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
- - Source: PubMed
Publication date: 2026/05/12
Chalasani NagaTillman Erik JBilles Sonja KRolph TimothyNoureddin Mazen - : Glucagon-like peptide-1 (GLP-1) is a nutritionally regulated incretin involved in the coordination of intestinal, hepatic, and adipose metabolic responses. Although plant-derived extracts are increasingly investigated for their metabolic effects, mechanistic evidence integrating multiple metabolic tissues remains limited. This study aimed to investigate the molecular effects of a combination of plant-derived extracts in an integrated in vitro gut-liver-adipose model. : Differentiated Caco-2 monolayers were exposed to a standardised combination of plant-derived extracts obtained from , , and . GLP-1 secretion and epithelial barrier integrity were assessed. Conditioned media from intestinal cells were applied to HepG2 hepatocytes, and downstream effects on lipid metabolism-related pathways were evaluated. Subsequently, conditioned media from hepatic cells were applied to differentiated 3T3-L1 adipocytes to assess lipid accumulation and metabolic signalling. : Exposure of intestinal cells to the extract combination significantly increased GLP-1 secretion without altering epithelial barrier integrity. Intestinal conditioned media were associated with reductions in intracellular triglyceride levels in hepatocytes and with modulation of markers linked to lipid handling, including resistin, FGF21, SREBP-1c, NRF2, Src, AMPK, SIRT1, and PGC1α, suggesting GLP-1-associated effects. In adipocytes, hepatic conditioned media decreased lipid accumulation and increased the levels of metabolic markers associated with adipocyte browning-related signalling, including UCP1, NOS, SIRT1, and STAT3. : Within the limitations of this in vitro multi-organ model, these findings suggest that the tested combination of plant-derived extracts modulates cellular pathways related to GLP-1-associated metabolic signalling across intestinal, hepatic, and adipose systems. These results should be interpreted as mechanistic and hypothesis-generating, and further in vivo and clinical studies are required to confirm their physiological relevance. - Source: PubMed
Publication date: 2026/04/28
Uberti FrancescaGalla RebeccaMulè SimoneParini FrancescaMolinari Claudio - Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder shaped by genetic variants and network-level interactions beyond obesity and insulin resistance. This study aimed to define the genetic and proteomic architecture of MASLD by integrating GWAS and plasma proteomic profiling from the UK Biobank. Genome-wide association analyses were conducted under additive and dominant models, with functional annotations performed using SIFT, PolyPhen-2, PROVEAN, REVEL, CADD, MutationTaster, and conservation metrics (GERP++, phyloP, phastCons, and B-statistic). Differential protein expression was assessed using the Olink platform, and STRING was applied for protein-protein interaction analysis. MASLD patients showed male predominance and significant differences in hepatic (AST, ALT, GGT, PDFF), metabolic (glucose, triglycerides, TyG index), and inflammatory markers (CRP, neutrophils, NLR, CAR). GWAS confirmed (rs738409, I148M) and (rs58542926, E167K) as major risk variants, while and showed weaker but conserved associations. Proteomics revealed downregulation of IGFBP2, IGFBP1, PON3, CKB, and APOF and upregulation of CPM, IGSF9, GUSB, ACY1, AFM, LEP, and GSTA1/3. PPI analysis identified ADIPOQ, LEP, FGF21, and ADH1B as central hubs in metabolic and inflammatory regulation. MASLD should be regarded as a network disease involving lipid metabolism, insulin/IGF signaling, mitochondrial function, and ECM-inflammatory pathways. These findings highlight and as major genetic drivers, while , , and peripheral proteins contribute regulatory roles, suggesting novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/28
Kang Sang WookKim Su KangBan Ju YeonPark Min Su - This study aimed to investigate the genetic causal relationship between obesity and urolithiasis using a two-sample Mendelian randomization (MR) approach. It further explored the potential mediating role of inflammatory factors in this causal pathway. Single nucleotide polymorphisms (SNPs) associated with body mass index, waist-to-hip ratio, and urolithiasis were obtained from publicly available genome-wide association study datasets and employed as instrumental variables. A bidirectional two-sample MR analysis was performed to assess the causal effect of obesity on the risk of urolithiasis. The inverse variance weighted method served as the primary analytical strategy, supplemented by sensitivity analyses using the simple mode, weighted median, weighted mode, and MR-Egger regression methods. To explore potential mediation, mediation MR and multivariable MR analyses were conducted. Additional sensitivity analyses were carried out to evaluate the robustness of the findings. MR analysis revealed a significant positive causal associations of both body mass index (odds ratio = 1.190, 95% confidence interval: 1.082-1.308, P = 3.27 × 10-4) and waist-to-hip ratio (odds ratio = 1.245, 95% confidence interval: 1.107-1.401, P = 2.63 × 10-4) with urolithiasis. Mediation analysis identified fibroblast growth factor 21 as a significant mediator in the pathway linking obesity to urolithiasis. This study provides genetic evidence supporting a causal association between obesity and an increased risk of urolithiasis. The inflammatory marker fibroblast growth factor 21 may partially mediate this relationship. - Source: PubMed
Chen JinganSong ChengChen ChongyangYou MingpoChen Bin - Gestational diabetes mellitus (GDM) is among the most common complications during pregnancy. It is characterized by hyperglycemia that is first identified during pregnancy, typically in the second or third trimesters. However, the relatively late diagnosis limits timely glycemic control and preventive interventions. The present study aimed to evaluate the diagnostic potential of serum afamin and fibroblast growth factor 21 (FGF21) as early predictive biomarkers for GDM. The study involved 17 healthy pregnant women and 26 pregnant women with one or more risk factors for developing GDM. Fasting blood samples were collected in the 1st (8-12 weeks) and 2nd (22-28 weeks) trimesters of pregnancy. Higher serum afamin level was observed in GDM group at 1st trimester (92.9 ± 34.51 ng/ml) compared to normal pregnancy (57.1 ± 25.15 ng/ml). At 2nd trimester, no significant difference in circulated serum afamin was noted between the two groups (73.2 ± 20.30 ng/ml and 68.3 ± 18.74 ng/ml, for GDM and normal pregnancy, respectively). The study also indicated higher serum FGF21 in pregnancy complicated with GDM compared to normal pregnancy at both sampling times (1st trimester: 140.8 ± 32.83 and 97.1 ± 21.43 Pg/ml for GDM and normal; 2nd trimester: 123.8 ± 41.85 and 89.4 ± 32.53 Pg/ml for GDM and normal). At 1st trimester no significant correlations were noted between afamin and all parameters in normal pregnancy, however, in pregnancy complicated with GDM, positive correlations were noted between the hormone and the diabetic profile parameters and baby birth weight. At both 1st and 2nd trimesters, no correlation between FGF21 with all tested parameters, either in normal or complicated pregnancies. ROC curve analysis demonstrated that afamin (AUC = 0.826, P < 0.001), FGF21 (AUC = 0.877, P < 0.001), and their combined assessment (AUC = 0.9, P < 0.001) were strong predictors of GDM development at 1st trimester before the development of the disease than expectant mothers with normal pregnancy. - Source: PubMed
Publication date: 2026/05/11
Sabri Abdelrahman OElhady Mostafa MHemida Eman H AZaki Radwa M MNoureldeen Amani F H