Monocyte and Neutrophil Adhesion Molecule Expression During Acute Hyperglycemia and After Antioxidant Treatment in Type 2 Diabetes and Control Patients

Sampson, Michael J.; Davies, I. R.; Brown, J. C.; Ivory, Kamal; Hughes, David A.

doi:10.1161/01.atv.0000021759.08060.63

Cited by 92 publications

(58 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In vivo leukocyte activation induced by glucose has also been shown with oral glucose tolerance tests. 10 The present study suggests that short-term leukocyte activation by glucose is less likely than by triglycerides, which is in agreement with previous observations. 9 Although the total transport of TRLs by leukocytes is limited, this is the first study showing changes in fatty acid composition in leukocytes.…”

Section: Discussionsupporting

confidence: 93%

Leukocyte Activation by Triglyceride-Rich Lipoproteins

Alipour

Oostrom²,

Izraeljan³

et al. 2008

ATVB

190

152

View full text Add to dashboard Cite

Objective-Postprandial lipemia has been linked to atherosclerosis and inflammation. Because leukocyte activation is obligatory for atherogenesis, leukocyte activation by triglyceride-rich lipoproteins (TRLs) was investigated. Methods and Results-The expression of CD11b and CD66b after incubation with glucose and native and artificial TRLs (NTRL and ATRL) in vivo and in vitro was evaluated by flowcytometry. Oral fat loading tests showed an increased expression of CD11b on monocytes and neutrophils and CD66b on neutrophils. In 11 volunteers, postprandial leukocytes became enriched with meal-derived fatty acids ([1-13 C]16:0) suggesting uptake of exogenous fat. ApoB binding on leukocytes measured by flowcytometry in 65 subjects was highest on neutrophils and monocytes suggesting adherence of apoB-containing lipoproteins. Physiological concentrations of TRLs showed 62% increased neutrophil CD11b and a dose-dependent increased monocyte CD11b up to 84% in vitro. Incubations with lipid emulsions in the hypertriglyceridemic range showed a 5-fold increased monocyte CD11b expression, which was higher than the positive control (fMLP), and a dose-dependent 2-to 3-fold increased neutrophil CD11b and CD66b. The oxidative scavenger DMTU decreased the neutrophil CD66b expression by 36%. Conclusion-Acute hypertriglyceridemia is a leukocyte activator most likely by direct interaction between TRLs and leukocytes and uptake of fatty acids. TG-mediated leukocyte activation is an alternative proinflammatory and proatherogenic mechanism of hypertriglyceridemia in part associated to the generation of oxidative stress.

show abstract

Section: Discussionsupporting

confidence: 93%

Leukocyte Activation by Triglyceride-Rich Lipoproteins

Alipour

Oostrom²,

Izraeljan³

et al. 2008

ATVB

190

152

View full text Add to dashboard Cite

show abstract

“…in diabetic patients without any signs of vascular complications, we and others [21] found no elevation of Mac-1 in spite of the different basal glucose levels. in contrast, we found a significantly higher expression of Mac-1 on monocytes binding platelets, compared to single monocytes.…”

Section: Discussioncontrasting

confidence: 53%

Elevation of monocyte-platelet aggregates is an early marker of type 2 diabetes

Patkó

Császár

Acsády

et al. 2012

IMAS

View full text Add to dashboard Cite

Background: Diabetes has been shown to be an accelerating factor in the progression of atherosclerosis. The metabolic changes in diabetes contribute to modified platelet function and enhanced leukocyte-platelet aggregate formation. The attachment of activated platelets leads to the activation of leukocytes causing enhanced cytokine production and upregulation of surface adhesion molecules. Therefore, plateletleukocyte aggregates may be of great importance in the development of cardiovascular complications. Materials and Methods: Monocyte-platelet aggregates and monocyte Mac-1 expression were measured by flow cytometry to obtain differences between type 2 diabetic and healthy subjects. inflammatory mediators were evaluated to assess the presence of inflammation. Results: We found no signs of inflammation in type 2 diabetes; however, we observed enhanced aggregation level of monocytes and platelets. The expression of Mac-1 did not differ between diabetic and control subjects, but it was significantly higher on monocytes bearing platelets in both groups. Conclusions: Elevation of monocyte-platelet aggregates is an early marker of diabetes, which precedes the signs of inflammation. Enhanced Mac-1 expression can be observed on monocytes bearing platelets, independent from the presence of diabetes.

show abstract

“…Increased ROS generation causes activation of transcriptional factors, growth factors, and secondary mediators. Through direct tissue injury or via activation of these secondary mediators, hyperglycemia-induced oxidative stress causes cell and tissue injury (58,59,62,70,72,74,80,(121)(122)(123)(124)(125)(126)(127). In all cases studied, abnormalities were reversed by antioxidants or by restoring euglycemia (58,59,70,72,80,122,127).…”

Section: Hyperglycemia and Oxidative Stressmentioning

confidence: 94%