4.7 Article

Arterial wall inflammation assessed by 18F-FDG-PET/CT is higher in individuals with Type 1 diabetes and associated with circulating inflammatory proteins

期刊

CARDIOVASCULAR RESEARCH
卷 119, 期 10, 页码 1942-1951

出版社

OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvad058

关键词

F-18-FDG-PET; CT; Diabetes; Vascular inflammation; Atherosclerosis; Type 1 diabetes

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This study investigates the association between chronic hyperglycaemia in Type 1 diabetes (T1D) and a proinflammatory immune signature as well as arterial wall inflammation, which contribute to the development of atherosclerosis. The results show that T1D patients have higher levels of arterial wall inflammation and haematopoietic activity compared to healthy controls. The expressions of CCR2 and CD36 on circulating monocytes are also higher in T1D patients, along with increased levels of several circulating inflammatory proteins. Furthermore, the degree of hyperglycaemia does not significantly influence this inflammatory response in T1D patients.
Aims The article investigates whether chronic hyperglycaemia in Type 1 diabetes (T1D) is associated with a proinflammatory immune signature and with arterial wall inflammation, driving the development of atherosclerosis. Methods and results Patients with T1D (n = 41), and healthy age-, sex-, and body mass index-matched controls (n = 20) were recruited. Arterial wall inflammation and haematopoietic activity were measured with 2 '-deoxy-2 '-(F-18)-fluoro-D-glucose (F-18-FDG) positron emission tomography/computed tomography. In addition, flow cytometry of circulating leucocytes was performed as well as targeted proteomics to measure circulating inflammatory markers. F-18-FDG uptake in the wall of the abdominal aorta, carotid arteries, and iliac arteries was higher in T1D compared with that in the healthy controls. Also, F-18-FDG uptake in the bone marrow and spleen was higher in patients with T1D. CCR2 and CD36 expressions on circulating monocytes were higher in patients with T1D, as well as several circulating inflammatory proteins. In addition, several circulating inflammatory markers (osteoprotegerin, transforming growth factor-alpha, CX3CL1, and colony-stimulating factor-1) displayed a positive correlation with FDG uptake. Within T1D, no differences were found between people with a high and low HbA(1c). Conclusion These findings strengthen the concept that chronic hyperglycaemia in T1D induces inflammatory changes that fuel arterial wall inflammation leading to atherosclerosis. The degree of hyperglycaemia appears to play a minor role in driving this inflammatory response in patients with T1D.

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