Key result
T2DM shows no link to altered leptin or cellular marker expression in atherosclerotic plaques.
Why the study?
Leptin and other inflammatory markers may contribute to the progression of atherosclerosis and local inflammation in patients with diabetes mellitus, prompting investigation into plaque immunophenotypes.
Does type 2 diabetes mellitus alter the immunophenotype (leptin, leptin receptor, CD68, -SMA, CD34) of atherosclerotic plaques in patients undergoing vascular surgery?
Cross-Sectional (n=24)
Yes
Does type 2 diabetes mellitus alter the immunophenotype (leptin, leptin receptor, CD68, -SMA, CD34) of atherosclerotic plaques in patients undergoing vascular surgery?
In a small cohort, type 2 diabetes mellitus was not significantly associated with altered expression of leptin, leptin receptor, or inflammatory markers in atherosclerotic plaques, though non-significant trends were noted.
Answers are grounded in this paper and cite their sources.
No association seen in this cross-sectional cohort; leaves open diabetes effects on plaque immunophenotype in larger studies.
BACKGROUND: Diabetes mellitus (DM) is a significant predictor of atherosclerosis, cardiovascular disease, and cardiovascular mortality. It is known that atherosclerosis occurs earlier in patients with diabetes, reducing the duration of their life. Leptin as well as other inflammatory markers can contribute to the progression of atherosclerosis in patients with DM, participate in the development of a local inflammatory reaction. AIM: Determine the cells immunophenotype of atherosclerotic plaques in patients with diabetes. MATERIALS AND METHODS: We analyzed 24 patients (20 men and 4 women), who underwent aortofemoral bypass, femoral-tibial bypass or carotid endarterectomy. During the operation, a fragment of the arterial wall with an atherosclerotic plaque was obtained for further immunohistochemical studies. Five histologic plaque characteristics (CD68+, -SMA, CD34, leptin and leptin receptor) were compared. RESULTS: No difference in the expression of CD68 (p=0.922), -SMA (p=0.192), CD34 (p=0.858), leptin receptor (p=0.741) and leptin (p=0.610) in atherosclerotic plaques were observed between patients with and without DM. The lack of significant differences between the two groups was possibly due to the small number of observations with DM. In particular, when assessing the expression of selected markers in atherosclerotic plaques, patients with DM showed significantly more leptin receptors than patients without DM (2160.716 and 1205.88 respectively); and also significantly less CD68+ (0.39 and 0.98 respectively) and -SMA+ (6.5 and 13.5 respectively). CONCLUSION: Based on the expression of CD68, -SMA, CD34, leptin receptor and leptin, no significant differences were observed in atherosclerotic plaque between patients with and without DM. At the same time, despite the limitations of the study (a small number of patients, moderate severity of DM, elderly patients in the DM group), we found a tendency in the increased number of leptin receptors and a decreased number of -SMA+, CD68+ in DM atherosclerotic plaques. Further study needed, taking into account the limitations of this work.
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Dimitrova et al. (2021) conducted a cross-sectional in Atherosclerosis in patients with type 2 diabetes mellitus (n=24). Type 2 diabetes mellitus vs. Patients without diabetes mellitus was evaluated on Leptin receptor expression in atherosclerotic plaques (p=0.741). Type 2 diabetes mellitus was not associated with significant differences in the expression of leptin, leptin receptors, CD68, α-SMA, or CD34 in atherosclerotic plaques compared to patients without diabetes.
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