Metabolic inflammation (metaflammation) is characteristic of obesity-related metabolic disorders, associated with increased risk of development of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), or cardiovascular disease. Metaflammation refers to a chronic, low-grade systemic inflammation as opposed to the classical transient and acute inflammatory responses of the innate immune system. Metaflammation is driven by a range of adverse dietary factors, including saturated fatty acids and some sugars, suggesting that certain dietary triggers may be particularly relevant beyond simple excessive dietary intake presenting as obesity. Importantly, obese patients with diabetes have a higher risk of infection and display gut microbiota profiles characteristic of dysfunctional immunity. Targeting metaflammation has also emerged as a strategy to attenuate metabolic disease. In this review we explore how different nutrition interventions may reconfigure disrupted metabolic inflammation in type 2 diabetes and nonalcoholic fatty liver disease by reestablishing a conventional proinflammatory program in innate immune cells and/or correcting dysbiosis to dampen systemic inflammation. We begin by reviewing concepts of metabolic inflammation relating to IL-1β inflammation and how it is induced by dietary and/or metabolic stressors. We then explore whether and how dietary interventions may attenuate processes pertaining to metaflammation, either directly or indirectly via the microbiome. Hence, we hope to bring new perspectives to alleviate the metaflammation typifying metabolic disease.
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http://dx.doi.org/10.1016/j.jaci.2020.08.013 | DOI Listing |
Cell Rep
January 2025
School of Infection, Inflammation and Immunology, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK. Electronic address:
Interleukin (IL)-7 promotes T cell expansion during lymphopenia. We studied the metabolic basis in CD4 T cells, observing increased glucose usage for nucleotide synthesis and oxidation in the tricarboxylic acid (TCA) cycle. Unlike other TCA metabolites, glucose-derived citrate does not accumulate upon IL-7 exposure, indicating diversion into other processes.
View Article and Find Full Text PDFCell Mol Biol (Noisy-le-grand)
January 2025
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Türkiye.
J Cell Mol Med
January 2025
Ataturk Vocational School of Health Services, Department of Medical Laboratory Techniques, Afyonkarahisar Health Sciences University, Afyonkarahisar, Turkey.
The development and progression of osteoarthritis (OA) are believed to involve inflammation. This study aimed to investigate the effects of applying therapeutic ultrasound (US) to human osteoarthritic chondrocytes in continuous and pulsed modes on cell proliferation and proinflammatory cytokine levels. Human osteoarthritic chondrocytes (HC-OA 402OA-05a) were proliferated in appropriate media and then seeded into culture plates.
View Article and Find Full Text PDFPak J Pharm Sci
January 2025
Department of Psychiatry, Wenzhou Seventh People's Hospital, Wenzhou, China.
The objective of this study was to evaluate the therapeutic effects of Chiglitazar combined with Rosa roxburghii Tratt (RRT) in inpatients diagnosed with psychiatric disorders and antipsychotic-induced metabolic syndrome (MetS).100 cases were included and divided into the Siglitazar group (n=50) and the Siglitazar + RRT group (n=50) Anthropometric measurements, lipid and glucose metabolism indicators, inflammatory markers and PANSS scores were assessed at baseline, 8 weeks and 12 weeks post-treatment. Both treatment groups exhibited significant reductions in waist circumference and improvements in lipid profiles and glucose metabolism indicators over the 12-week study period.
View Article and Find Full Text PDFXi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Neonatology, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200062, China. *Corresponding author, E-mail:
Necrotizing enterocolitis (NEC) is an intestinal inflammatory and necrotic disease seen in premature infants, and remains the leading cause of death resulted from gastrointestinal diseases in premature infants. The specific pathogenesis of NEC is still unclear. In recent years, a lot of studies have reported that Toll-like receptor 4 (TLR4) plays a key role in the pathogenesis of NEC.
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