Currently, a search is underway for non-drug biologically active agents that help restore impaired metabolism in metabolic syndrome. The attention of many researchers is drawn to L-carnitine and its role in the metabolism of fats and carbohydrates in both normal and pathological conditions.
The review is devoted to an urgent topic the theoretical justification of increasing the biogenic potential of drinking mineral waters in order to use them in the non-drug treatment of metabolic syndrome. The choice of a biologically active substance for the modification of drinking mineral waters, namely, L-carnitine, is based on its direct involvement in the energy exchange of body cells.
L-carnitine plays an irreplaceable role in lipid metabolism: it participates in the transport of fatty acids and products of their incomplete oxidation across the mitochondrial membrane, potentiating -oxidation of long-chain fatty acids, which leads to the activation of energy metabolism in various tissues. Thus, it can be assumed that the addition of L-carnitine to the diet of patients with metabolic syndrome and type 2 diabetes mellitus may be an effective tool in the treatment and prevention of the progression of these diseases.
The data of experimental and clinical studies justifying the preventive effect of drinking mineral waters were analyzed. In addition, we have conducted searching for scientific publications over the past 5 years in the electronic databases PubMed, Web of Science, e-Library on the study of L-carnitine and drinking mineral waters of various compositions, taking into account their influence on the components of metabolic syndrome. The search terms provided criteria that included full text, related data, clinical trials, meta-analysis, randomized controlled trials, and systematic reviews.
Based on the results of independent scientific studies, it is unambiguous to conclude that there is both a direct (due to dissolved ions) and a more complex (mediated through regulatory systems) effect of mineral waters on impaired metabolism caused by magnesium and calcium deficiency in this group of patients.
Background. Due to the fact that it is not always possible to reproduce all known manifestations of carbohydrate and lipid metabolism disorders, for example, in rodents, it is necessary to verify individual pathogenetic links in animals when modeling the metabolic syndrome in order to select the most optimal natural biotropic factors for studying the effect on them.
Aims: To analyze metabolic disorders in the modeling of metabolic syndrome of alimentary genesis in comparison with the combined effect of alimentary factor and chemical agents to select the most appropriate model in the study of natural and weak preformed physical factors.
Materials and methods. Metabolic syndrome was modeled in 47 sexually mature outbred white male rats using a hypercaloric diet (HD) of various duration and medications. The first series was the 1st control group (CG1) and the 1st experimental group (EG1). They received HD during 180 days, they were withdrawn from the experiment 30 days after the cancellation of HD. The second series was the 2nd control group (CG2) and three experimental groups. They received HD for 60 days, where the 2nd group (EG2) in association with HD received Mercazolil (10 mg/kg of animal weight) intragastrically for 14 days starting from the 21st day; the 3rd group (EG3) had the same scheme of treatment as in EG2, besides, after taking Mercazolil, they were intramuscularly injected with Nitox 200 at 25 mg/kg once per day during 5 days. Animals of EG2 and EG3 were withdrawn from the experiment 60 days after ending of HD. Animals of the 4th experimental group (EG4) got HD and the same medicine as in EG3. They left the experiment 30 days after ending HD. The content of hormones and biochemical parameters of protein, fat, and carbohydrate in peripheral blood was evaluated using multiple inter-group comparisons and intra-group relationships by Spearmans rank correlation method.
Results. There have been detected a large number of biochemical signs of dependence of metabolism regulation on leptin level after long-term HD (180 days), while there were fewer biochemical signs of protein exchange disorder less than with the combined use of HD (60 days) and drugs.
Conclusion. It is more appropriate and promising to use a long-term HD as a model of MS close to the natural conditions of its formation, to study the influence of natural and weak preformed physical factors.
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