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.

The aim of this study was to evaluate the relationship between early blood pressure (BP) changes (detected using ambulatory BP monitoring; ABPM) with different markers of inflammation and endothelial dysfunction in patients with type 1 diabetes mellitus (T1DM). The study design was observational cross-sectional in 85 T1DM patients, clinically normotensive and with normo-albuminuria. We analyzed the relationships between ABPM-measured BP alterations over 24 h with the inflammatory cytokines (interleukin-6 (IL-6), tumor necrosis factor-α and vascular endothelial growth factor (VEGF)) and the markers of endothelial damage (vascular adhesion molecule, intercellular adhesion molecule and plasminogen activator inhibitor-1 (PAI)). Despite being recorded as normotensive, 27 (31.8%) subjects presented with an average of pathological BP. VEGF levels were significantly elevated in the patients with an altered mean diurnal values compared with normotensives (112.33 (72.87-213.53) pg ml vs 71.03 (37.71-107.92) pg ml; P=0.007). Further, VEGF levels correlated significantly with the parameters of diurnal BP and of 24 h values. IL-6 concentration was a risk factor in the patients with hypertension (OR=1.406; P=0.027). There were no modifications in the levels of markers of endothelial damage. Summarizing, there is an increase in pro-inflammatory cytokines, but not the endothelial adhesion molecules, in early stages of arterial hypertension in patients with T1DM.

No abstract

No abstract

No abstract