Abstract：
INTRODUCTION:Iron overload leads to multiple organ damage including endocrine organ dysfunctions. Hypogonadism is the most common non-diabetic endocrinopathy in primary and secondary iron overload syndromes. AIM:To explore the molecular determinants of iron overload-induced hypogonadism with specific focus on hypothalamic derangements. A dysmetabolic male murine model fed iron-enriched diet (IED) and cell-based models of gonadotropin-releasing hormone (GnRH) neurons were used. RESULTS:Mice fed IED showed severe hypogonadism with a significant reduction of serum levels of testosterone (-83%) and of luteinizing hormone (-86%), as well as reduced body weight gain, body fat and plasma leptin. IED mice had a significant increment in iron concentration in testes and in the pituitary. Even if iron challenge of in vitro neuronal models (GN-11 and GT1-7 GnRH cells) resulted in 10- and 5-fold iron content increments, respectively, no iron content changes were found in vivo in hypothalamus of IED mice. Conversely, mice placed on IED showed a significant increment in hypothalamic GnRH gene expression (+34%) and in the intensity of GnRH-neuron innervation of the median eminence (+1.5-fold); similar changes were found in the murine model HFE-/-, resembling human hemochromatosis. CONCLUSIONS:IED-fed adult male mice show severe impairment of hypothalamus-pituitary-gonadal axis without a relevant contribution of the hypothalamic compartment, which thus appears sufficiently protected from systemic iron overload.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Macchi C,Steffani L,Oleari R,Lettieri A,Valenti L,Dongiovanni P,Romero-Ruiz A,Tena-Sempere M,Cariboni A,Magni P,Ruscica Mdoi
10.1016/j.mce.2017.06.019subject
Has Abstractpub_date
2017-10-15 00:00:00pages
135-145eissn
0303-7207issn
1872-8057pii
S0303-7207(17)30346-5journal_volume
454pub_type
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