Abstract:Insulin resistance is associated with an enhanced degree of erythrocyte adhesiveness/aggregation and this is related to the presence of enhanced inflammation-sensitive plasma proteins that are part of the acute-phase response. These findings might have hemorheological consequences and might contribute to the pathophysiology of the insulin-resistance syndrome.
“…However, we disagree about the standardization issue. In fact, we have by now analyzed approximately 2000 samples from different inflammatory conditions and found that the results of the slide test are generally not inferior to those obtained by other commonly used markers of the acute-phase response [9][10][11][12][13][14][15]. We do agree, however, that our slide test is not affected to a significant degree by protein-independent aggregability.The slide test was developed as a low-cost real-time and point of care methodology to reveal the presence of enhanced red cell adhesiveness / aggregation in the peripheral blood [16].…”
“…However, we disagree about the standardization issue. In fact, we have by now analyzed approximately 2000 samples from different inflammatory conditions and found that the results of the slide test are generally not inferior to those obtained by other commonly used markers of the acute-phase response [9][10][11][12][13][14][15]. We do agree, however, that our slide test is not affected to a significant degree by protein-independent aggregability.The slide test was developed as a low-cost real-time and point of care methodology to reveal the presence of enhanced red cell adhesiveness / aggregation in the peripheral blood [16].…”
“…For example, enhanced erythrocyte aggregation has been described in hypertension [38,39], hypercholesterolemia [40,41], hypertriglyceridemia [42], obesity [43] as well as in insulin resistance [5]. Thus, the aggregability of the cells might indeed reflect the presence of lowgrade inflammation and enhanced synthesis of adhesive proteins [44].…”
Section: Discussionmentioning
confidence: 97%
“…The aggregation of red blood cells in the peripheral blood was performed by the ERYTHROSENSE technology [5,18,19]. In brief, blood from the antecubital vein was obtained between 8 and 11 AM following an overnight fast.…”
Section: The Erythrosense Technologymentioning
confidence: 99%
“…In a recent work, we have evaluated the possibility that low-grade inflammation and the presence of inflammation sensitive proteins, can be associated with enhanced erythrocyte aggregation in individuals with insulin resistance [5]. A significant correlation was noted between insulin resistance expressed as HOMA index and the degree of erythrocyte aggregation in a group of 129 participants who were also evaluated for the presence of low-grade inflammation.…”
The multiplicity of components of the metabolic syndrome is associated with enhanced erythrocyte aggregation, probably related to the presence of multiple adhesive macromolecules in the peripheral blood. The enhanced aggregation might contribute to capillary slow flow, tissue deoxygenation as well as vasomotor tone changes in the presence of multiple components of this syndrome.
“…Erythrocyte deformability and/or aggregation is an important determinant of passage of blood through capillaries. The degree of erythrocyte aggregation is correlated with the IR index HOMA [ 189 , 405 ]. High hematocrit is inversely related to small vessel endothelial‐dependent vasodilatation [ 280 ].…”
Section: Microcirculation and The Metabolic Syndromementioning
The present review, to the authors' knowledge, is the first to specifically address the relationships between microcirculation and metabolic syndrome, a cluster of metabolic and cardiovascular modifications highly prevalent in the general population. Its close link to overweight and insulin resistance makes it the main cause of the worldwide burden of type 2 diabetes. However, metabolic syndrome is also observed in many other diseases, particularly, but not exclusively, those where insulin resistance is a main feature. Analysis of the literature reveals that this clinical situation is invariably linked to microvascular disturbances, such as abnormalities in arteriolar reactivity, capillary recruitment, permeability, and hemorheology. A particularly interesting observation is that these defects in small vessel structure and function are seen very early in life or disease. Very importantly, they further suggest that microcirculatory abnormalities may be not only secondary but also causal to the development and/or aggravation of insulin resistance and metabolic syndrome. Mechanisms responsible for these modifications remain largely unknown, but insulin's vascular effects in the microvascular network, detailed in this review, are at least one example of such connections. The existing data point to a clear, at least bidirectional, relationship between microcirculation and metabolic syndrome. Additional studies should determine the level of reciprocal causality.
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