Malthe E. B. Hviid, Lea A. N. Christoffersen, Mette K. Klausen, Thorsten Brodersen, Ole B. Pedersen, Sisse R. Ostrowski, Margit H. Larsen, Mette Kongstad, Mathias E. Jensen, Tina Vilsbøll, Anders Fink-Jensen
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This study aimed to compare the pro-inflammatory and metabolic biomarker profiles in individuals with AUD with individuals without AUD, and to evaluate the effect of exenatide on these biomarkers in individuals with AUD.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>Serum concentrations of 25 biomarkers (interferon-γ [IFN-γ], tumor necrosis factor-α [TNF-α], interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, monocyte chemoattractant protein-1 [MCP-1], C-peptide, gastric inhibitory polypeptide [GIP], glucagon-like peptide [GLP-1], glucagon, insulin, leptin, pancreatic polypeptide [PP], adiponectin, high sensitivity C-reactive protein [hsCRP], fibroblast growth factor 21 [FGF-21], total cholesterol [CHOL], high-density lipoprotein [HDL], low-density lipoprotein [LDL], and triglycerides [TG]) from individuals with AUD were measured at baseline and after 26 weeks of treatment with the GLP-1 receptor agonist (GLP-1RA) exenatide once-weekly or placebo, using multiplexed immunoassays, enzyme-linked immunosorbent assay (ELISA), and line immunoassays. Serum samples from 23 individuals with no record of AUD or treatment with a GLP-1RA were measured once for comparison with individuals with AUD.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>IL-6 (1.56 vs. 0.62 pg/mL), hsCRP (3.30 vs. 1.34 mg/L), and FGF-21 (1794.97 vs. 306.11 pg/mL) were significantly higher, whereas GIP (63.06 vs. 111.07 pg/mL) was significantly lower in individuals with AUD (<i>n</i> = 124) than in those without AUD (<i>n</i> = 23). No significant changes in biomarker levels were observed after treatment with exenatide (<i>n</i> = 40) compared with treatment with placebo (<i>n</i> = 37).</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Our findings support the well-established link between AUD and inflammation. However, treatment with the GLP-1 receptor agonist exenatide did not impact pro-inflammatory and metabolic biomarkers.</p>\n </section>\n </div>","PeriodicalId":72145,"journal":{"name":"Alcohol (Hanover, York County, Pa.)","volume":"49 8","pages":"1659-1666"},"PeriodicalIF":2.7000,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acer.70110","citationCount":"0","resultStr":"{\"title\":\"Effect of the GLP-1 receptor agonist exenatide on pro-inflammatory and metabolic biomarkers in individuals with alcohol use disorder: Post hoc results from a randomized, double-blinded, placebo-controlled clinical trial\",\"authors\":\"Malthe E. B. Hviid, Lea A. N. Christoffersen, Mette K. Klausen, Thorsten Brodersen, Ole B. Pedersen, Sisse R. Ostrowski, Margit H. Larsen, Mette Kongstad, Mathias E. 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引用次数: 0
摘要
背景：酒精使用障碍（AUD）与炎症、代谢综合征和全因死亡风险增加有关。本研究旨在比较AUD患者与非AUD患者的促炎和代谢生物标志物特征，并评估艾塞那肽对AUD患者这些生物标志物的影响。方法:血清25项生物标志物(干扰素-γ [IFN-γ]、肿瘤坏死因子-α [TNF-α]、白细胞介素(IL)-1β、IL-2、IL-4、IL-6、IL-8、IL-10、IL-12p70、IL-13、单核细胞化学吸引蛋白-1 [MCP-1]、c肽、胃抑制多肽[GIP]、胰高血糖素样肽[GLP-1]、胰高血糖素、胰岛素、瘦素、胰多肽[PP]、脂联素、高敏c反应蛋白[hsCRP]、成纤维细胞生长因子21 [FGF-21]、总胆固醇[CHOL]、高密度脂蛋白[HDL]、使用多重免疫测定法、酶联免疫吸附测定法（ELISA）和线免疫测定法，在基线时和接受每周一次GLP-1受体激动剂（GLP-1RA）艾塞那肽或安慰剂治疗26周后，测量AUD患者的低密度脂蛋白（LDL）和甘油三酯（TG）。对23名无AUD记录或未接受GLP-1RA治疗的患者的血清样本进行一次测定，与AUD患者进行比较。结果：AUD患者（n = 124） IL-6 （1.56 vs. 0.62 pg/mL）、hsCRP （3.30 vs. 1.34 mg/L）和FGF-21 （1794.97 vs. 306.11 pg/mL）显著高于非AUD患者（n = 23），而GIP （63.06 vs. 111.07 pg/mL）显著低于AUD患者（n = 23）。与安慰剂治疗组（n = 37）相比，艾塞那肽治疗组（n = 40）的生物标志物水平无显著变化。结论：我们的研究结果支持AUD与炎症之间的既定联系。然而，用GLP-1受体激动剂艾塞那肽治疗不会影响促炎和代谢生物标志物。
Effect of the GLP-1 receptor agonist exenatide on pro-inflammatory and metabolic biomarkers in individuals with alcohol use disorder: Post hoc results from a randomized, double-blinded, placebo-controlled clinical trial
Background
Alcohol use disorder (AUD) has been associated with inflammation, metabolic syndrome, and increased risk of all-cause mortality. This study aimed to compare the pro-inflammatory and metabolic biomarker profiles in individuals with AUD with individuals without AUD, and to evaluate the effect of exenatide on these biomarkers in individuals with AUD.
Methods
Serum concentrations of 25 biomarkers (interferon-γ [IFN-γ], tumor necrosis factor-α [TNF-α], interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, monocyte chemoattractant protein-1 [MCP-1], C-peptide, gastric inhibitory polypeptide [GIP], glucagon-like peptide [GLP-1], glucagon, insulin, leptin, pancreatic polypeptide [PP], adiponectin, high sensitivity C-reactive protein [hsCRP], fibroblast growth factor 21 [FGF-21], total cholesterol [CHOL], high-density lipoprotein [HDL], low-density lipoprotein [LDL], and triglycerides [TG]) from individuals with AUD were measured at baseline and after 26 weeks of treatment with the GLP-1 receptor agonist (GLP-1RA) exenatide once-weekly or placebo, using multiplexed immunoassays, enzyme-linked immunosorbent assay (ELISA), and line immunoassays. Serum samples from 23 individuals with no record of AUD or treatment with a GLP-1RA were measured once for comparison with individuals with AUD.
Results
IL-6 (1.56 vs. 0.62 pg/mL), hsCRP (3.30 vs. 1.34 mg/L), and FGF-21 (1794.97 vs. 306.11 pg/mL) were significantly higher, whereas GIP (63.06 vs. 111.07 pg/mL) was significantly lower in individuals with AUD (n = 124) than in those without AUD (n = 23). No significant changes in biomarker levels were observed after treatment with exenatide (n = 40) compared with treatment with placebo (n = 37).
Conclusion
Our findings support the well-established link between AUD and inflammation. However, treatment with the GLP-1 receptor agonist exenatide did not impact pro-inflammatory and metabolic biomarkers.
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