Ask about this productRelated genes to: FGF21 antibody
- Gene:
- FGF21 NIH gene
- Name:
- fibroblast growth factor 21
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2014-11-18
Related products to: FGF21 antibody
Related articles to: FGF21 antibody
- Depressive symptoms in late life are often accompanied by altered appetite and dietary behavior, yet the biological mechanisms linking metabolic signals to eating behavior remain poorly understood. Fibroblast growth factor 21 (FGF21) is a carbohydrate responsive hepatokine that suppresses sweet preference via central pathways. We examined whether depressive symptoms modify the association between FGF21 and sucrose intake in Japanese older adults, focusing on post-glucose FGF21 response. - Source: PubMed
Publication date: 2026/08/22
Sakamoto ShotaKakehi SaoriKaga HideyoshiTabata HirokiSomeya YukiNaito HitoshiTajima TsubasaIto NaoakiKogai ToshikiYoshizawa YasuyoKawamori RyuzoWatada HirotakaTamura Yoshifumi - The liver, with its unique physiology and powerful metabolic activity, represents an ideal 'protein factory' for gene therapy. Yet efficient, cell-specific transfection of hepatocytes remains a significant challenge. To address this, we engineered a novel ternary nanocomplex through a modular design. A stable binary core was first formed by electrostatically condensing plasmid DNA (pDNA) with a fluorinated ROS-cleavable (TK) polyethylenimine (FRP), enhancing cellular uptake and facilitating endosomal escape. This core was subsequently coated with a surface layer of galactose-modified hyaluronic acid-polyethylene glycol (GPH), enabling dual-receptor-mediated hepatocyte targeting. Galactose (Gal) engages the asialoglycoprotein receptor (ASGPR) and hyaluronic acid (HA) interacts with CD44 on hepatocytes, while the PEG corona improves complex stability. studies demonstrated that the FRP/pDNA and GP (GPH-coated FRP/pDNA) complexes achieved highly efficient and specific gene transfection in AML12 hepatocytes, significantly outperforming the commercial reagent Lipofectamine 3000. In a cellular model of metabolic dysfunction-associated steatotic liver disease (MASLD), successful FGF21 gene delivery FRP or GP effectively alleviated lipid accumulation. This work highlights the potential of the GP nanocomplex as a powerful platform for hepatocyte-targeted gene delivery, offering a promising strategy for treating liver-centric metabolic disorders. - Source: PubMed
Publication date: 2026/08/20
Liu XiaoweiWang MeilinLiao JiahaoFu WenguangYang Suleixin - Regular physical activity exerts systemic metabolic benefits that are pivotal for preventing and managing metabolic diseases. These effects are mediated in part by exerkines, which are signaling molecules released from various organs in response to exercise. Exerkines encompass polypeptides, nucleic acids, and bioactive lipids that collectively orchestrate metabolic adaptations. Recent metagenomic analyses have identified the gut microbiota as an additional source of exercise-responsive factors that modulate host metabolism and may influence individual responsiveness to training. Together, these diverse exerkines coordinate interorgan communication, enhance insulin sensitivity, maintain glucose and lipid homeostasis, and modulate inflammatory pathways. This review summarizes representative exerkines from skeletal muscle, adipose tissue, and liver, including interleukin-6, myostatin, fibroblast growth factor 21, adiponectin, and growth differentiation factor 15, which have shown promising therapeutic efficacy in preclinical studies and clinical trials for complex metabolic diseases. We also discuss microbiota-derived metabolites such as short-chain fatty acids that improve glucose and lipid metabolism, as well as host-derived metabolites including N-lactoyl-phenylalanine, betaine, and β-aminoisobutyric acid that regulate appetite, substrate utilization, and insulin action. Furthermore, we highlight recent progress in understanding how dynamic regulation of these exerkines mediates the metabolic benefits of exercise and their potential as targets for precision management of metabolic diseases. Understanding these molecular mediators of exercise provides a framework for integrating physical activity with pharmacological and nutritional strategies to improve metabolic health. - Source: PubMed
Publication date: 2026/08/19
Jin LeigangLin YifenZheng YixuanWang AnliLiao PengLuo YuchengSui ZhonghengNi XiayunZhang JiananShen QingXu Aimin - Biallelic pathogenic variants in SORD (Sorbitoldehydrongenase gene), encoding sorbitol dehydrogenase, are a common cause of autosomal recessive axonal Charcot-Marie-Tooth disease type 2 (CMT2). Recent evidence suggests direct involvement of skeletal muscle in addition to peripheral nerve degeneration. We investigated muscle biopsies from 4 genetically confirmed CMT-SORD patients using an integrative approach. Histological evaluation revealed features of chronic denervation with grouped fiber atrophy, fiber-type grouping and central nuclei, ie, non-specific neurogenic muscle atrophy. Ultrastructural studies demonstrated mitochondrial abnormalities and expansion of the sarcoplasmic reticulum (SR). Proteomic profiling identified 220 significantly dysregulated proteins in CMT-SORD muscle, including alterations in mitochondrial complex I components, redox enzymes, and metabolic regulators distinct from changes observed in other rare recessive CMTs. Quantitative PCR validated increased levels of NNMT, POSTN, TACO1, as well as complement and immunomodulatory factors, suggesting mitochondrial stress, compensatory metabolic activation and tissue remodeling. Despite mitochondrial vulnerability, serum studies indicated that GDF-15 and FGF-21 did not appear to be suitable biomarkers for CMT-SORD. These findings demonstrate that SORD deficiency induces molecular and structural changes in skeletal muscle that extend beyond denervation, implicating impaired sorbitol metabolism, oxidative stress, and mitochondrial dysfunction as intrinsic myopathic features of SORD-related CMT2. They indicate the need for therapeutic strategies targeting both neuronal and muscular compartments. - Source: PubMed
Publication date: 2026/08/19
Kölbel HeikeHentschel AndreasPreuße CorinnaTiet MayDohrn Maike FMuhmann Davidvan den Ameele JelleChen LeiSchara-Schmidt UlrikeWeis JoachimHorvath RitaMensch AlexanderRoos Andreas - The Paris International Liver Meeting (January 19-21, 2026) brought together leading hepatology experts to discuss transformative advances in chronic liver disease management. The meeting highlighted pivotal developments reflecting the field's evolution from disease characterisation toward precision, mechanism-based therapeutics. Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), were highlighted, marking the transition to an era of approved disease-modifying therapies. Resmetirom and semaglutide are now approved for MASH with F2-F3 fibrosis, with a robust pipeline generating anti-fibrotic signals through FGF21 analogs, pan-peroxisome proliferator-activated receptor (PPAR) agonists, and incretin-based dual and triple agonists. Non-invasive tests have evolved beyond their original diagnostic role to enable prognostic stratification, screening of at-risk populations, treatment selection, and monitoring of therapeutic response. This evolution is not limited to MASLD, but extends to other chronic liver diseases, including primary biliary cholangitis (PBC) and portal hypertension, as highlighted by the recommendations of the Baveno Consensus Workshops. Hepatitis B and D are moving toward functional cure strategies, with simplified HBV treatment algorithms based on fibrosis and viral load, supported by biomarkers for risk stratification and safe treatment discontinuation. In parallel, HDV management is transitioning from a severe disease to one with emerging suppressive and potential curative l through bulevirtide and novel HBsAg-targeting and RNA-silencing therapies, respectively. Management of PBC has advanced with novel PPAR agonists that improve cholestatic biochemistry and pruritus, supported by individualised risk stratification. However, significant treatment gaps persist, with fewer than half of eligible PBC patients receiving second-line therapy, and fatigue remains a major unmet clinical need. Furthermore, effective pharmacotherapies for primary sclerosing cholangitis (PSC) remain a major challenge, and no approved disease-modifying treatments are currently available. Finally, for patients with hepatocellular carcinoma (HCC), immunotherapy combinations can achieve unprecedented long-term survival in selected populations of patients. Collectively, these advances define a new era of hepatology centered on precision medicine, earlier intervention, and mechanism-driven therapeutic strategies. - Source: PubMed
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