Alcohol, clinical & experimental research · 2025
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.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
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Hviid Malthe E B, Christoffersen Lea A N, Klausen Mette K, Brodersen Thorsten, Pedersen Ole B, Ostrowski Sisse R, Larsen Margit H, Kongstad Mette, Jensen Mathias E, Vilsbøll Tina, Fink-Jensen Anders
Аннотация
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.
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.