ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2026
MerTK Inhibition Aggravates Pancreatic Inflammation and Structural Damage via the NF-κB Pathway in an in vivo Type 2 Diabetic Rat Model.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Type 2 diabetes mellitus (T2DM) is characterized by chronic inflammation and progressive pancreatic β-cell dysfunction. The Mer receptor tyrosine kinase (MerTK) regulates immune homeostasis and inflammation, but its role in T2DM-related islet injury remains unclear. This study aimed to investigate the effects of MerTK and its inhibition on pancreatic structure, metabolic parameters, and NF-κB-mediated inflammation in a rat model of T2DM. Methods: Seventy male Sprague-Dawley rats were randomized into five groups: normal control (CON), CON+MRX-2843 (MerTK inhibitor), T2DM 2-week (T2DM-2; assessed 2 weeks after diabetes induction), T2DM 12-week (T2DM-12; assessed 12 weeks after diabetes induction), and T2DM-12+MRX-2843. T2DM was induced by a high-fat/high-sugar diet plus streptozotocin injection. In the intervention groups, MRX-2843, a selective MerTK inhibitor (65 mg/kg/day) was administered by gavage for two weeks after successful diabetes induction, including after 10 weeks of diabetes exposure in the T2DM-12+MRX-2843 group. Serum MerTK, glucose, lipids, insulin, and pro-inflammatory cytokines (NF-κB, TNF-α, IL-1β) were measured by ELISA, and pancreatic histology was evaluated by HE staining. Results: Serum MerTK expression increased with diabetes duration, peaking in the T2DM-12 group (47.5% higher than CON). MerTK inhibition significantly reduced MerTK levels by 21.3% versus T2DM-12 but aggravated metabolic dysfunction, with higher fasting glucose (+13.3%), HbA1c (+2.5%), total cholesterol (+16.9%), triglycerides (+32.6%), and insulin (+8.5%) compared to non-inhibited T2DM rats. Pro-inflammatory cytokines were markedly elevated after MRX-2843 treatment, particularly NF-κB (+35.2%), TNF-α (+48.2%), and IL-1β (+70.3%) in the T2DM-12+MRX-2843 group. Histological analysis showed progressive islet atrophy and vacuolation with diabetes, which became more severe after MerTK inhibition, indicating enhanced structural damage. Conclusion: MerTK expression is dynamically upregulated in T2DM and exerts a compensatory protective effect by limiting NF-κB-driven inflammation and preserving pancreatic integrity. Pharmacological inhibition of MerTK exacerbates cytokine release, metabolic disturbances, and pancreatic injury, suggesting that MerTK may represent a promising candidate for further therapeutic investigation in T2DM.
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