Abstract
Metabolic syndrome (MetS) is a cluster of several disorders, such as hypertension, central obesity, dyslipidemia, hyperglycemia, insulin resistance and non-alcoholic fatty liver disease. Despite health policies based on the promotion of physical exercise, the reduction of calorie intake and the consumption of healthy food, there is still a global rise in the incidence and prevalence of MetS in the world. This phenomenon can partly be explained by the fact that adverse events in the perinatal period can increase the susceptibility to develop cardiometabolic diseases in adulthood. Individuals born after intrauterine growth restriction (IUGR) are particularly at risk of developing cardiovascular diseases (CVD) and metabolic disorders later in life. It has been shown that alterations in the structural and functional integrity of the endothelium can lead to the development of cardiometabolic diseases. The endothelial progenitor cells (EPCs) are circulating components of the endothelium playing a major role in vascular homeostasis. An association has been found between the maintenance of endothelial structure and function by EPCs and their ability to differentiate and repair damaged endothelial tissue. In this narrative review, we explore the alterations of EPCs observed in individuals with cardiometabolic disorders, describe some mechanisms related to such dysfunction and propose some therapeutical approaches to reverse the EPCs dysfunction.
Highlights
Neonatal Research Laboratory, Department Woman-Mother-Child, Clinic of Neonatology, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland; Division of Pediatrics, DOHaD Laboratory, Department Woman-Mother-Child, Lausanne University Hospital, 1011 Lausanne, Switzerland
endothelial progenitor cells (EPCs) angiogenesis abilitybeen and observed left ventricular ejection fraction, and endothelium, an increased left ventricular remodeling have in the ejection fraction, to and an increased left ventricular remodeling have been observed in the obese compared control mice [91]
non-alcoholic fatty liver disease (NAFLD) is currently well recognized as a hepatic manifestation of Metabolic syndrome (MetS) [95] and has NAFLD is currently well recognized as a hepatic manifestation of MetS [95] and been associated with obesity, insulin resistance, systemic inflammation and advanced has been associated with obesity, insulin resistance, systemic inflammation and advanced atherosclerosis[96,97]
Summary
The incidence and prevalence of metabolic syndrome (MetS) are increasing worldwide and MetS is becoming a global health problem. MetS affects 20–30% of the population in developed countries [1]. The major components of the MetS cluster are obesity, in particular abdominal body fat accumulation, impaired glucose metabolism, dyslipidemia and arterial hypertension [2,3]. Non-alcoholic fatty liver disease (NAFLD), which is defined as excess fat (>5% weight or volume) deposition in the liver in the absence of excessive alcohol intake, has been identified as a hepatic manifestation of MetS [4]. MetS has been identified as an epidemiologic tool related to cardiovascular disease (CVD) risk. Each component of the MetS represents an independent risk factor for the development of CVD [5,6,7]
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