Metabolic syndrome now represents a major public health problem at the root of the twin global epidemics of type 2 diabetes and cardiovascular disease. There are many consequences associated with metabolic syndrome. One such consequence is oxidative stress, induced by both hyperglycemia and hyperlipidemia.
Metabolic syndrome and oxidative stress, a note about these two notions
Metabolic syndrome refers to the presence of physiological factors (elevated glucose levels, abdominal obesity, hypertriglyceridemia, low HDL cholesterol level, high blood pressure) which increase the likelihood of type 2 diabetes, heart disease and stroke. This syndrome is defined by the presence of at least three of these factors.
Oxidative stress appears in a cell when the balance between oxidizing and antioxidant molecules is disturbed, resulting in a shift toward an oxidizing state. It is characterised by the overproduction of free radicals, which are also known as Reactive Oxygen Species (ROS). This oxidative stress causes extensive damage: oxidation of cell membranes, denaturation of proteins, etc.
How are metabolic syndrome and oxidative stress linked?
Oxidative stress is brought on by different factors such as tobacco, ultraviolet exposure, alcohol, hyperlipidemia or hyperglycemia. These last two factors are linked to metabolic syndrome.
Hyperglycemia causes the production of free radicals through two different reactions: protein glycation and activation of the polyol pathway:
- In the phenomenon of glycation, glucose reacts with the amino groups of proteins to produce Schiff bases, a combination of glucose and proteins which eventually form advanced glycosylation end products. The glycated proteins activate membrane receptors such as RAGE (Receptor for Advanced Glycosylation End products), inducing intracellular oxidative stress1, the regulation of the inflammation through the interaction of the AGEs and increased expression of inflammatory cytokines (TNF alpha, beta IL1, IL6 and others).
- The polyol pathway is also activated by an accumulation of glucose in the tissues. It primarily involves two enzymes, aldose reductase and sorbitol-deshydrogenase. The first enzyme helps transform glucose into sorbitol while the second produces uses the sorbitol to produce fructose. This increased production of fructose also stimulates protein glycation.
Hyperlipidemia is also responsible for producing free radicals since it increases the lipid peroxidation at the root of oxidative stress.
Oxidative stress and the associated free radicals, caused by metabolic syndrome, lead to cell and vascular damage which in turn lead to diabetes-related complications and insulin resistance. Moreover, diabetic individuals often have lowered antioxidant defences, which further compounds oxidative stress.
How to combat oxidative stress?
Antioxydants contained in food are an important means of combating and preventing oxidative stress, whether associated with metabolic syndrome or in general. Some of the most powerful antioxidants are copper, zinc, iron, manganese, selenium, vitamins C, D and E, folic acid and beta-carotene.
In addition, carcinine, a peptide which comes from crustaceans, has an anti-glycation and de-glycation effect, therefore making it possible to limit oxidative stress and the associated consequences. Our Glycoxil® ingredient, made from natural carcinine, exhibits excellent stability and very good bioavailability. It helps prevent the production of glycated proteins and deglycate proteins which have already been affected in a long-lasting, effective way2.
1. Anti-glycation effect of carcinine (alistin): highlighting of its capacity to limit glucosone-induced collagen reticulation and yellowing, Exsymol, May 2016
2. Evaluation of carcinine supplementation: results of immunostainings and classical histology, Sedifa Laboratory, September 2008