ICEECE2012 Poster Presentations Diabetes (248 abstracts)
Iron overload induces visceral adipose tissue insulin resistance
P. Dongiovanni , M. Ruscica , S. La Spina , L. Steffani , V. Borroni , R. Rametta , S. Recalcati , G. Cairo , S. Gatti , P. Magni , S. Fargion & L. Valenti
Università degli Studi di Milano, Milan, Italy.
Excess body iron is associated with the metabolic syndrome, but whether it has a causal role in the pathophysiology of insulin resistance (IR) is not well understood. Aim of this study was to assess (a) the effect of dietary modulation of iron status on IR in Wild-type or ob/ob C57Bl/6 male mice fed a standard iron concentration (8 mg/kg) or an iron enriched diet (30 g/kg; IED), as well as in high-fructose diet (HFD) mice and (b) to investigate the mechanisms whereby. IED determined a progressive increase in glucose levels due to IR, as confirmed by the insulin tolerance test, associated with a reduction in visceral adipose tissue (VAT) mass (perigonadal fat pad:−60%, P=0.02), whereas in ob/ob mice IED led to overt diabetes. Moreover, in HFD fed mice increased IR by about 100%, was associated with decreased VAT despite no changes in total body mass, thus suggesting VAT-IR. IED induced iron accumulation in VAT, which was associated with IR, as shown by decreased phospho-AKT/AKT ratio (−80%, P=0.03). Gene expression analysis of VAT showed that IED upregulated iron-responsive genes (ferritin and hepcidin) and adipokines associated with IR (resistin and visfatin, both P=0.005), whereas downregulated inflammation. This resulted in hyper-resistinemia (P=0.01) and in increased levels of SOCS3 (p<0.05), a target of resistin and hepcidin implicated in adipose tissue IR. Furthermore, iron treatment induced hepcidin and inhibited the differentiation of human mesenchymal stem cells towards adipocytes. In conclusion, iron overload may induce IR and hyperglycemia by affecting VAT iron metabolism, endocrine function, and differentiation.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details unavailable.
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Endocrine Abstracts
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