Interaction between HFE and haptoglobin polymorphisms and its relation with plasma glutathione levels in obese children

Abstract

Obesity among children has emerged as a serious public health problem. The growing prevalence of childhood obesity has led to the appearance of serious complications, including a chronic systemic inflammation associated with oxidative stress. In the present study, we analysed the interaction between two genes related with iron metabolism -HFE and haptoglobin -and the plasmatic concentration of glutathione, as a way to evaluate the antioxidant response capacity in obesity. To achieve this, 118 obese children and 89 eutrophic children were recruited for the study. Results showed that although obese children present a significantly decreased tGSH levels, once we analysed separately children based on their haptoglobin phenotype, the decreased tGSH levels is significant only for the Hp 2 allele. Additionally, Hp 2.2 obese children carrying H63D polymorphism show significantly lower tGSH/GSSG values. Our results found an association of haptoglobin and HFE with oxidative stress in childhood obesity.

Iron Metabolism in Obesity and Metabolic Syndrome

“…Moreover, the haptoglobin phenotype has been related to oxidative stress in obesity, since the presence of the Hp 2 allele seems to be associated to lower levels of reduced glutathione (tGSH) in obese children. This difference is even higher if the Hp phenotype is accompanied by H63D polymorphism in the HFE gene [ 138 ]. CD163 expression is also elevated in obese subjects and positively correlates with insulin resistance, as measured by HOMA-IR [ 139 ].…”

Pathophysiological disorders in iron metabolism in the development of obesity and metabolic syndrome

“…Более того, фенотип гаптоглобина был связан с окислительным стрессом при ожирении, поскольку наличие аллеля Hp 2, по-видимому, ассоциировано с более низкими уровнями восстановленного глутатиона (tGSH) у детей с ожирением. Это различие становится еще более заметным, если фенотип Hp сопровождается полиморфизмом H63D в гене HFE [77]. Экспрессия CD163 также увеличена у лиц с ожирением и положительно коррелирует с инсулинорезистентностью при измерении с помощью HOMA-IR [78].…”