Two previous studies [18, 27] have demonstrated that hepcidin GSK2656157 mRNA expression in AbScAT and visceral adipose tissue from obese women did not differ significantly. However, it is well understood that adipose tissue is not homogenous . Therefore, despite reporting that the AbScAT does not release hepcidin, we cannot exclude the possibility that the visceral adipose depot secretes hepcidin and has an influential role in systemic or localized iron regulation. Collectively, previous research and findings from this study suggest that liver- and not adipose-derived hepcidin may be associated with the increased systemic hepcidin concentrations and the iron dysregulation observed in obesity.
First, hepatic selleck DNA Methyltransferase inhibitor hepcidin mRNA expression was reported to be significantly greater than that observed in AbScAT and visceral adipose tissue from obese women [18, 27]; in one study, it was reported to be more than 700 times greater . Also, Tussing-Humphreys and colleagues  reported that liver hepcidin mRNA expression was positively correlated with serum hepcidin concentrations, whereas adipose mRNA expression was not. However, Bekri and colleagues  reported that liver hepcidin mRNA expression was similar in hepatic biopsies from obese and lean premenopausal women suggesting that the liver is not the source of increased hepcidin in obesity. But this observation is somewhat flawed as the iron status of the lean women was not described  and could have differed considerably from the obese women. As reported by Bekri et al.
, iron status was depleted, based on transferrin saturation (<20%), in 60% (n = 15) of the obese women. Matching the iron status Mianserin HCl of obese and lean subjects is critical as hepatic hepcidin expression is simultaneously regulated by body iron stores, inflammation, hypoxia, and anemia [2�C6]. It is also critical that when matching on iron status, gender and age are also considered, as iron status differs between men and women and also with menopause . Several studies have investigated the regulation of hepatic hepcidin by opposing stimuli and suggest that the strength of the individual stimuli, rather than the hierarchy of signaling pathways, determines hepatic hepcidin production [6, 7].