Relation between serum high molecular weight adiponectin and serum ferritin or prohepcidin in patients with type 2 diabetes

Aso, Yoshimasa; Takebayashi, Kohzo; Wakabayashi, Shigeo; Momobayashi, Atsushi; Sugawara, Naoto; Terasawa, Tomoko; Naruse, Rika; Hara, Kenji; Suetsugu, Mariko; Morita, Kimio; Iwamoto, Toshihiko

doi:10.1016/j.diabres.2010.09.008

Cited by 38 publications

(24 citation statements)

References 29 publications

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“…It was also found in other HFD rat models that hepcidin expression remained unchanged (33,38) or began decreasing only when fasting blood glucose was increased (39). Clinical studies (16,17,34) showed that the prohepcidin or hepcidin level in blood was significantly decreased in DM2 patients with hyperferritinemia. All of these findings support the results of the current study.…”

Section: Discussionmentioning

confidence: 80%

“…Hepcidin, a circulatory antimicrobial peptide mainly expressed in the liver, plays a critical role in the regulation of iron metabolism by negatively regulating intestinal iron absorption and macrophage iron release and lowering the level of circulating iron (15). Decreased serum prohepcidin was recently reported in DM2 patients with hyperferritinemia (16,17), suggesting that hepcidin plays a potential role in iron overload in DM2.…”

Section: Hepcidin Is Directly Regulated By Insulin and Plays An Impormentioning

confidence: 99%

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Hepcidin Is Directly Regulated by Insulin and Plays an Important Role in Iron Overload in Streptozotocin-Induced Diabetic Rats

et al. 2014

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Iron overload is frequently observed in type 2 diabetes mellitus (DM2), but the underlying mechanisms remain unclear. We hypothesize that hepcidin may be directly regulated by insulin and play an important role in iron overload in DM2. We therefore examined the hepatic iron content, serum iron parameters, intestinal iron absorption, and liver hepcidin expression in rats treated with streptozotocin (STZ), which was given alone or after insulin resistance induced by a high-fat diet. The direct effect of insulin on hepcidin and its molecular mechanisms were furthermore determined in vitro in HepG2 cells. STZ administration caused a significant reduction in liver hepcidin level and a marked increase in intestinal iron absorption and serum and hepatic iron content. Insulin obviously upregulated hepcidin expression in HepG2 cells and enhanced signal transducer and activator of transcription 3 protein synthesis and DNA binding activity. The effect of insulin on hepcidin disappeared when the signal transducer and activator of transcription 3 pathway was blocked and could be partially inhibited by U0126. In conclusion, the current study suggests that hepcidin can be directly regulated by insulin, and the suppressed liver hepcidin synthesis may be an important reason for the iron overload in DM2.

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Section: Discussionmentioning

confidence: 80%

Section: Hepcidin Is Directly Regulated By Insulin and Plays An Impormentioning

confidence: 99%

Hepcidin Is Directly Regulated by Insulin and Plays an Important Role in Iron Overload in Streptozotocin-Induced Diabetic Rats

et al. 2014

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“…The response appears to be peroxisome proliferated and may involve PPAR gamma (Storey et al 2009;Wang et al 2010). Adipokines are known to induce inflammation and can stimulate ferritin expression (Aso et al 2010).…”

Section: Ferritin Gene Regulationmentioning

confidence: 99%

The many faces of the octahedral ferritin protein

Watt

2011

Biometals

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Iron is an essential trace nutrient required for the active sites of many enzymes, electron transfer and oxygen transport proteins. In contrast, to its important biological roles, iron is a catalyst for reactive oxygen species (ROS). Organisms must acquire iron but must protect against oxidative damage. Biology has evolved siderophores, hormones, membrane transporters, and iron transport and storage proteins to acquire sufficient iron but maintain iron levels at safe concentrations that prevent iron from catalyzing the formation of ROS. Ferritin is an important hub for iron metabolism because it sequesters iron during times of iron excess and releases iron during iron paucity. Ferritin is expressed in response to oxidative stress and is secreted into the extracellular matrix and into the serum. The iron sequestering ability of ferritin is believed to be the source of the anti-oxidant properties of ferritin. In fact, ferritin has been used as a biomarker for disease because it is synthesized in response to oxidative damage and inflammation. The function of serum ferritin is poorly understood, however serum ferritin concentrations seem to correlate with total iron stores. Under certain conditions, ferritin is also associated with pro-oxidant activity. The source of this switch from anti-oxidant to pro-oxidant has not been established but may be associated with unregulated iron release from ferritin. Recent reports demonstrate that ferritin is involved in other aspects of biology such as cell activation, development, immunity and angiogenesis. This review examines ferritin expression and secretion in correlation with anti-oxidant activity and with respect to these new functions. In addition, conditions that lead to pro-oxidant conditions are considered.

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“…The relationship between the regulator of iron metabolism, hepcidin/Hamp, and type 2 diabetes remains controversial (13,14). The expression of hepcidin/Hamp refl ects iron storage in the liver (15).…”

Section: Discussionmentioning

confidence: 99%

A Long-Term High-Fat Diet Changes Iron Distribution in the Body, Increasing Iron Accumulation Specifically in the Mouse Spleen

Yamano

Ikeda

Sakama

et al. 2015

J Nutr Sci Vitaminol

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Summary Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifi cally accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD. Key Words iron/spleen/diet, high fat/diabetes mellitus, type 2/DMT1 protein (iron transporter)

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Relation between serum high molecular weight adiponectin and serum ferritin or prohepcidin in patients with type 2 diabetes

Cited by 38 publications

References 29 publications

Hepcidin Is Directly Regulated by Insulin and Plays an Important Role in Iron Overload in Streptozotocin-Induced Diabetic Rats

Hepcidin Is Directly Regulated by Insulin and Plays an Important Role in Iron Overload in Streptozotocin-Induced Diabetic Rats

The many faces of the octahedral ferritin protein

A Long-Term High-Fat Diet Changes Iron Distribution in the Body, Increasing Iron Accumulation Specifically in the Mouse Spleen

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