Obesity has been described as a global epidemic and is a low-grade chronic inflammatory disease that arises as a consequence of energy imbalance. Obesity increases the risk of type 2 diabetes (T2D), by mechanisms that are not entirely clarified. Elevated circulating pro-inflammatory cytokines and free fatty acids (FFA) during obesity cause insulin resistance and ß-cell dysfunction, the two main features of T2D, which are both aggravated with the progressive development of hyperglycemia. The inflammatory kinase c-jun N-terminal kinase (JNK) responds to various cellular stress signals activated by cytokines, free fatty acids and hyperglycemia, and is a key mediator in the transition between obesity and T2D. Specifically, JNK mediates both insulin resistance and ß-cell dysfunction, and is therefore a potential target for T2D therapy.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7140703 | PMC |
| http://dx.doi.org/10.3390/cells9030706 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Resolvin D1 suppresses inflammation in human fibroblast-like synoviocytes via the p-38, NF-κB, and AKT signaling pathways.
In Vitro Cell Dev Biol Anim
March 2025
Department of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-Ku, Hiroshima-Shi, Hiroshima Prefecture, Japan.
Synovitis represents the initial pathological change in osteoarthritis and contributes to its progression. Resolvin D1 (RV-D1) is a novel and endogenous docosahexaenoic acid-derived lipid mediator, which regulates the duration and magnitude of inflammation by downregulating pro-inflammatory genes and mediators. However, the effects of RV-D1 on synovitis remain unknown.
View Article and Find Full Text PDFutilizes vimentin to internalize human keratinocytes.
Front Cell Infect Microbiol
March 2025
Research and Development Center, Skin Biotechnology Center Co. Ltd., Yongin, Republic of Korea.
Introduction: Vimentin is an intermediate filamentous cytoskeletal protein involved in cell migration, adhesion, and division. Recent studies have demonstrated that several bacteria and viruses interact with vimentin to facilitate entry and trafficking within eukaryotic cells. However, the relationship between and vimentin remains unclear.
View Article and Find Full Text PDFSingle-nucleus transcriptomics reveal the cytological mechanism of conjugated linoleic acids in regulating intramuscular fat deposition.
Elife
March 2025
College of Animal Sciences, Zhejiang University, Hangzhou, China.
Conjugated linoleic acids (CLAs) can serve as a nutritional intervention to regulate quality, function, and fat infiltration in skeletal muscles, but the specific cytological mechanisms remain unknown. Here, we applied single-nucleus RNA-sequencing (snRNA-seq) to characterize the cytological mechanism of CLAs regulates fat infiltration in skeletal muscles based on pig models. We investigated the regulatory effects of CLAs on cell populations and molecular characteristics in pig muscles and found CLAs could promote the transformation of fast glycolytic myofibers into slow oxidative myofibers.
View Article and Find Full Text PDFThe role of the PKCζ/JNK signaling pathway in regulating the development of femoral head necrosis.
Braz J Med Biol Res
March 2025
Department of Orthopedics, Zhuji People's Hospital of Zhejiang Province, Shaoxing, China.
Osteonecrosis of the femoral head (ONFH) is a debilitating condition characterized by the death of bone cells in the hip joint, resulting in profound disability. This condition has a significant global prevalence. Glucocorticoid (GC)-induced apoptosis of bone cells serves as a crucial cellular mechanism underlying ONFH.
View Article and Find Full Text PDFG protein-coupled oestrogen receptor regulates branched-chain amino acid metabolism through c-Jun N-terminal kinase.
FEBS Lett
March 2025
Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati, India.
Branched-chain amino acids (BCAA) are essential requirements for overall protein turnover, signalling and energy balance, and dysregulation of their metabolic pathway has been associated with many pathophysiological events. Despite the importance of BCAA in human health, our understanding of their metabolic regulation is limited. Here, we present evidence that G protein-coupled oestrogen receptor (GPER) activation inhibits the key BCAA metabolic regulatory enzyme branched-chain α-keto acid dehydrogenase complex (BCKDH) by phosphorylating S293.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!