TRACE ELEMENTS IN MEDICINE (MOSCOW)
2015. 16(2): 3-9
TOPICAL PAPERS

IRON IN OBESITY: A VICTIM OR SUSPECT

А.А. Nikonorov1, A.A. Tinkov1,2, E.V. Popova1, O.N. Nemereshina1, E.R. Gatiatulina1, M.G. Skalnaya3, A.V. Skalny2,3

1 Orenburg State Medical University, Sovetskaya str. 6, Orenburg, 460000, Russia
2 P.G. Demidov Yaroslavl State University, Sovetskaya str. 14, Yaroslavl, 150000, Russia
3 ANO Centre for Biotic Medicine, Zemlyanoi val 46, Moscow, 105064, Russia

DOI: 10.19112/2413-6174-2015-16-2-3-9 

ABSTRACT. Numerous indications of the interrelationship between obesity and impaired iron homeostasis exist. At the same time, the exact pathways are unknown. A review of data regarding interaction between iron and obesity was performed. Two sides of such interaction have been revealed: at first, obesity-induced iron deficiency (iron as a victim), and at second, excessive iron cumulation as a risk factor for obesity development (iron as a suspect). Obesity-induced hypoferremia may be formed as a result of hepcidin and lipocalin-2 hyperproduction, leading to iron sequestration in reticuloendothelial cells and decreased iron absorption. Literature data indicating intimate mechanisms of hepcidin and lipocalin-2 induction in obesity are reviewed. It is shown that iron accumulation in adipose tissue results in its toxicity by endoplasmic reticulum and oxidative stress, proinflammatory changes, and adipocyte endocrine dysfunction. The latter processes are known to play a key role in obesity pathogenesis. It is concluded that a circus vitiosus, where hypoferremia, iron cumulation in adipose tissue and obesity are self-sustaining processes, is formed. All components of this circus vitiosus should be taken into account while planning therapeutic approaches to obesity treatment. In particular, iron chelation along with anti-inflammatory treatment may hypothetically break the circus vitiosus and improve metabolic health in obese individuals. At the same time, further studies in this field are required.

KEYWORDS: iron, obesity, inflammation, hepcidin, lipocalin-2, oxidative stress, endoplasmic reticulum stress.