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Obesity has been regarded as an epidemic in recent years. Various treatments have been developed, with bariatric surgery showing the highest levels of safety and effectiveness. This has increased its popularity and demand not only among young adults but also among elderly patients.

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Intestinal epithelial cell NCoR deficiency ameliorates obesity and metabolic syndrome.

Acta Pharm Sin B

December 2024

State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

Nuclear receptor corepressor (NCoR1) interacts with various nuclear receptors and regulates the anabolism and catabolism of lipids. An imbalance in lipid/energy homeostasis is also an important factor in obesity and metabolic syndrome development. In this study, we found that the deletion of NCoR1 in intestinal epithelial cells (IECs) mainly activated the nuclear receptor PPAR and attenuated metabolic syndrome by stimulating thermogenesis.

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Lymphedema is a chronic condition caused by the accumulation of protein-rich fluid in the interstitial tissue, resulting in edema and a diminished quality of life. When first-line treatments like complete decongestive therapy (CDT) fail, surgical options are considered. These include physiological procedures like lymphaticovenous anastomosis (LVA) and vascularized lymph node transfer (VLNT), which aim to restore lymphatic function, as well as reductive procedures such as liposuction and excisional techniques, which reduce limb volume.

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Absence of MCJ/DnaJC15 promotes brown adipose tissue thermogenesis.

Nat Commun

January 2025

Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.

Obesity poses a global health challenge, demanding a deeper understanding of adipose tissue (AT) and its mitochondria. This study describes the role of the mitochondrial protein Methylation-controlled J protein (MCJ/DnaJC15) in orchestrating brown adipose tissue (BAT) thermogenesis. Here we show how MCJ expression decreases during obesity, as evident in human and mouse adipose tissue samples.

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