Hypertriglyceridemia Enhances Monocyte Binding to Endothelial Cells in NIDDM

Hoogerbrugge, Nicoline; Verkerk, Anton; Jacobs, M. L.; Postema, P. T. E.; Jongkind, J. F.

doi:10.2337/diacare.19.10.1122

Cited by 25 publications

(21 citation statements)

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“…No mention of vascular complications was made in that study. However, another study did not report increased monocyteendothelial adhesion in normolipidemic type 1 diabetic patients (39); some of the patients in that study did have vascular complications. Thus, although two of the three studies to date have reported increased monocyte adhesion in type 1 diabetes, it needs to be emphasized that all three studies were small (n Ͻ20).…”

Section: Discussionmentioning

confidence: 95%

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Glaser²,

et al. 2006

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, and monocyte function). High-sensitive CRP, soluble intracellular adhesion molecule (sICAM), sCD40L, and nitrotyrosine levels were significantly elevated in type 1 diabetic subjects compared with in control subjects (P < 0.05). Monocyte superoxide anion release was significantly increased in the resting (37%; P < 0.05) and activated state (26%; P < 0.005) in type 1 diabetic compared with in control subjects. Monocyte interleukin (IL)-6 levels were significantly elevated in type 1 diabetic subjects compared with in control subjects in the resting state (51%; P < 0.05) and after lipopolysaccharide activation (31%; P < 0.01). Monocyte IL-1␤ levels were increased in the activated monocytes in type 1 diabetic compared with in control subjects. There were no significant differences in monocyte tumor necrosis factor levels or adhesion between the two groups. Thus type 1 diabetes is a proinflammatory state, as evidenced by increased levels of monocyte IL-6, superoxide anion, and plasma CRP, sICAM, sCD40L, and nitrotyrosine levels. These results have a major implication on our understanding of the role of inflammation in vasculopathies in type 1 diabetes. Diabetes 55: 774 -779, 2006

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Section: Discussionmentioning

confidence: 95%

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Glaser²,

et al. 2006

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“…Evidence that endothelial LOX-1 supports adhesion of monocytes and is upregulated in diabetes (19 -21) suggests a role for this receptor in the enhanced binding of monocytes documented in patients with diabetes (28,49,50). Previous studies have shown that glucose may contribute to the increased monocyte adherence to endothelium in diabetes (25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Glucose Enhances Endothelial LOX-1 Expression

Sawamura

Renier

2003

Diabetes

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Endothelial dysfunction is an early and key determinant of diabetic vascular complications that is elicited at least in part by oxidized LDL (oxLDL). The recent observation that lectin-like oxLDL receptor-1 (LOX-1) expression is increased in the vascular endothelium of diabetic rats suggests a role for LOX-1 in the pathogenesis of diabetic vascular dysfunction. Because postprandial plasma glucose has been recently proposed as an independent risk factor for cardiovascular diseases in patients with diabetes, we evaluated, in the current study, the in vitro effect of high glucose on LOX-1 expression by human aortic endothelial cells (

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“…In addition, DNA damage may lead to injury in the endothelium and induce inflammation and, subsequently, the development of atherosclerosis (45). Monocytes from subjects with diabetes have elevated oxidative stress, inflammation response (46), and binding to endothelium compared with cells from individuals without diabetes (47,48). Furthermore, human atherosclerotic plaques showed high levels of DNA damage (49).…”

Section: Discussionmentioning

confidence: 99%

PPARGC1A Variation Associated With DNA Damage, Diabetes, and Cardiovascular Diseases

et al. 2008

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OBJECTIVE-Individuals with type 2 diabetes exhibit higher DNA damage and increased risk of cardiovascular disease (CVD). However, mechanisms underlying the association between DNA damage and development of type 2 diabetes and CVD are not understood. We sought to link peroxisome proliferatoractivated receptor-␥ coactivator-1 ␣ (PPARGC1A), a master transcriptional regulator of mitochondrial oxidative phosphorylation and cellular energy metabolism, with DNA damage, type 2 diabetes, and CVD.RESEARCH DESIGN AND METHODS-We measured DNA damage as urinary 8-hydroxydeoxyguanosine (8-OHdG) concentration and examined the relationship between nine PPARGC1A genetic variants, DNA damage, type 2 diabetes, and self-reported CVD in 959 participants of the Boston Puerto Rican Health Study.RESULTS-With respect to urinary 8-OHdG, PPARGC1A variants showed significant association, and PPARGC1A haplotypes exhibited significant association after correction for multiple testing. Two independent PPARGC1A variants associated significantly with type 2 diabetes (odds ratios [ORs] 1.35 and 2.46; P ϭ 0.045 and Ͻ0.001). Carriers of minor alleles of two other PPARGC1A variants, both in strong linkage disequilibrium and associated with lower DNA damage, showed lower prevalence of CVD (ORs 0.53 and 0.65; P ϭ 0.030 and 0.175). Moreover, we found that physical activity correlated negatively with DNA damage.CONCLUSIONS-It is plausible that low physical activity combined with risk haplotyes contribute to the high prevalence of type 2 diabetes in this population. We propose that PPARGC1A influences development of type 2 diabetes and CVD via DNA damage. Increasing physical activity, which induces PPARGC1A expression, is a potential strategy to slow DNA damage, thereby decreasing the risk of CVD for individuals with type 2 diabetes.

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Hypertriglyceridemia Enhances Monocyte Binding to Endothelial Cells in NIDDM

Abstract: The results suggest that in NIDDM hypertriglyceridemia should be treated to reduce the high risk for atherosclerosis.

Cited by 25 publications

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Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Increased Monocytic Activity and Biomarkers of Inflammation in Patients With Type 1 Diabetes

Glucose Enhances Endothelial LOX-1 Expression

PPARGC1A Variation Associated With DNA Damage, Diabetes, and Cardiovascular Diseases

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