Fasting hyperglycemia and postprandial : an aid to a more targeted prognosis.
A state of persistent hyperglycaemia continued over time acts in concert with other cardiovascular risk factors within or in the context of the metabolic syndrome * , to cause vascular damage .
Patients with hyperglycemia often have :insulin resistance and hyperinsulinemia ;
- increased blood pressure
- increased triglycerides , increased LDL and low HDL cholesterol levels
- central obesity
- high levels of inhibitors of plasminogen activator and low-grade inflammation
Nevertheless, experimental models confirm the importance of the direct effect of even slight alterations of glucose homeostasis in the atherosclerotic process .
Today , we know that the exposure glucose and glucose variability contribute to the development of atherosclerosis : the arterial wall , in fact , is a critical target for these insults glucose .
The glycosylation of proteins ( caused by the presence of elevated glucose levels that persisted in the body end up reacting with the -NH2 groups of the residues of proteins) due crosslinks with collagen and other extracellular matrix proteins in the arterial wall , and increasing favoring the formation of atherosclerotic processes .
Glycosylation of LDL particles ( caused by the presence of elevated glucose levels that persisted in the body end to react with LDL oxidization, stimulates the activation of macrophages, and the formation of foam cells first mover for the formation of the atheromatous plaque.
Even more direct action is exerted by the glucose molecules in long stay in the bloodstream that react with the NH2 – terminal of the endothelial cells , causing endothelial dysfunction , an early manifestation of atherosclerosis, and an important prognostic factor for cardiovascular disease .
In type 2 diabetes , blood sugar fluctuations during the post prandial or, more generally , all the extreme fluctuations seem to have a more specific triggering effect on oxidative stress than chronic hyperglycemia : In vitro studies have demonstrated increased expression of markers of oxidative stress in cells exposed to fluctuating concentrations of glucose.
The hyperglycemia in non-insulin- dependent tissues , such as endothelial cells , causes a super production of free radicals and superoxide by the mitochondrial respiratory chain ; free radicals may mediate some of the effects associated with hyperglycemia such as vasoconstriction , activation of the coagulation , increased expression of adhesion molecules , etc. .
The post-prandial hyperglycemia and glucose variability are also associated with an inflammatory state reported by the formation of advanced glycosylation products (AGE ‘s) , with a marked increase in the levels of C-reactive protein and TNF -a.
Acute hyperglycaemia activates the formation of carbonyls , leading to the formation of highly reactive species such as methylglyoxal or 3 – deossiglucusone .
Today, most of the scholars of both the diabetes but also metabolic diseases agrees to judge the disglicemia a factor not to be overlooked at all.
Article by GIOACCHINO DI LEO
The image is a watercolor by BRUNA MILANI