From Metabolic Syndrome to Neurological Diseases: Role of Autophagy

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.

Short cognitive screening in elderlies as a part of advanced pharmaceutical care in Slovak community pharmacies - The pilot study KOGNIMET-SK

“…Abdominal obesity was the second most prevalent component of MetS, and it also occurred concomitantly with hypertension in 31% of our elderly population, which is in line with the findings described in the study ofHildrum et al (2007). It is important to identify and establish the management of all patients with MetS and also of those who are not affected yet but show early signs of features of MetS(Yates et al, 2012;Maiuolo et al, 2021;Feinkohl et al, 2019). Moreover, it is crucial to act as early as possible because these signs are modifiable and can help to manage patients' cognitive impairment and identify individuals with a high risk of cognitive dysfunction(Liu et al, 2015).…”

“…Moreover, it is crucial to act as early as possible because these signs are modifiable and can help to manage patients' cognitive impairment and identify individuals with a high risk of cognitive dysfunction(Liu et al, 2015). , and support the formation of Alzheimer's disease pathogenesis(Muller et al, 2014;Maiuolo et al, 2021).…”

Elevated plasma levels of the appetite-stimulator ACBP/DBI in fasting and obese subjects

“…Weight gain in mice correlated with enhanced circulating ACBP/DBI concentrations. Since obesity is coupled to an inhibition of autophagy [ 20 – 22 ], it appears improbable that this effect may be explained by an enhanced autophagy-dependent release of ACBP/DBI protein from the intracellular space. Rather, an autophagy-independent release mechanism must account for this observation.…”

Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms

“…Metabolic syndrome (MS) is a multifactorial condition that increases the risk of developing cardiovascular diseases (CVD), type 2 diabetes (T2D), nonalcoholic fatty liver disease (NAFLD), neurodegenerative diseases, and several types of cancer ( 1 – 5 ). The cardinal signs of the MS are 1) abdominal obesity, 2) dyslipidemia (including hypertriglyceridemia and low levels of high-density lipoprotein cholesterol), 3) hypertension, 4) impaired fasting glucose, and 5) insulin resistance ( 1 , 2 , 6 ).…”