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Abstract
The rising prevalence of childhood obesity in the past decades has made Non-Alcoholic Fatty Liver Disease (NAFLD) the most common cause of pediatric chronic liver disease worldwide. Currently, a growing body of evidence links NAFLD with cardiovascular disease (CVD) even at an early age. Data on the pediatric population have shown that NAFLD could represent an independent risk factor not only for cardiovascular events but also for early subclinical abnormalities in myocardial structure and function. Briefly, we review the current knowledge regarding the relationship between pediatric NAFLD and cardiovascular risk in an attempt to clarify our understanding of NAFLD as a possible cardiovascular risk factor in childhood.
Highlights
In the last 20 years, Non-Alcoholic Fatty Liver Disease (NAFLD) has become the major cause of chronic liver disease in childhood, as a result of an increased prevalence of pediatric obesity [1,2]
It has been widely recognized that NAFLD represents an independent risk factor for cardiovascular diseases (CVD) in adulthood, but this association is still debated in the pediatric population [4,5,6,7,8]
Recent studies have focused on fibroblast growth factor 21 (FGF-21), a hepatoprotective protein with modulatory effects on glucose and insulin sensitivity, that shows a condition of resistance in subjects with NAFLD, with further worsening in the case of Non-Alcoholic Steatohepatitis (NASH) [11]
Summary
In the last 20 years, Non-Alcoholic Fatty Liver Disease (NAFLD) has become the major cause of chronic liver disease in childhood, as a result of an increased prevalence of pediatric obesity [1,2]. It has been widely recognized that NAFLD represents an independent risk factor for cardiovascular diseases (CVD) in adulthood, but this association is still debated in the pediatric population [4,5,6,7,8]. The association between NAFLD and cardiovascular derangements has not been fully elucidated in children, but increased visceral adipose tissue and insulin resistance seem to play a critical role [8,10,11]. Recent studies have focused on fibroblast growth factor 21 (FGF-21), a hepatoprotective protein with modulatory effects on glucose and insulin sensitivity, that shows a condition of resistance in subjects with NAFLD, with further worsening in the case of Non-Alcoholic Steatohepatitis (NASH) [11]. In order to stop this vicious circle, a comprehensive treatment of NAFLD (weight loss, lifestyle interventions, control of risk factors) is strongly recommended
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