Key result
Type 2 diabetes was associated with increased aortic Syndecan-1 expression compared to controls, but this did not correlate with fasting plasma GLP-1 levels.
Why the study?
Thoracic aortic aneurysm prevalence is reduced in type 2 diabetes, leading investigators to hypothesize that elevated fasting plasma GLP-1 increases aortic Syndecan-1 expression in type 2 diabetes.
Does Type 2 Diabetes alter aortic Syndecan-1 expression in surgical patients with aortic valve pathology?
Observational
Does Type 2 Diabetes alter aortic Syndecan-1 expression in surgical patients with aortic valve pathology?
Answers are grounded in this paper and cite their sources.
Increased aortic Syndecan-1 expression in patients with Type 2 diabetes may contribute to the reduced prevalence of thoracic aortic aneurysms in this population, independent of fasting plasma GLP-1 levels.
A reduced prevalence of a thoracic aortic aneurysm (thoracic AA) is observed in type 2 diabetes (T2D). Glucagon-like peptide-1 (GLP-1)/GLP-1-based anti-diabetic therapy has indicated protective effects in thoracic AA and regulates the processes controlling the vascular tissue expression of Syndecan-1 (Sdc-1). Sdc-1 expression on macrophages infiltrating the aortic tissue contributes to a counter-regulatory response to thoracic AA formation in animal models through the interplay with inflammation/proteolytic activity. We hypothesized that elevated fasting plasma GLP-1 (fpGLP-1) increases the aortic Sdc-1 expression in T2D, which may contribute to a reduced prevalence of thoracic AA. Consequently, we determined whether T2D/thoracic AA associates with an altered Sdc-1 expression in the aortic tissue and the possible associations with fpGLP-1 and inflammation/proteolytic activity. From a cohort of surgical patients with an aortic valve pathology, we compared different disease groups (T2D/thoracic AA) with the same sub-cohort group of controls (patients without T2D and thoracic AA). The MMP-2 activity and Sdc-1, GLP-1R and CD68 expression were analyzed in the aortic tissue. GLP-1, Sdc-1 and cytokines were analyzed in the plasma. The aortic Sdc-1 expression was increased in T2D patients but did not correlate with fpGLP-1. Thoracic AA was associated with an increased aortic expression of Sdc-1 and the macrophage marker CD68. CD68 was not detected in T2D. In conclusion, an increased aortic Sdc-1 expression may contribute to a reduced prevalence of thoracic AA in T2D.
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Ntika et al. (2021) conducted an observational in Type 2 diabetes and thoracic aortic aneurysm. Type 2 diabetes vs. Patients without T2D and thoracic AA was evaluated on Aortic Sdc-1 expression. Type 2 diabetes was associated with increased aortic Syndecan-1 expression compared to controls, but this did not correlate with fasting plasma GLP-1 levels.
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