Carbohydrates Consumption and Cardiovascular Pathophysiology
Gaetano Crepaldi and Angelo Avogaro.
University of Padova. Italy.
The term 'postprandial' is broadly defined as 'the period following a meal'. The duration of this period depends on the composition of the meal. The postprandial period a meal high in glucose, would be around 2—3 h, there is a great interest in the use of postprandial glucose levels as predictors of diabetic complications and related mortality. The question of whether postprandial blood glucose levels are independent predictors of risk for atherosclerotic disease and total mortality in patient with diabetes was by several studies. A recently published meta-regression analysis of 20 studies including 95,783 nondiabetic individuals who had 3,707 cardiovascular events and who were followed for 12.4 years showed that high fasting, 1-h, and 2-h glucose values increased the risk for cardiovascular events, but that casual glucose did not. 1-h fasting glucose of 6.1 mmol/1 increased the risk of cardiovascular events by 1.33 (1.06—1.67) compared with a fasting glucose of 4.2 mmol/l. Similarly, 2-h glucose of 7.8 mmol/i (140 mg/dl) was associated with a relative risk of cardiovascular events of 1.58 (1.19—2.10). Postprandial hyperglycemia alters each component of the so-called Wirchow triad which encompasses the vascular wall integrity, blood haemodynamics, and the blood cells. Hyperglycemia increases the intra-organ forearm blood flow which is thought to be crucial for the development and progression of long-term diabetic complication. Postprandial hyperglycemia increases ICAM-1 (intracellular adhesion molecule 1) as well as d-dimer concentration and F1 + 2 which are prothrombin fragments: Therefore postprandial hyperglycemia not only activate thrombin but also alters the interaction between endothelial cells and leukocytes. This effect appears to be secondary to an oxidative stress since they are partially reversed by the administration of antioxidant agents such as reduced glutathione. Acute hyperglycemia has also been shown to alter the release of nitric oxide by endothelium. The interaction between endothelium and circulating leucocytes is a key step in the pathogenesis of atherosclerotic lesion. Hyperglycemia has been shown to increase the number of adherence cell to cultured endothelial cells. This interaction appears to dependent upon the activation of protein kinase C, a serine/threonine kinase, which has been shown to be activated by hyperglycemia. Increased PKC activity is linked to the rolling and adhesion of leucocytes to the vessel wall. We have shown that hyperglycemia also increase the PKC in monocytes and this phenomenon is observed not only in diabetic patients but also in normal subjects made hyperglycemic. Hyperglycemia increases selectively the ß2 glucose responsive isoform. In conclusion, postprandial hyperglycemia may contribute to cardiovascular pathophysiology by increasing the concentration of soluble adhesion molecules; by increasing the coagulation pathway; by decreasing the endothelium-mediated vasodilation; by increasing the vascular oxidative stress; by altering the permeability of endothelial cell to albumin; by stimulating the PKC of mononuclear cells thus activating the rolling and the adhesion of leucocytes to the vessel wall.