VITAMIN B12 AND METABOLIC SYNDROME (literature review)

Abstract

Metabolic syndrome (MetS) is a cluster of interrelated and often coexisting conditions and diseases, such as impaired glucose tolerance, dyslipidemia, hypertension, and abdominal obesity, each of which is independently associated with an increased risk of cardiovascular disease, diabetes mellitus, stroke, and overall mortality.

Enriching the diet with certain biofactors may be a useful adjunct to conventional therapy for the prevention and treatment of MetS, since, on the one hand, MetS is associated with a systemic deficiency of a number of biofactors, and on the other hand, their beneficial effects are observed even in patients without such a deficiency.

A number of epidemiological and experimental studies have demonstrated a link between the importance of vitamin B12 and various components of MetS. Vitamin B12 (cyanocobalamin, cobalamin) is an essential cofactor in two important biochemical pathways: the metabolism of methylmalonic acid and the synthesis of methionine from homocysteine (Hcy). In addition, attention has been drawn to a possible link between low levels of vitamins B6, B12, and folates, or elevated blood Hcy levels, and an increased risk of MetS, as abnormalities in these levels may also contribute to changes involved in the pathogenesis of this syndrome. This may serve as a rationale for the use of vitamin B12 in the treatment of MetS, even in the early subclinical stages.

The interactions between vitamin B12 and MetS are extremely complex and not yet fully understood, as they involve multifaceted biochemical and physiological processes. Studies demonstrate that a deficiency of key nutrients, such as folates, vitamins B6 and B12, can lead to the development of low-grade chronic inflammation, dyslipidemia, impaired vascular endothelial function, and impaired glucose tolerance, and also contributes to the onset of insulin resistance. These pathophysiological conditions are most often caused by the effects of oxidative stress, which plays a significant role in the development of MetS. In addition to low-grade chronic inflammation, cobalamin deficiency disrupts nitric oxide synthesis, a process closely linked to key mechanisms of MetS pathophysiology. Thus, cobalamin, regardless of its classical function as a cofactor, may act as an intracellular, specifically an intramitochondrial, antioxidant. Evidence of a link between levels of cyanocobalamin, folates, and Hcy with MetS will open the possibility of investigating the use of these vitamins as a preventive therapy for MetS or its complications.

The aim of this review is to synthesize current understanding of the role of vitamin B12 in the prevention and treatment of metabolic syndrome, as well as to identify promising areas for further research in this field. The search was conducted in Scopus, ScienceDirect (from Elsevier), and PubMed, including the Medline databases. The keywords used were “vitamin B12,” “cobalamin,” “metabolic syndrome,” “obesity,” “insulin resistance,” and “dyslipidemia.” To identify study results that could not be found during the online search, a manual search of the bibliographies of publications was conducted.