Gluconeogenic signals regulate iron homeostasis via hepcidin in mice.

ABSTRACT:

Background & aims

Hepatic gluconeogenesis provides fuel during starvation, and is abnormally induced in obese individuals or those with diabetes. Common metabolic disorders associated with active gluconeogenesis and insulin resistance (obesity, metabolic syndrome, diabetes, and nonalcoholic fatty liver disease) have been associated with alterations in iron homeostasis that disrupt insulin sensitivity and promote disease progression. We investigated whether gluconeogenic signals directly control Hepcidin, an important regulator of iron homeostasis, in starving mice (a model of persistently activated gluconeogenesis and insulin resistance).

Methods

We investigated hepatic regulation of Hepcidin expression in C57BL/6Crl, 129S2/SvPas, BALB/c, and Creb3l3-/- null mice. Mice were

SUBMITTER: Vecchi C 

PROVIDER: S-EPMC3989026 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature