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Adipocyte iron regulates leptin and food intake. | LitMetric

AI Article Synopsis

  • * In patients with metabolic syndrome and mice on a high-iron diet, a negative correlation was found between serum ferritin and leptin levels, suggesting that excess iron reduces leptin production.
  • * Iron regulates leptin expression through the activation of CREB, with specific binding sites identified in the leptin promoter, indicating dietary iron influences both appetite and metabolism.

Article Abstract

Dietary iron supplementation is associated with increased appetite. Here, we investigated the effect of iron on the hormone leptin, which regulates food intake and energy homeostasis. Serum ferritin was negatively associated with serum leptin in a cohort of patients with metabolic syndrome. Moreover, the same inverse correlation was observed in mice fed a high-iron diet. Adipocyte-specific loss of the iron exporter ferroportin resulted in iron loading and decreased leptin, while decreased levels of hepcidin in a murine hereditary hemochromatosis (HH) model increased adipocyte ferroportin expression, decreased adipocyte iron, and increased leptin. Treatment of 3T3-L1 adipocytes with iron decreased leptin mRNA in a dose-dependent manner. We found that iron negatively regulates leptin transcription via cAMP-responsive element binding protein activation (CREB activation) and identified 2 potential CREB-binding sites in the mouse leptin promoter region. Mutation of both sites completely blocked the effect of iron on promoter activity. ChIP analysis revealed that binding of phosphorylated CREB is enriched at these two sites in iron-treated 3T3-L1 adipocytes compared with untreated cells. Consistent with the changes in leptin, dietary iron content was also directly related to food intake, independently of weight. These findings indicate that levels of dietary iron play an important role in regulation of appetite and metabolism through CREB-dependent modulation of leptin expression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4588289PMC
http://dx.doi.org/10.1172/JCI81860DOI Listing

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