Metabolic syndrome and neuroprotection

Abstract

Introduction. Over the years, the prevalence of metabolic syndrome has increased dramatically in developing countries as a major byproduct of industrialization. Many factors, such as the consumption of high-calorie diets and a sedentary lifestyle, favor the spread of this disorder. Without a doubt, the massive and still growing incidence of metabolic syndrome places this epidemic as an important public health problem. Metabolic syndrome is also a neurological and psychiatric risk factor. In this work, an exploratory review of literature on the topic will be carried out. In this work, we review the information regarding what is known about metabolic syndrome beyond its classic association with cardiovascular disease and type 2 diabetes mellitus, since metabolic syndrome also represents a risk factor for nervous tissue and a threat neuronal function. First, we present some essential concepts of the pathophysiology of metabolic syndrome. Secondly, we explore some neuroprotective approaches in metabolic syndrome related to cerebral hypoxia. Goals. Update, exploratory review, and synthesize the literature regarding the neurological impact of metabolic syndrome, beyond its classic association with cardiovascular disease and type 2 diabetes mellitus. Define and review essential concepts of the pathophysiology of metabolic syndrome. Explore neuroprevention and neuroprotection strategies in metabolic syndrome related to therapeutic cerebral hypoxia. Material and methods. An exploratory survey of scientific literature from the period January 1989-November 2022 was carried out. Selection/inclusion criteria: scientific publications containing data and exploratory information on metabolic syndrome and neurological comorbidity and possible neurotherapeutic approaches. Pathophysiology. The metabolic pathways characteristically impaired in metabolic syndrome lead to hyperglycemia, insulin resistance, inflammation and hypoxia, all closely related to a generalized pro-oxidative state. Oxidative stress is well known to cause the destruction of cellular structures and tissue architecture. Disruption of redox homeostasis and oxidative stress alter the macromolecular matrix of nuclear genetic material, lipids and proteins, which in turn alters biochemical pathways necessary for normal cellular function. Neuroprotection. Different neuroprotective strategies are discussed that involve lifestyle changes, medications aimed at mitigating the cardinal symptoms of metabolic syndrome, and treatments aimed at reducing oxidative stress. It is well known that routine physical exercise, particularly aerobic activity, and a complete and balanced diet are key factors in preventing metabolic syndrome. However, pharmacological control of the metabolic syndrome as a whole and the corresponding hypertension, dyslipidemia and endothelial injury contribute to the improvement of neuronal health. Conclusion. The development of metabolic syndrome is presented as a risk factor for the development and/or exacerbation of neurological disorders. Therapeutic strategies include multidisciplinary approaches aimed at addressing, in a concerted manner, different pathways involved in its pathophysiology.