Key result
Semaglutide is linked to an ~19% reduction in circulating CD16+ monocytes in type 2 diabetes.
Why the study?
GLP-1 receptor agonists reduce cardiovascular disease in type 2 diabetes and have anti-inflammatory effects, but their mechanism of action in humans remains unclear.
Does semaglutide reduce circulating inflammatory monocytes and markers of endothelial inflammation in individuals with type 2 diabetes?
Observational (n=16)
Does semaglutide reduce circulating inflammatory monocytes and markers of endothelial inflammation in individuals with type 2 diabetes?
p-value: p=0.034
Semaglutide reduces circulating inflammatory monocytes and bone marrow inflammation in patients with type 2 diabetes, providing a potential mechanism for its cardioprotective effects.
Semaglutide was associated with reduced inflammatory monocytes in type 2 diabetes; hypothesis-generating for GLP-1 cardioprotective mechanisms and requires prospective validation.
BACKGROUND AND AIMS: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce cardiovascular disease (CVD) in type 2 diabetes (T2D) and have anti-inflammatory effects in experimental studies, but their mechanism of action in humans remains unclear. This study characterized the cardiovascular-haematopoietic axis in individuals with T2D receiving semaglutide, as a potential mediator of GLP-1RA cardioprotective properties. METHODS: In 16 individuals with T2D [63.2 ± 6.1 years, 37.5% female, weight 82.3 ± 15.3 kg, body mass index (BMI) 28.33 ± 3.5 kg/m2, LDL cholesterol 2.2 ± 0.9 mmol/L, glycated haemoglobin (HbA1c) 78.1 ± 13.1 mmol/mol, high-sensitivity C-reactive protein (hsCRP) 1.9 (1.2, 5.8) mg/L], blood and sternal bone marrow aspirates (subset, n = 14) were collected at baseline and after 6 months of semaglutide ≤2.0 mg weekly. Circulating monocytes and haematopoietic precursors were quantified by flow cytometry, plasma cytokines using an nELISA™ assay (Nomic Bio) and inflammatory macrophages in coronary arteries, bone marrow, and spleen by gallium-68-labelled DOTA-(Tyr3)-octreotate (68Ga-DOTATATE) positron emission tomography-computed tomography scans. RESULTS: After 6 months of semaglutide, significant reductions in HbA1c (-21.1 mmol/mol, P < .0001), weight (-6.7 kg, P < .001), BMI (-2.5 kg/m2, P < .001), and hsCRP (-1.0 mg/L, P = .005) were observed. Circulating CD16+ monocytes were markedly lower (-18.8%, P = .034), with increased bone marrow retention correlating with weight loss, alongside reductions in interleukin-1 receptor antagonist, leptin, E-selectin, intercellular adhesion molecule-1 (ICAM-1), C-C motif chemokine ligand 2, C-C motif chemokine ligand 11, and C-X-C motif chemokine ligand 13. Gallium-68-labelled DOTA-(Tyr3)-octreotate PET-CT showed lower bone marrow uptake (-17.5%, P = .037), but not in spleen or coronary arteries. CONCLUSIONS: Semaglutide in T2D potentially reduces circulating inflammatory monocytes, increases bone marrow retention, and lowers markers of endothelial inflammation, with no reduction in coronary artery inflammatory macrophages. Semaglutide is associated with lower bone marrow 68Ga-DOTATATE uptake, which may relate to anti-inflammatory effects relevant to CVD risk.
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Teunis et al. (2026) conducted an observational in Type 2 diabetes (n=16). Semaglutide vs. Baseline (before-after comparison) was evaluated on Circulating CD16+ monocytes (p=0.034). Six months of semaglutide therapy in patients with type 2 diabetes significantly reduced circulating CD16+ monocytes (-18.8%, P=0.034) and bone marrow uptake (-17.5%, P=0.037).
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