Project description:It has been found that fat oxidation is reduced in the skeletal muscle of obese humans. This study aims to identify the mRNA of proteins involved in fat oxidation that may be reduced in obese and morbidly obese individuals. Information gathered will help in understanding how obesity contributes to cardiovascular disease via insulin resistance. Keywords: other

2003-07-16 | GSE474 | GEO

Resolvin D1 Enhances Necroptotic Cell Clearance Through Promoting Macrophage Fatty Acid Oxidation and Oxidative Phosphorylation.

Project description: Not available

| S-EPMC8174560 | biostudies-literature

Rao2014 - Fatty acid beta-oxidation (reduced model)

Project description: Not available

| MODEL1403250000 | biostudies-other

The omega-3 fatty acid docosahexaenoic acid favorably modulates the inflammatory pathways and macrophage polarization within aorta of LDLR(-/-) mice.

Project description: Not available

| S-EPMC4172650 | biostudies-literature

Aspirin increases mitochondrial fatty acid oxidation.

Project description: Not available

| S-EPMC5195905 | biostudies-literature

Carnitine transport and fatty acid oxidation.

Project description: Not available

| S-EPMC4967041 | biostudies-literature

Mitochondrial fatty acid oxidation drives senescence.

Project description: Not available

| S-EPMC11506141 | biostudies-literature

ROLE OF FATTY ACID ß-OXIDATION IN LYMPHANGIOGENESIS

Project description:Lymphatic vessels are involved in fluid drainage and are critical for health. To date, only genetic signaling pathways have been implicated in lymphatic development, and a role for metabolism has not been described. Here, we report that transcription factor Prox1 increases fatty acid ß-oxidation (FAO) through upregulation of CPT1a, a rate-controlling step of FAO. Lymphatic endothelial cells (LECs) oxidize fatty acids to proliferate and migrate. By providing acetyl-CoA, FAO is also critical for the maintenance of differentiated LECs through the regulation of histone acetylation of key lymphangiogenic genes. Loss of CPT1a in LEC precursors causes lymphatic defects in vivo, while restoration of acetyl-CoA by supplementing acetate to replenish cellular acetyl-CoA levels rescues this process.

2017-02-13 | GSE71230 | GEO

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