FGF19
- Known as:
- FGF19
- Catalog number:
- GTX101012
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- FGF19
Related genes to: FGF19
- Gene:
- FGF19 NIH gene
- Name:
- fibroblast growth factor 19
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: FGF19
Related articles to: FGF19
- Post-pancreatitis diabetes mellitus after acute pancreatitis (PPDM-A) is increasingly recognized as a distinct metabolic complication rather than a simple subtype of type 2 diabetes. This narrative review summarizes current evidence on PPDM-A, with emphasis on terminology, diagnostic timing, epidemiology, pathophysiology, risk factors, clinical phenotypes, screening, prevention, and long-term follow-up. A structured literature search was conducted in PubMed/MEDLINE, Scopus, and Google Scholar to identify relevant studies. PPDM-A may develop after mild, moderately severe, or severe acute pancreatitis, although the risk is greatest in patients with pancreatic necrosis, recurrent attacks, exocrine pancreatic dysfunction, obesity, dyslipidemia, fatty liver disease, metabolic comorbidities, and marked in-hospital glycemic variability. A major diagnostic challenge is distinguishing transient stress hyperglycemia and previously unrecognized diabetes from incident PPDM-A. Formal diagnosis should generally be established no earlier than 90 days after the index episode of acute pancreatitis to minimize misclassification due to transient stress-related dysglycemia. Follow-up assessment should combine fasting plasma glucose and HbA1c, whereas a 75-g oral glucose tolerance test (OGTT) may provide greater sensitivity during early recovery, particularly when HbA1c is unreliable, results are borderline or discordant, or isolated postprandial dysglycemia is suspected. Current evidence indicates that PPDM-A develops through interacting pathogenic domains, including pancreatic endocrine injury with impaired β-cell reserve, metabolic dysregulation characterized by insulin resistance and persistent inflammation, exocrine pancreatic dysfunction with nutritional consequences, and emerging mechanisms involving gut microbiome alterations, bile acid-FGF19 signaling, and extracellular vesicle-mediated communication. Available data support a trajectory-based model in which some patients recover normal glucose metabolism, some develop persistent intermediate dysglycemia, and others progress to overt diabetes over months or years. Structured post-discharge surveillance, risk-stratified follow-up, assessment of exocrine dysfunction, and prevention of recurrent pancreatic injury are essential for improving early detection, reducing diagnostic misclassification, and optimizing long-term clinical outcomes. - Source: PubMed
Publication date: 2026/08/12
Chooklin SergeChuklin Serhii - Traditional risk factors do not fully account for the residual cardiometabolic risk of major adverse cardiovascular events (MACE) in coronary artery disease (CAD). We aimed to identify circulating metabolic signatures associated with MACE susceptibility and uncover potential pathobiological mechanisms underlying the gut-liver-heart axis. - Source: PubMed
Publication date: 2026/08/12
Lin Min-QingWong Chun-KaAu Ka-WingCheung Chloe Yu-YanLau Yee-ManLiao Song-YanLam Karen Siu-LingXu AiminTse Hung-Fat - This study aimed to explore the association of long-term left ventricular assist device (LVAD) support with changes in inflammation and cardiac remodelling in subjects with advanced heart failure (HF). - Source: PubMed
Publication date: 2026/08/11
Hlavacek DanielCinkajzlova AnnaKollar MarekKasperova Barbora JuditaMelenovsky VojtechMraz MilosHaluzik MartinIvak PeterStemberkova Hubackova Sona - Endocrine fibroblast growth factors (FGF19 subfamily) play a key role in regulating metabolic homeostasis in vertebrates. However, their functional diversification in salmonids remains poorly understood. In this study, we conducted an integrative characterisation of Fgf19 and Fgf21 signalling in rainbow trout (Oncorhynchus mykiss) by combining phylogenetic, structural and expression analyses. Phylogenetic analyses revealed the conservation of single fgf19 and fgf21 genes, despite the extensive expansion of receptors post-Ss4R (salmonid-specific fourth-round whole genome duplication). Structural modelling and molecular dynamics simulations demonstrated the stable interactions of both ligands to multiple Fgfr isoforms, with receptor-specific energetic profiles and conserved core interaction residues. Tissue expression profiling revealed clear differences from mammalian models, such as predominant hepatic fgf19 expression and the absence of hepatic fgf21 under basal conditions. In addition, there were complex and tissue-dependent distributions of fgfr and klotho transcripts. These findings support a receptor-driven diversification model of endocrine Fgf signalling in salmonids, suggesting enhanced endocrine plasticity associated with the retention of receptors following post-genomic duplication. Taken together, our findings provide new insights into the structural and regulatory organisation of endocrine Fgf signalling, as well as its potential role in metabolic regulation in rainbow trout. - Source: PubMed
Publication date: 2026/08/06
Calo JessicaFerreiro DavidPérez-Tierra GabrielSoengas José LuisVelasco Cristina - Cholestatic liver fibrosis is a progressive liver disease characterized by disrupted bile acid homeostasis, persistent inflammation, and excessive extracellular matrix deposition, for which effective pharmacological therapies remain limited. Although Notoginsenoside R1 (NG-R1), a major bioactive saponin from Panax notoginseng, exhibits anti-fibrotic activity in experimental liver injury, its disease-specific mechanism in cholestatic liver fibrosis remains unclear. Here, C57BL/6 mice subjected to bile duct ligation (BDL) were treated with NG-R1 for 14 days. NG-R1 significantly improved liver function, alleviated hepatic and intestinal injury, suppressed inflammatory responses, and attenuated liver fibrosis. Mechanistically, NG-R1 restored intestinal FXR-FGF15 endocrine signaling by enhancing ileal FXR expression and increasing circulating FGF15 levels, thereby contributing to improved gut-liver bile acid homeostasis. Consistent with these changes, hepatic CYP7A1 expression was reduced, bile acid transporters were coordinately regulated (upregulation of BSEP and OSTα/β and downregulation of NTCP), and hepatic bile acid accumulation was decreased. In Caco-2 cells, NG-R1 increased the expression of FXR, FGF19, Occludin, and ZO-1, whereas these effects were partially abolished by the FXR antagonist guggulsterone, supporting direct activation of intestinal FXR signaling. NG-R1 also partially corrected BDL-induced gut microbial dysbiosis. Collectively, these findings suggest that modulation of the intestinal FXR-FGF15 endocrine axis and restoration of gut-liver bile acid homeostasis contribute to the protective effects of NG-R1 against cholestatic liver fibrosis, providing a mechanistic basis for its therapeutic potential. - Source: PubMed
Publication date: 2026/08/05
Yang MinMa QiaolianYang BairongLi JieChang WeiyuCui XiumingNiu BenGe Feng