and high-throughput model for investigating CGA's regulatory mechanism on metabolism in vitro. While previous studies have explored CGA's important regulatory role in human metabolism, its specific impact on hESCs metabolism remains undisclosed. Metabolites of hESCs are critical targets for enhancing stem cell function regulation. Prior research has emphasized the essential nature of de novo synthesis and β-oxidation of fatty acids for regulating hESCs; however, CGA's roles and mechanisms in regulating fatty acid metabolism within hESCs remain unelucidated. This study utilizes transcriptome analysis combined with epigenetics to investigate CGA's regulation of fatty acid metabolism within hESCs while analyzing the molecular mechanisms involved—providing a theoretical foundation for future regulation of HESC metabolism by CGA and offering potential optimizations for hESCs culture systems.

2025-01-20 | GSE268203 | GEO

Mitochondrial fatty acid synthesis coordinates mitochondrial oxidative metabolism

Project description:Mitochondrial fatty acid synthesis coordinates mitochondrial oxidative metabolism

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CARM1 reprograms fatty acid metabolism to promote ovarian cancer

Project description:Fatty acids are critical energy sources and structural components of cells. We investigate how CARM1 reprograms fatty acid metabolism to promote ovarian cancer

2023-03-29 | GSE202259 | GEO

CARM1 reprograms fatty acid metabolism to promote ovarian cancer

Project description:CARM1 reprograms fatty acid metabolism to promote ovarian cancer

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NAT10 depletion suppresses fatty acid metabolism in MCF7 breast cancer cells

Project description:NAT10 is an RNA cytidine transferase known to add acetyl group on RNA transcripts thereby promoting translational efficiency. It was reported that NAT10 regulates epithelial to mesenchymal transition (EMT), DNA damage, and cell proliferation in cancers. However, weather NAT10 regulates other crucial pathways is unknown. In our study we conducted gene expression profiling analysis using data obtained from RNA-seq of MCF7 NAT10 KO and scramble control. High throughput sequencing revealed fatty acid metabolism as the top enriched pathway with fatty acid metabolic genes such ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB, and ACAT1 were found to be differentially down-regulated. Overall our results revealed NAT10 depletion suppresses fatty acid metabolism in MCF7.

2022-08-03 | GSE210086 | GEO

A synthetic gene-metabolic circuit preferentially increased fatty acid metabolism in human hepatocytes

Project description:Obesity is becoming increasingly widespread in developed countries, and is often associated with heart diseases and diabetes. Elevated levels of plasma free fatty acids are a biochemical hallmark of obesity. Unlike plants and bacteria, mammals cannot utilize fatty acids to generate glucose because of the lack of glyoxylate shunt enzymes. Instead, fatty acids are used for energy storage, and their utilization is regulated at multiple levels ranging from hormonal to metabolic ensuring that glucose is preferentially oxidized before fatty acids. Here we designed a synthetic gene-metabolic circuit to alter the intracellular signaling and metabolic pathways that control fatty acid metabolism. By introducing the Escherichia coli glyoxylate shunt enzymes, isocitrate lyase (AceA) and malate synthase (AceB), into the mitochondria of human hepatocytes, we demonstrated that fatty acid utilization is preferentially increased while glucose uptake is significantly reduced. This bacterial pathway diverts signal metabolites (citrate, acetyl-CoA, and malonyl-CoA) that inhibits fatty acid uptake and provides an additional channel for fatty acid utilization. Remarkably, the hepatocytes readily adapted to the synthetic circuit by a series of global transcriptional and post-translational changes in metabolic and signal transduction pathways that further advanced our design objective. This systems approach illustrates the logic of the synergistic interaction between metabolism and signal transduction. The ready acceptance of this non-native pathway by hepatocytes suggests the plasticity of liver metabolism and opens a possibility for the synthetic approach in regulating human metabolism. Keywords: Fatty acid response, synthetic circuit, carbohydrate metabolism, stably transfected HepG2 cell line, glyoxylate shunt

2009-06-05 | GSE5903 | GEO

Hepatocyte-specific deletion of SIRT1 alters fatty acid metabolism

Project description:Hepatic metabolic derangements are key components in the development of fatty liver, insulin resistance, and atherosclerosis. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Here we demonstrate that hepatic SIRT1 regulates fatty acid metabolism by positively regulating PPAR-alpha. Hepatocyte-specific deletion of SIRT1 impairs PPAR-alpha signaling and decreased fatty acid beta-oxidation in the liver. When challenged with a high-fat diet, liver-specific SIRT1 knockout mice develop hepatic steatosis, hepatic inflammation, and endoplasmic reticulum stress. Taken together, our data indicate that SIRT1 plays a vital role in the regulation of hepatic lipid homeostasis.

2009-04-07 | GSE14921 | GEO

Srebf1-mediated fatty acid metabolism is crucial to sustain sugmented pigmentation SREBF1-mediated metabolic reprogramming through fatty acid metabolism sustains augmented melanogenesis

Project description:Srebf1-mediated fatty acid metabolism is crucial to sustain sugmented pigmentation SREBF1-mediated metabolic reprogramming through fatty acid metabolism sustains augmented melanogenesis

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Bacteria modulate tamoxifen-induced death via host fatty acid metabolism

Project description:Bacteria modulate tamoxifen-induced death via host fatty acid metabolism

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The role of fatty acid metabolism on Th9 cells differentiation

Project description:The role of fatty acid metabolism on Th9 cells differentiation

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