It is generally accepted that metainflammation, a state of chronic and low-grade inflammation in obesity, plays a great role in metabolic disorder like insulin resistance. To gain further insight into the mechanism of metainflammation and find feasible therapy of obesity, diet-induced obesity (DIO) rats model and Electroacupuncture (EA) treatment were established in this trail. The results indicated that rising Lee's index, hyperlipidemia, insulin resistance, and increasing inflammation factors including NF-B, TNF-, and Macrophages 1 were determined in DIO rats while EA is exhibiting an effective intervention. Furthermore, to clarify this phenomenon and provide new recognition of alternative medicine for the treatment of metainflammation, we found that EA activating Sirt1 and Sirt1-dependent deacetylation of histone (H3K9) was the key of modulation. It should be noted that, while possible, the activating of Sirt1 could lead to deacetylation of NF-B also. In this study, the deacetylation of NF-B depended on higher level of Sirt1 than H3K9, which suggested that the deacetylation via Sirt1 in metainflammation could be specific and programmed.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6217753 | PMC |
http://dx.doi.org/10.1155/2018/5302049 | DOI Listing |
Diabetol Metab Syndr
January 2025
Laboratory of Immunopharmacology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation-Fiocruz, Campus Maré. Centro de Pesquisa, Inovação e Vigilância em Covid-19 e Emergências Sanitárias. Endereço: Av. Brasil, 4036-Bloco 2. Manguinhos, Rio de Janeiro, RJ, CEP 21040-361, Brazil.
Introduction: Metabolic syndrome (MetS) is a metabolic disorder related to obesity and insulin resistance and is the primary determinant of the development of low-intensity chronic inflammation. This continuous inflammatory response culminates in neuroimmune-endocrine dysregulation responsible for the metabolic abnormalities and morbidities observed in individuals with MetS. Events such as the accumulation of visceral adipose tissue, increased plasma concentrations of free fatty acids, tissue hypoxia, and sympathetic hyperactivity in individuals with MetS may contribute to the activation of the innate immune response, which compromises cerebral microcirculation and the neurovascular unit, leading to the onset or progression of neurodegenerative diseases.
View Article and Find Full Text PDFImmun Ageing
January 2025
Institute for Behavioral Medicine Research, Ohio State University, 460 Medical Center Drive, Columbus, OH, 43210, USA.
Background: Obesity and metabolic syndrome are major public health concerns linked to cognitive decline with aging. Prior work from our lab has demonstrated that short-term high fat diet (HFD) rapidly impairs memory function via a neuroinflammatory mechanism. However, the degree to which these rapid inflammatory changes are unique to the brain is unknown.
View Article and Find Full Text PDFEMBO J
January 2025
Department of Immunology and Regenerative Biology, Weizmann Institute of Science, 76100, Rehovot, Israel.
Mitochondrial carrier homolog 2 (MTCH2) is a regulator of apoptosis, mitochondrial dynamics, and metabolism. Loss of MTCH2 results in mitochondrial fragmentation, an increase in whole-body energy utilization, and protection against diet-induced obesity. In this study, we used temporal metabolomics on HeLa cells to show that MTCH2 deletion results in a high ATP demand, an oxidized cellular environment, and elevated utilization of lipids, amino acids, and carbohydrates, accompanied by a decrease in several metabolites.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA.
Outer mitochondrial membrane (OMM) proteins communicate with the cytosol and other organelles, including the endoplasmic reticulum. This communication is important in thermogenic adipocytes to increase the energy expenditure that controls body temperature and weight. However, the regulatory mechanisms of OMM protein insertion are poorly understood.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
National Key Laboratory of Veterinary Public Health Security, College of Veterinary Medicine, China Agricultural University, Haidian, Beijing 100193, China. Electronic address:
Obesity is a contributing factor that increases the likelihood of developing chronic kidney disease. In recent years, studies have found that light pollution worldwide promoted obesity, which was known to be a consequence of circadian rhythm disruption. Nevertheless, the impact of light pollution on kidney disease associated with obesity remains mostly unknown, and potential processes have been minimally investigated.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!