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Endothelial dysfunction in diabetes mellitus.

Hadi HA, Suwaidi JA - Vasc Health Risk Manag (2007)

Bottom Line: A complete biochemical understanding of the mechanisms by which hyperglycemia causes vascular functional and structural changes associated with the diabetic milieu still eludes us.Control of hyperglycemia thus remains the best way to improve endothelial function and to prevent atherosclerosis and other cardiovascular complications of diabetes.In the present review we provide the up to date details on this subject.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology and Cardiovascular Surgery, Hamad General Hospital, Hamad Medical Corporation, Doha, State of Qatar, UAE. hadi968@hotmail.com

ABSTRACT
Diabetes mellitus is associated with an increased risk of cardiovascular disease, even in the presence of intensive glycemic control. Substantial clinical and experimental evidence suggest that both diabetes and insulin resistance cause a combination of endothelial dysfunctions, which may diminish the anti-atherogenic role of the vascular endothelium. Both insulin resistance and endothelial dysfunction appear to precede the development of overt hyperglycemia in patients with type 2 diabetes. Therefore, in patients with diabetes or insulin resistance, endothelial dysfunction may be a critical early target for preventing atherosclerosis and cardiovascular disease. Microalbuminuria is now considered to be an atherosclerotic risk factor and predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. It has been implicated as an independent risk factor for cardiovascular disease and premature cardiovascular mortality for patients with type 1 and type 2 diabetes mellitus, as well as for patients with essential hypertension. A complete biochemical understanding of the mechanisms by which hyperglycemia causes vascular functional and structural changes associated with the diabetic milieu still eludes us. In recent years, the numerous biochemical and metabolic pathways postulated to have a causal role in the pathogenesis of diabetic vascular disease have been distilled into several unifying hypotheses. The role of chronic hyperglycemia in the development of diabetic microvascular complications and in neuropathy has been clearly established. However, the biochemical or cellular links between elevated blood glucose levels, and the vascular lesions remain incompletely understood. A number of trials have demonstrated that statins therapy as well as angiotensin converting enzyme inhibitors is associated with improvements in endothelial function in diabetes. Although antioxidants provide short-term improvement of endothelial function in humans, all studies of the effectiveness of preventive antioxidant therapy have been disappointing. Control of hyperglycemia thus remains the best way to improve endothelial function and to prevent atherosclerosis and other cardiovascular complications of diabetes. In the present review we provide the up to date details on this subject.

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Progression of endothelial dysfunction in relation the progression of insulin resistance (Hsueh et al 2004).
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fig1: Progression of endothelial dysfunction in relation the progression of insulin resistance (Hsueh et al 2004).

Mentions: The insulin resistance syndrome encompasses more than a subnormal response to insulin-mediated glucose disposal. Patients with this syndrome also frequently display elevated blood pressure, hyperlipidemia and dysfibinolysis even without any clinically demonstrable alteration in plasma glucose concentrations. Of note, endothelial dysfunction also has been demonstrated in patients with hypertension (Landin et al 1990; Luscher 1990; Bonner 1994; Briner and Luscher 1994; Kamide et al 1996; Lemne and de Faire 1996; Hedner and Sun 1997; Khder et al 1998), which is one of the features of the insulin resistance syndrome. It is tempting to speculate that loss of endothelial-dependent vasodilation and increased vasoconstrictors might be etiological factors of hypertension. Moreover loss of activity and/or quantity of endothelium-bound protein lipase activity may contribute to hyperlipidemia, which is typical of the insulin resistance syndrome. A synergistic interaction and vicious cycle may exist in which endothelial dysfunction contributes to insulin resistance and vice versa (Figure 1).


Endothelial dysfunction in diabetes mellitus.

Hadi HA, Suwaidi JA - Vasc Health Risk Manag (2007)

Progression of endothelial dysfunction in relation the progression of insulin resistance (Hsueh et al 2004).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2350146&req=5

fig1: Progression of endothelial dysfunction in relation the progression of insulin resistance (Hsueh et al 2004).
Mentions: The insulin resistance syndrome encompasses more than a subnormal response to insulin-mediated glucose disposal. Patients with this syndrome also frequently display elevated blood pressure, hyperlipidemia and dysfibinolysis even without any clinically demonstrable alteration in plasma glucose concentrations. Of note, endothelial dysfunction also has been demonstrated in patients with hypertension (Landin et al 1990; Luscher 1990; Bonner 1994; Briner and Luscher 1994; Kamide et al 1996; Lemne and de Faire 1996; Hedner and Sun 1997; Khder et al 1998), which is one of the features of the insulin resistance syndrome. It is tempting to speculate that loss of endothelial-dependent vasodilation and increased vasoconstrictors might be etiological factors of hypertension. Moreover loss of activity and/or quantity of endothelium-bound protein lipase activity may contribute to hyperlipidemia, which is typical of the insulin resistance syndrome. A synergistic interaction and vicious cycle may exist in which endothelial dysfunction contributes to insulin resistance and vice versa (Figure 1).

Bottom Line: A complete biochemical understanding of the mechanisms by which hyperglycemia causes vascular functional and structural changes associated with the diabetic milieu still eludes us.Control of hyperglycemia thus remains the best way to improve endothelial function and to prevent atherosclerosis and other cardiovascular complications of diabetes.In the present review we provide the up to date details on this subject.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology and Cardiovascular Surgery, Hamad General Hospital, Hamad Medical Corporation, Doha, State of Qatar, UAE. hadi968@hotmail.com

ABSTRACT
Diabetes mellitus is associated with an increased risk of cardiovascular disease, even in the presence of intensive glycemic control. Substantial clinical and experimental evidence suggest that both diabetes and insulin resistance cause a combination of endothelial dysfunctions, which may diminish the anti-atherogenic role of the vascular endothelium. Both insulin resistance and endothelial dysfunction appear to precede the development of overt hyperglycemia in patients with type 2 diabetes. Therefore, in patients with diabetes or insulin resistance, endothelial dysfunction may be a critical early target for preventing atherosclerosis and cardiovascular disease. Microalbuminuria is now considered to be an atherosclerotic risk factor and predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. It has been implicated as an independent risk factor for cardiovascular disease and premature cardiovascular mortality for patients with type 1 and type 2 diabetes mellitus, as well as for patients with essential hypertension. A complete biochemical understanding of the mechanisms by which hyperglycemia causes vascular functional and structural changes associated with the diabetic milieu still eludes us. In recent years, the numerous biochemical and metabolic pathways postulated to have a causal role in the pathogenesis of diabetic vascular disease have been distilled into several unifying hypotheses. The role of chronic hyperglycemia in the development of diabetic microvascular complications and in neuropathy has been clearly established. However, the biochemical or cellular links between elevated blood glucose levels, and the vascular lesions remain incompletely understood. A number of trials have demonstrated that statins therapy as well as angiotensin converting enzyme inhibitors is associated with improvements in endothelial function in diabetes. Although antioxidants provide short-term improvement of endothelial function in humans, all studies of the effectiveness of preventive antioxidant therapy have been disappointing. Control of hyperglycemia thus remains the best way to improve endothelial function and to prevent atherosclerosis and other cardiovascular complications of diabetes. In the present review we provide the up to date details on this subject.

Show MeSH
Related in: MedlinePlus