Journal of physiology and biochemistry最新文献

{"title":"Activation of TRPA1 prevents metabolic dysfunction-associated steatotic liver disease in diet-induced obese mice through stimulating the AMPK/CPT1A signaling pathway.","authors":"Dan Wang, Sen Liu, Jindong Wan, Shichao Chen, Kaige Feng, Jixin Hou, Yi Yang, Peijian Wang","doi":"10.1007/s13105-025-01081-y","DOIUrl":"10.1007/s13105-025-01081-y","url":null,"abstract":"<p><p>Mitochondrial dysfunction plays an important role in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). Transient receptor potential ankyrin-1 (TRPA1) activation improves mitochondrial dysfunction in a variety of cells. The present study tested the effects of Trpa1 knockout and activation in diet-induced MASLD in mice and palmitate-induced lipid deposition in HepG2 cells. Mice were fed with a high-fat diet (HFD) for 24 weeks to establish the animal model of MASLD. TRPA1 was downregulated in the liver of mice with MASLD and in HepG2 cells with palmitate-treated steatosis. Compared with HFD-fed wild-type mice, Trpa1^-/- mice on HFD demonstrated exacerbated lipid deposition and mitochondrial damage in hepatocytes. AMP-activated protein kinase (AMPK) and carnitine palmitoyl transferase 1 A (CPT1A) in the liver were downregulated by HFD and to a greater extent in Trpa1^-/- mice. Similarly, knockdown of Trpa1 worsened palmitate-induced lipid accumulation, mitochondrial morphological damage, mitochondrial ATP reduction and dysfunction, and downregulation of AMPK and CPT1A in HepG2 cells. Oral administration of cinnamaldehyde significantly reduced lipid deposition and improved mitochondrial damage in hepatocytes, which were abolished by HC030031, a TRPA1 antagonist. In HepG2 cells, cinnamaldehyde remarkably attenuated palmitate-induced lipid accumulation, mitochondrial damage, ATP reduction, and mitochondrial dysfunction, which were blunted by HC030031. Cinnamaldehyde reversed downregulation of AMPK and CPT1A in the liver of HFD-fed mice and palmitate-treated HepG2 cells through activating TRPA1. In conclusion, these findings suggest that the downregulation of TRPA1 may be involved in the pathogenesis of MASLD and activation of TRPA1 holds potential in the prevention and treatment of MASLD.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"359-373"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Soluble alpha-klotho and 25-hydroxivitamin D are not associated with brown adipose tissue metabolism in young healthy adults.","authors":"Francisco J Amaro-Gahete, Héctor Vázquez-Lorente, Guillermo Sanchez-Delgado, Jonatan R Ruiz","doi":"10.1007/s13105-025-01072-z","DOIUrl":"10.1007/s13105-025-01072-z","url":null,"abstract":"<p><strong>Background: </strong>Soluble Alpha-Klotho (S-αklotho) protein and 25-Hydroxyvitamin D (25-OH-D) have emerged as potential modulators for activating and recruiting Brown Adipose Tissue (BAT). The present study aimed to investigate whether circulating S-αklotho and 25-OH-D levels are related to BAT volume, ¹⁸Fluorine-Fluorodeoxyglucose (¹⁸F-FDG) uptake, and BAT radiodensity in young healthy adults.</p><p><strong>Methods: </strong>A total of 128 participants (68% women) aged 18-25 years old participated in this cross-sectional study. Serum levels of S-αklotho were determined by a solid-phase sandwich enzyme-linked immunosorbent assay kit and 25-OH-D serum levels were analyzed using a competitive chemiluminescence immunoassay, both in blood samples collected after an overnight fast. All participants underwent a personalized cold exposure to determine their BAT volume, ¹⁸F-FDG uptake, and radiodensity, using a static positron emission tomography combined with computed tomography scan.</p><p><strong>Results: </strong>After adjusting for multiple covariates, serum levels of S-αklotho (all R² ≤ 0.228 and P ≥ 0.364), 25-OH-D as continuous (all R² ≤ 0.242 and P ≥ 0.088) or by vitamin D status (all R² ≤ 0.767 and P ≥ 0.061) were not associated with either BAT volume and ¹⁸F-FDG uptake, or BAT radiodensity.</p><p><strong>Conclusion: </strong>Serum S-αklotho and 25-OH-D levels within the physiological range are not related to BAT-related variables in young healthy adults. Further studies are needed to fully understand the underlying mechanisms involved in BAT metabolism in humans. (ACTIBATE; ClinicalTrials.gov identifier: not applicable).</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"291-298"},"PeriodicalIF":4.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary-Based Diabetes Risk Score and breast cancer: a prospective evaluation in the SUN project.","authors":"Inmaculada Aguilera-Buenosvinos, Miguel A Martínez-González, Andrea Romanos-Nanclares, Rodrigo Sánchez-Bayona, Carlos E de Andrea, Ligia J Domínguez, Estefania Toledo","doi":"10.1007/s13105-024-01036-9","DOIUrl":"10.1007/s13105-024-01036-9","url":null,"abstract":"<p><p>An association between type 2 diabetes (T2D) and breast cancer risk has been reported. This association can be potentially explained by alteration of the insulin/IGF system. Therefore, we aimed to prospectively investigate whether a previously reported Dietary-Based Diabetes Risk Score (DDS) inversely associated with T2D was also associated with breast cancer risk in the SUN (\"Seguimiento Universidad de Navarra\") cohort. We followed up 10,810 women (mean age = 35 years, SD = 11 years) for an average of 12.5 years during which 147 new cases of invasive breast cancer were diagnosed. A validated 136-item FFQ was administered at baseline and after 10 years of follow-up. The DDS (range: 11 to 55 points) positively weighted vegetables, fruit, whole cereals, nuts, coffee, low-fat dairy, fiber, PUFA; while it negatively weighted red meat, processed meats, and sugar-sweetened beverages. The DDS was categorized into tertiles. Self-reported medically diagnosed breast cancer cases were confirmed through medical records. We found a significant inverse association between the intermediate tertile of the DDS score and overall breast cancer risk (Hazard ratio, HR_{T2 vs. T1}= 0.55; 95% CI: 0.36-0.82) and premenopausal breast cancer risk (HR_T2= 0.26; 95% CI: 0.13-0.53), but not for the highest tertile. This association was stronger among women with a BMI < 25 kg/m² (p_interaction: 0.029). In conclusion, moderate adherence to the DDS score was associated with a lower risk of breast cancer, especially among premenopausal women and women with a lower BMI. These findings underscore the importance of antidiabetic diet in reducing the risk of breast cancer.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"459-469"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: miR-9 inhibits the metastatic ability of hepatocellular carcinoma via targeting beta galactoside alpha-2,6-sialyltransferase 1.","authors":"Yi Han, Yubo Liu, Xirao Fu, Huang Huang, Cheng Zhang, Wenli Li, Jianing Zhang","doi":"10.1007/s13105-025-01074-x","DOIUrl":"10.1007/s13105-025-01074-x","url":null,"abstract":"<p><p>This erratum addresses corrections to the article titled 'miR-9 inhibits the metastatic ability of hepatocellular carcinoma via targeting beta galactoside alpha-2,6-sialyltransferase 1' published in Journal of physiology and biochemistry on 13 July 2018. In the original article, the transwell microscope images presented in Fig. 4C of the Hca-P mimic group and Fig. 5E of Hca-P PF group were accidentally misused during the assembly of the figures. These errors have now been corrected and does not change the conclusions of the study. The authors apologize for this oversight and any confusion it may have caused.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"375-377"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial special issue: Frontiers in cancer, obesity and metabolism.","authors":"Ana B Crujeiras, José Ángel Martínez-Climent, Miguel Burgos","doi":"10.1007/s13105-025-01107-5","DOIUrl":"10.1007/s13105-025-01107-5","url":null,"abstract":"<p><p>This Special Issue contains 7 contributions elaborated in the context of the workshop \"Frontiers in Cancer, Obesity and metabolism\" organized by the Journal of Physiology and Biochemistry (Pamplona, Spain, 2022). It contains basic, translational and epidemiological research that sheds light in our understanding of the molecular mechanisms underlying how the excess of adipose tissue in obesity promotes tumor growth and progression, and highlights the role of nutrition in preventing tumor development and improving treatment outcomes in cancer patients with obesity and related comorbidities. Two review articles and one systematic review are included in this special issue, which describe the effects of nutrient deprivation that potentially enhance cancer immunotherapy, reveal the importance of the glucose transporter GLUT12 in obesity and cancer, and analyze recently described molecular mechanisms that connect obesity and the development of different types of cancer. Additionally, four original articles demonstrate a metabolic inflammatory pathway in patients with obesity in which dysfunctional adipose tissue alters the tumor microenvironment favoring tumor progression, offers mechanistic support for exploring low-fat ketogenic diets as adjuvant therapy in obesity-related breast cancer prevention or therapy by linking nutritional ketosis to epigenetic regulation of cancer‑related genes, indicate the use of genes related to amino acid metabolism as prognostic biomarkers in breast cancer, and associate a moderate adherence to a dietary-based diabetes-risk score to a lower risk of breast cancer among premenopausal women and women with low body mass index. Globally, the articles included in this special issue contribute to better understand the molecular mechanisms beyond nutritional aspects linked to obesity and cancer development.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"379-381"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ESR1-dependent suppression of LCN2 transcription reverses autophagy-linked ferroptosis and enhances sorafenib sensitivity in hepatocellular carcinoma.","authors":"Mingfang Xu, Tran Sy Trung, Zhiyong Zhu, Shijia Li, Shicheng Gong, Nuo Cheng, Peng Zhou, Shuai Wang","doi":"10.1007/s13105-025-01073-y","DOIUrl":"10.1007/s13105-025-01073-y","url":null,"abstract":"<p><p>Sorafenib resistance is a significant hurdle in the treatment landscape of hepatocellular carcinoma (HCC). Lipocalin 2 (LCN2), a secretory glycoprotein that transports lipophilic molecules across cell membranes, is thought to affect the s therapeutic efficacy of sorafenib. Despite its importance, the detailed regulatory pathways involving LCN2 are still being deciphered. We probed the correlation between LCN2 expression and sorafenib resistance in HCC cells. Through the modulation of LCN2 levels, we investigated its role in cell proliferation, apoptosis, and its regulatory effects on autophagy-driven ferroptosis. With the aid of hTFtarget and JASPAR databases, ESR1 was pinpointed as a transcriptional inhibitor of LCN2. The impact of the ESR1-LCN2 axis on sorafenib resistance in HCC was then examined in vitro and validated in a xenograft tumor mouse model. In HCC cells, elevated LCN2 levels were found to be associated with resistance to sorafenib. Depletion of LCN2 resulted in attenuated HCC cell growth and elevated rates of apoptosis and ferroptosis. Overexpression of LCN2 had the opposite effect, promoting cell proliferation and suppressing cell death pathways, a response that could be overridden by autophagy agonists. ESR1 suppressed LCN2 transcription, which in turn activated autophagy-mediated ferroptosis, mitigating sorafenib tolerance in HCC and enhancing the therapeutic index. ESR1 targets LCN2 transcription to initiate autophagy-driven ferroptosis, thereby reducing sorafenib resistance in HCC cells.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"299-312"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Matrix stiffening induces hepatocyte functional impairment and DNA damage via the Piezo1‒ERK1/2 signaling pathway.","authors":"Yanan Fan, Caizhelin An, Zhihui Wang, Jia Luo, Wenbin Wang, Qing Luo, Guanbin Song","doi":"10.1007/s13105-025-01070-1","DOIUrl":"10.1007/s13105-025-01070-1","url":null,"abstract":"<p><p>Hepatocytes are the primary functional cells in the liver, and the malignant transformation of hepatocytes significantly contributes to hepatocellular carcinoma (HCC) progression. Liver fibrosis and cirrhosis caused by extracellular matrix (ECM) remodeling during liver lesions is a pivotal driver of HCC. However, the impact of matrix stiffness on hepatocytes and the underlying molecular mechanisms are not fully understood. Herein, using gelatin/sodium alginate hydrogels with different stiffnesses to simulate the change of matrix stiffness during liver lesions, we found that matrix stiffening leads to a notable decrease in the expression of hepatocyte nuclear factor 4α (HNF4α) and functional hepatocyte genes and a significant increase in the expression of interleukin 6 (IL‒6) in human hepatocyte line L‒02 cells, indicating obvious damage of hepatocyte function. In addition, matrix stiffening causes extensive DNA damage to L‒02 cells. Mechanistically, matrix stiffening upregulates piezo‒type mechanosensitive ion channel component 1 (Piezo1) expression and activates extracellular signal‒regulated kinase 1/2 (ERK1/2) signaling. Piezo1 knockdown suppresses matrix stiffening‒induced functional impairment and DNA damage in L‒02 cells. Moreover, Piezo1 knockdown blocks matrix stiffening‒activated ERK1/2 signaling in L‒02 cells. U0126 (a selective inhibitor of ERK1/2 activation) treatment could rescue matrix stiffening‒induced functional impairment and DNA damage. Taken together, these findings demonstrate that matrix stiffening induces functional impairment and DNA damage in L‒02 cells via the Piezo1‒ERK1/2 signaling pathway, which provides evidence for a better understanding of the hepatocyte function damage caused by tissue mechanical microenvironment change in liver diseases and the mechanotransduction in this process.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"273-289"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms underlying obesity-malignancy connection: a systematic narrative review.","authors":"Ayesha Sultana, Sobia Rana","doi":"10.1007/s13105-025-01084-9","DOIUrl":"10.1007/s13105-025-01084-9","url":null,"abstract":"<p><p>The association between obesity and cancer risk carries substantial public health ramifications as obesity promotes cancer advancement via many cellular and molecular mechanisms. This study utilizes Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and narrative systematic review guidelines to evaluate 221 research articles selected from an initial collection of 1,288 publications sourced from multiple databases. Obesity-driven cancer risk is linked to hormonal imbalances including increased oestrogen levels that heighten the likelihood of breast and endometrial cancers, and insulin resistance that activates the insulin/ Insulin and Insulin-like Growth Factor 1 (IGF-1) pathway promoting colorectal cancer progression. Chronic low-grade inflammation, metabolic dysfunction, and hypoxia in expanding adipose tissue contribute to pancreatic, oesophageal, colorectal, renal, and liver malignancies. Recent research has identified novel mechanisms that drive obesity-induced cancer progression. The adipose tissue secretome, extracellular vesicle-mediated lipid and RNA transfer, ferroptosis resistance, and metabolic reprogramming via Cluster of Differentiation 36 (CD36), Fatty Acid Binding Protein 4 (FABP4), and Carnitine Palmitoyl transferase 1A (CPT1A) create a tumour-permissive microenvironment. Obesity-induced epigenetic memory sustains cancer risk even after weight loss through persistent histone modifications (Histone H3 Lysine 4 Trimethylation (H3K4me3), Histone H3 Lysine 27 Trimethylation (H3K27me3), DNA methylation, and RNA modifications, particularly through the Fat Mass and Obesity-Associated (FTO) gene. Additionally, organ and cell size expansion increase mutation susceptibility. Emerging pathways including the Von Hippel-Lindau (VHL)-Hypoxia-Inducible Factor (HIF) axis, PR Domain Zinc Finger Protein 16 (PRDM16)/Uncoupling Protein 1 (UCP1) inhibition, Signal Transducer and Activator of Transcription 3 (STAT3)-driven FABP4 upregulation, and Yes-Associated Protein (YAP)/Transcriptional Co-Activator with PDZ-Binding Motif (TAZ) signalling, further highlight obesity's role in oncogenesis. Future research should investigate weight-loss drugs' effects on cancer pathways, expand demographic diversity, and develop biomarkers for adiposity. Integrating Mendelian randomization, multi-omics, and artificial intelligence could reveal novel therapeutic targets. A comprehensive prevention strategy combining lifestyle interventions, pharmacological therapies, and biomarker-driven diagnostics is crucial to reducing obesity-related cancer burden and improving patient outcomes.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"403-439"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular biomarkers for the prognosis of breast cancer: role of amino acid metabolism genes.","authors":"Yudong Zhou, Shibo Yu, Lizhe Zhu, Yalong Wang, Chenglong Duan, Danni Li, Jinsui Du, Jiaqi Zhang, Jianing Zhang, Ruichao Ma, Jianjun He, Yu Ren, Bin Wang","doi":"10.1007/s13105-025-01088-5","DOIUrl":"10.1007/s13105-025-01088-5","url":null,"abstract":"<p><p>The development of precise molecular biomarkers for breast cancer prognosis holds immense potential to improve treatment outcomes. This study aimed to investigate the role of amino acid metabolism genes as predictive markers for breast cancer prognosis and their association with the immune-tumour microenvironment. By employing advanced machine learning algorithms and bioinformatics analysis techniques, the impact of amino acid metabolism-related genes (AAMRGs) on the immune status and overall survival of patients with breast cancer was examined. An AAMRG-based risk model was established to assess the prognostic significance. Validated risk models (AIMP2, IYD, and QARS1) accurately predicted patient outcomes [1 y: 0.87 (0.96-0.78); 3 y: 0.82 (0.87-0.76); 5 y: 0.80 (0.86-0.75)]. Furthermore, this study revealed evidence suggesting that QARS1 may influence breast cancer cell proliferation through methionine metabolism. This analysis provides valuable insights into the mechanisms of breast cancer, emphasizing the significance of AAMRGs as prognostic biomarkers and potential therapeutic targets for optimizing personalized treatment strategies.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"441-457"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The importance of growth differentiation factor 15 and interleukin 6 serum levels in inflammatory bowel diseases.","authors":"Evgenia Koureta, Pantelis Karatzas, Panagiotis N Kanellopoulos, Angeliki Papapanagiotou, Vasileios Lekakis, Giorgos Bamias, George Karamanolis, Jiannis Vlachogiannakos, Athanasios G Papavassiliou, George V Papatheodoridis","doi":"10.1007/s13105-024-01057-4","DOIUrl":"10.1007/s13105-024-01057-4","url":null,"abstract":"<p><p>There are only scarce recent reports about the role of growth differentiation factor 15 (GDF-15) and some more data about interleukin-6 (IL-6) in inflammatory bowel diseases (IBD). We assessed GDF-15 and IL-6 serum levels in patients with IBD and associations with their characteristics. We included 122 and 71 stored samples from patients with Crohn's disease (CD) and ulcerative colitis (UC), respectively, and regular follow-up and 44 samples from healthy controls. Data regarding epidemiologic and disease characteristics were recorded. In CD, both GDF-15 and IL-6 levels were higher in active disease or all patients than controls (P ≤ 0.020) as well as patients with elevated CRP (P ≤ 0.008), endoscopically active disease (P ≤ 0.017), age ≥ 40 years (P ≤ 0.005) and active smokers (P ≤ 0.050) and were positively correlated with hospitalization numbers (P ≤ 0.019). GDF-15 levels were also positively correlated with flares within year-1 (P < 0.001). In UC, both GDF-15 and IL-6 levels were higher in clinically active or all patients than controls (P < 0.001), but they shared no other association with patient characteristics except for positive correlation with CRP. Only IL-6 levels were higher in active than inactive UC either clinically (P = 0.047) or endoscopically (P < 0.001) and were positively correlated with stool calprotectin (P = 0.021). GDF-15 was positively correlated to IL-6 levels only in UC (r_s=0.591, P < 0.001) but not in CD. In conclusion, in CD, GDF-15 and IL-6 levels could constitute indexes of activity and even offer a prognostic index of disease progression. In UC, IL-6 could also represent an activity index, but the role of GDF-15 needs further evaluation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"111-122"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}