Abstract

Metabolic syndrome is not a single pathology, but a constellation of cardiovascular disease risk factors including: central and abdominal obesity, systemic hypertension, insulin resistance (or type 2 diabetes mellitus), and atherogenic dyslipidemia. The global incidence of Metabolic syndrome is estimated to be about one quarter of the world population; for this reason, it would be desirable to better understand the underlying mechanisms involved in order to develop treatments that can reduce or eliminate the damage caused. The effects of Metabolic syndrome are multiple and wide ranging; some of which have an impact on the central nervous system and cause neurological and neurodegenerative diseases. Autophagy is a catabolic intracellular process, essential for the recycling of cytoplasmic materials and for the degradation of damaged cellular organelle. Therefore, autophagy is primarily a cytoprotective mechanism; even if excessive cellular degradation can be detrimental. To date, it is known that systemic autophagic insufficiency is able to cause metabolic balance deterioration and facilitate the onset of metabolic syndrome. This review aims to highlight the current state of knowledge regarding the connection between metabolic syndrome and the onset of several neurological diseases related to it. Furthermore, since autophagy has been found to be of particular importance in metabolic disorders, the probable involvement of this degradative process is assumed to be responsible for the attenuation of neurological disorders resulting from metabolic syndrome.

Highlights

  • Metabolic syndrome (MetS), known as syndrome X, insulin resistance syndrome, or Reaven syndrome; is not a single pathology, but a constellation of cardiovascular disease risk factors

  • Autophagy in MetS and Its Neurological Disorders characteristics of MetS; among these, we point out the one provided by the International Federation of Diabetes (IDF) of 2006 (Saklayen, 2018), which states that metabolic syndrome is represented by glucose in the blood above 5.6 mmol/L (100 mg/dl) along with the presence of two or more of the following conditions:

  • It has been highlighted that autophagy is fundamental for the maintenance of cellular metabolic homeostasis and that it plays a crucial role in the control of body metabolism, whose dysregulation could participate in the onset of Mets (Lim et al, 2018)

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Summary

Introduction

Metabolic syndrome (MetS), known as syndrome X, insulin resistance syndrome, or Reaven syndrome; is not a single pathology, but a constellation of cardiovascular disease risk factors. The global incidence of MetS is very high, afflicting one third of adults 18 years or older in the United States alone (Aguilar et al, 2015). During the last 15 years, the prevalence of MetS has increased (Pucci et al, 2017) and the main motivation is related to significant changes in lifestyle; the western lifestyle consists of numerous risk factors such as: high-fat diet, cigarette smoking, alcohol consumption, obesity, and physical inactivity (O’Doherty et al, 2016; Sarmiento Quintero et al, 2016; Finicelli et al, 2019). The western diet is based on high consumption of salt, refined sugars, and saturated fats that determine significant effects on body composition and metabolism such as: increased BMI, generalized and abdominal obesity, dyslipidemia, and type 2 diabetes (Misra and Khurana, 2008).

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