Abstract
Obesity is an excessive adipose tissue accumulation that may have detrimental effects on health. Particularly, childhood obesity has become one of the main public health problems in the 21st century, since its prevalence has widely increased in recent years. Childhood obesity is intimately related to the development of several comorbidities such as nonalcoholic fatty liver disease, dyslipidemia, type 2 diabetes mellitus, non-congenital cardiovascular disease, chronic inflammation and anemia, among others. Within this tangled interplay between these comorbidities and associated pathological conditions, obesity has been closely linked to important perturbations in iron metabolism. Iron is the second most abundant metal on Earth, but its bioavailability is hampered by its ability to form highly insoluble oxides, with iron deficiency being the most common nutritional disorder. Although every living organism requires iron, it may also cause toxic oxygen damage by generating oxygen free radicals through the Fenton reaction. Thus, iron homeostasis and metabolism must be tightly regulated in humans at every level (i.e., absorption, storage, transport, recycling). Dysregulation of any step involved in iron metabolism may lead to iron deficiencies and, eventually, to the anemic state related to obesity. In this review article, we summarize the existent evidence on the role of the most recently described components of iron metabolism and their alterations in obesity.
Highlights
Over 35% of obese children under 10 years of age present at least one cardiovascular risk factor or metabolic disturbance, with insulin resistance (IR) being the most common and the earliest to appear. It is already found in patients under five years old [4]. This situation, known as metabolic syndrome (MetS), is a group of cardiovascular risk factors associated with IR of which the main clinical alterations are cellular dysfunction, high fasting triglycerides and glucose, hypertension, low high density lipoprotein cholesterol (HDL-col), systemic inflammation and visceral obesity
Deletion of FXN in mice leads to an impaired oxidative metabolism accompanied by a higher predisposition of these animals to suffer from high-caloric diet-induced obesity [133], but again, to date, this has not been explored in human obesity
As pediatric obesity increases the risk of developing several comorbidities in both childhood and adulthood, it has become crucial to gather the existing knowledge on the molecular and cellular alterations found in these conditions
Summary
Known as non-communicable diseases (NCDs), are the result of a combination of behavioral, environmental, genetic and physiological factors, being responsible for the 75% of deaths in low- and middle-income countries. Obesity, along with cancer, cardiovascular diseases and diabetes, is one of the main NCDs worldwide [1]. Obesity is defined as an excessive fat accumulation that may have detrimental effects on health. Childhood obesity has become one of the main public health problems in the 21st century, since its prevalence has widely increased in recent years. In 2016, over 41 million children under five years of age were overweight or obese around the world. The prevalence of childhood obesity and overweight children has increased up to 30% of preschool children. If the actual growth rate is sustained, 70 million children will be obese or overweight in 2025. Obese children are more likely to become obese adults, with higher probabilities of suffering other NCDs like diabetes or cardiovascular diseases. Childhood obesity prevention and treatment strategies need to be given primary importance [2,3]
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