Journal of physiology and biochemistry最新文献

{"title":"The TWIK2-mtDNA-NLRP3 inflammasome signaling in hepatic macrophages facilitates exercise-induced attenuation of hepatic inflammation and insulin resistance in db/db mice.","authors":"Tan Zhang, Jingcheng Fan, Xin Wen, Xuemei Duan","doi":"10.1007/s13105-025-01077-8","DOIUrl":"https://doi.org/10.1007/s13105-025-01077-8","url":null,"abstract":"<p><p>Exercise has been proved to be effective in ameliorating diabetes but the underlying mechanisms remain obscure. It has been recently demonstrated that overactivation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome led to hepatic insulin resistance. Therefore, we aimed to explore the role and underlying mechanism of NLRP3 inflammasome in exercise-mediated hepatic insulin resistance. Wild type and db/db mice were sedentary or subjected to 8-week moderate intensity exercise, liver tissues and primary hepatic macrophages were isolated. Exercise mitigated hepatic steatosis and enhanced the hepatic insulin sensitivity of db/db mice. More importantly, exercise reduced the protein expression of two-pore domain weak inwardly rectifying K⁺ channel 2 (TWIK2) to suppress cellular K⁺ efflux, blunted the generation of mitochondrial ROS (mROS) and the release of oxidized mitochondrial DNA (ox-mtDNA) into cytosol, leading to the inhibition of NLRP3 inflammasome in hepatic macrophages of db/db mice. Accordingly, the hepatic macrophages switched from pro-inflammatory phenotype to anti-inflammatory phenotype and the infiltration of macrophages into liver was decreased in response to exercise. Moreover, inhibition of TWIK2 expression with TWIK2 inhibitor or shRNA interference in hepatic macrophages blunted the TWIK2-mtDNA-NLRP3 inflammasome signaling. The macrophages switched to anti-inflammatory phenotype upon TWIK2 deficiency. Additionally, the insulin sensitivity was elevated in primary hepatocytes which were exposed to culture medium from hepatic macrophages with TWIK2 deficiency, suggesting that inhibition of TWIK2-mtDNA-NLRP3 inflammasome signaling in hepatic macrophages could attenuate hepatic insulin resistance Taken together, we first observed the inhibition of TWIK2-mtDNA-NLRP3 inflammasome signaling in hepatic macrophages of diabetic mice in response to exercise intervention, implying a probable role for TWIK2-mtDNA-NLRP3 inflammasome signaling in exercise-mediated alleviation of hepatic inflammation and insulin resistance, hoping to provide theoretical basis and new target for the prevention and treatment of metabolic diseases.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795737","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":"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":"https://doi.org/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":""},"PeriodicalIF":3.7,"publicationDate":"2025-04-05","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":"Polarized or threshold training: is there a superior training intensity distribution to improve V̇O₂max, endurance capacity and mitochondrial function? A study in Wistar Rat models.","authors":"Pedro Oliveira, Miguel Anjos, Ariane Flores, Francisco Peixoto, Ana Isabel Padrão, Hélder Fonseca","doi":"10.1007/s13105-025-01079-6","DOIUrl":"https://doi.org/10.1007/s13105-025-01079-6","url":null,"abstract":"<p><p>Conflicting evidence exists regarding the superiority of Polarized Training (POL) vs other training intensity distribution models. Compare POL vs threshold (THR) training on V̇O₂max, endurance capacity (EC) and mitochondrial function. Fifteen male Wistar rats (336.1 ± 30.4 g) were divided in: POL (n = 5), THR (n = 5) or control (CON; n = 5) groups. V̇O₂max (indirect calorimetry) and EC (treadmill exhaustion test) were determined at baseline four and eight-weeks of training. POL consisted of 80% running volume at 60%V̇O₂max and 20% at 90%V̇O₂max while THR trained only at 75%V̇O₂max. Both protocols were isocaloric and performed 5d/week. All animals were housed in cages with access to running wheel to allow ad libitum activity. After training, animals were sacrificed and left ventricle (LV) myocardium, diaphragm, tibialis anterior and soleus muscles were collected for high-resolution respirometry, biochemical and histological analysis. There were no baseline differences between groups. After training V̇O₂max and EC were similar between POL and THR even though THR V̇O₂max was higher compared to CON. After training, there were also no significant differences in OXPHOS or any of the other major mitochondrial function markers assessed between POL and THR in any of the tissues analyzed. The expression of MFN1, MFN2, PGC-1α, TFAM, DRP1, OPA1 and TOM20 as well as the activity of citrate synthase were also similar between POL and THR in all tissues. There were no significant differences in endurance performance or markers of bioenergetic function between POL and THR after eight-weeks of training.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763494","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":"Nutritional ketosis modulates the methylation of cancer-related genes in patients with obesity and in breast cancer cells.","authors":"Paula M Lorenzo, Andrea G Izquierdo, Gemma Rodriguez-Carnero, Nicolas Costa-Fraga, Angel Díaz-Lagares, Cristina Porca, Daniel de Luis, Cristina Tejera, Laura De Paz, Juan Cueva, Diego Bellido, Ana B Crujeiras","doi":"10.1007/s13105-025-01076-9","DOIUrl":"https://doi.org/10.1007/s13105-025-01076-9","url":null,"abstract":"<p><p>Scientific evidence demonstrates that a very low-calorie ketogenic diet (VLCKD) is effective and beneficial in the treatment of obesity, capable of reversing the methylome associated with obesity and has immunomodulatory capacity. This effect is in part promoted by nutritional ketosis and could be involved in counteracting obesity-related cancer. The aim of this study was to evaluate the effect of nutritional ketosis on the methylation of genes related to tumor processes in patients with obesity and in breast cancer cells. Based on methylome data (Infinium MethylationEPIC BeadChip, Illumina) from patients with obesity treated with a VLCKD for weight loss (n = 10; n = 5 women, age = 48.8 ± 9.20 years, BMI = 32.9 ± 1.4 kg/m2), genes belonging to cancer-related pathways were specifically evaluated and further validated in vitro in MDA-MB-231 (triple negative) and MCF7 (RE positive) breast tumor cells pretreated for 72 h with βOHB, the main ketone body, secretome from visceral (VATs) or subcutaneous (SATs) adipose tissue of patients with obesity. The cell tumoral phenotype was evaluated by proliferation assay and expression of cancer-related genes. VLCKD-induced nutritional ketosis promoted changes in the methylation of 18 genes (20 CpGs; 17 hypomethylated, 3 hypermethylated) belonged to cancer-related pathways with MAPK10, CCN1, CTNNA2, LAMC3 and GLI2 being the most representative genes. A similar pattern was observed in the MDA-MB-231 cells treated with β-OHB, without changes in MCF7. These epigenetic changes paralleled the tumoral phenotype modulated by the treatments. Taking together these results highlight the potential role of VLCKD as an adjuvant to anticancer treatment in groups more susceptible to the development of cancer such as patients with obesity, exerting epigenetic regulation through nutritional ketosis and weight loss.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143719778","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":"https://doi.org/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":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","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":"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":"https://doi.org/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":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Candidate gene polymorphisms and power athlete status: a meta-analytical approach.","authors":"Gökhan İpekoğlu, Tuğba Çetin, Tülay Sırtbaş, Rabia Kılıç, Mustafa Odabaşı, Fahrettin Bayraktar","doi":"10.1007/s13105-025-01071-0","DOIUrl":"https://doi.org/10.1007/s13105-025-01071-0","url":null,"abstract":"<p><p>Recent studies have focused on genetic polymorphisms that may influence athlete status. This meta-analysis aimed to investigate the association between athlete status and specific candidate genetic polymorphisms (AGTR2 rs11091046, FTO rs9939609, GALNTL6 rs558129, GNB3 rs5443, MCT1 rs1049434, NOS3 rs2070744). Only case-control studies collected from PubMed and Web of Science databases, published between 2009 and 2022, were included. A total of 23 studies were included in the meta-analysis according to the criteria of the research, and analyses were performed using random or fixed effects models. Effect size, odds ratio, or risk ratio were evaluated with a suitable 95% confidence interval. The results showed that the GALNTL6 rs558129 T/T genotype, MCT1 rs1049434 T/T genotype, and NOS3 rs2070744 T allele and T/T genotype were more prevalent in power athletes than in controls (p < 0.05). Conversely, the GALNTL6 rs558129 C allele, C/C genotype, and AGTR2 rs11091046 C allele and C/C genotype were more common in the control group. These findings indicate that some genetic polymorphisms may be important markers in athlete status and should be supported by future studies.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586115","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":"https://doi.org/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":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-25","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":"The link between Mitochondria and Sarcopenia.","authors":"Nurul Tihani Kamarulzaman, Suzana Makpol","doi":"10.1007/s13105-024-01062-7","DOIUrl":"10.1007/s13105-024-01062-7","url":null,"abstract":"<p><p>Sarcopenia, a widespread condition, is characterized by a variety of factors influencing its development. The causes of sarcopenia differ depending on the age of the individual. It is defined as the combination of decreased muscle mass and impaired muscle function, primarily observed in association with ageing. As people age from 20 to 80 years old, there is an approximate 30% reduction in muscle mass and a 20% decline in cross-sectional area. This decline is attributed to a decrease in the size and number of muscle fibres. The regression of muscle mass and strength increases the risk of fractures, frailty, reduced quality of life, and loss of independence. Muscle cells, fibres, and tissues shrink, resulting in diminished muscle power, volume, and strength in major muscle groups. One prominent theory of cellular ageing posits a strong positive relationship between age and oxidative damage. Heightened oxidative stress leads to early-onset sarcopenia, characterized by neuromuscular innervation breakdown, muscle atrophy, and dysfunctional mitochondrial muscles. Ageing muscles generate more reactive oxygen species (ROS), and experience decreased oxygen consumption and ATP synthesis compared to younger muscles. Additionally, changes in mitochondrial protein interactions, cristae structure, and networks may contribute to ADP insensitivity, which ultimately leads to sarcopenia. Within this framework, this review provides a comprehensive summary of our current understanding of the role of mitochondria in sarcopenia and other muscle degenerative diseases, highlighting the crucial need for further research in these areas.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"1-20"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449338","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}