Abstract
Type 2 diabetes patients are less likely to develop an abdominal aortic aneurysm (AAA). Since macrophages play a crucial role in AAA development, we hypothesized that this decrease in AAA risk in diabetic patients might be due to diabetes-induced changes in macrophage biology. To test this hypothesis, we treated primary macrophages obtained from healthy human volunteers with serum from non-diabetic vs. diabetic AAA patients and observed differences in extracellular acidification and the expression of genes involved in glycolysis and lipid oxidation. These results suggest an increase in metabolism in macrophages treated with serum from diabetic AAA patients. Since serum samples used did not differ in glucose content, these changes are not likely to be caused by differences in glycemia. Macrophage functions have been shown to be linked to their metabolism. In line with this, our data suggest that this increase in macrophage metabolism is accompanied by a shift towards an anti-inflammatory state. Together, these results support a model where diabetes-induced changes in metabolism in macrophages might lead to a reduced risk for AAA development.
Highlights
Cardiovascular diseases represent important causes of mortality and morbidity, and rank first of the most frequently occurring diseases
To study the differential effects of serum from diabetic vs. non-diabetic abdominal aortic aneurysm (AAA) patients on human macrophage biology, we selected serum samples from six non-diabetic and six diabetic AAA patients that were matched for age, body mass index (BMI), AAA diameter, glycemia, and risk factors such as smoking, high blood pressure, and dyslipidemia (Table 1)
In this study we investigated the differential effects of serum from diabetic vs. nondiabetic AAA patients on human macrophage biology
Summary
Cardiovascular diseases represent important causes of mortality and morbidity, and rank first of the most frequently occurring diseases. Abdominal aortic aneurysm (AAA), defined as a focal dilatation of the aorta superior to 30 mm in diameter, is an early inflammation process causing degradation of the aorta wall, loss of arterial wall parallelism and progressive dilation until eventual fatal rupture [1], representing a life-threatening disease. It is of crucial importance to better understand the cellular/biological mechanism beyond AAA formation/progression to develop novel therapeutic strategies. AAA formation results from a complex process mainly involving the remodeling of the extracellular matrix (ECM), infiltration of inflammatory cells within the aortic wall ( monocytes/macrophages), as well as impairment of the vascular smooth muscle cell (SMC) homeostasis and increased local oxidative stress [2]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
