Circulating Visfatin Is Associated With Parameters of Iron Metabolism in Subjects With Altered Glucose Tolerance

Fernández-Real, José Manuel; Moreno, José María Ruiz; Chico, B. N. Diaz; López‐Bermejo, Abel; Ricart, Wifredo

doi:10.2337/dc06-1581

Cited by 49 publications

(45 citation statements)

References 37 publications

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“…Associations between levels of serum visfatin, an adipokine secreted prevalently by the visceral adipose tissue, and different parameters of iron metabolism (serum prohepcidin and sTfR) were observed in obese patients and patients with T2D; these associations differed according to obesity and glucose tolerance status (61). The meaning of such associations remains unclear, even though visfatin mRNA is enriched in iron-rich tissues (liver, muscle, bone marrow) (61).…”

Section: Iron Status May Influence the Release Of Adipokines From Adimentioning

confidence: 99%

Mechanisms Linking Glucose Homeostasis and Iron Metabolism Toward the Onset and Progression of Type 2 Diabetes

2015

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OBJECTIVEThe bidirectional relationship between iron metabolism and glucose homeostasis is increasingly recognized. Several pathways of iron metabolism are modified according to systemic glucose levels, whereas insulin action and secretion are influenced by changes in relative iron excess. We aimed to update the possible influence of iron on insulin action and secretion and vice versa. RESEARCH DESIGN AND METHODSThe mechanisms that link iron metabolism and glucose homeostasis in the main insulin-sensitive tissues and insulin-producing b-cells were revised according to their possible influence on the development of type 2 diabetes (T2D). RESULTSThe mechanisms leading to dysmetabolic hyperferritinemia and hepatic overload syndrome were diverse, including diet-induced alterations in iron absorption, modulation of gluconeogenesis, heme-mediated disruption of circadian glucose rhythm, impaired hepcidin secretion and action, and reduced copper availability. Glucose metabolism in adipose tissue seems to be affected by both iron deficiency and excess through interaction with adipocyte differentiation, tissue hyperplasia and hypertrophy, release of adipokines, lipid synthesis, and lipolysis. Reduced heme synthesis and dysregulated iron uptake or export could also be contributing factors affecting glucose metabolism in the senescent muscle, whereas exercise is known to affect iron and glucose status. Finally, iron also seems to modulate b-cells and insulin secretion, although this has been scarcely studied. CONCLUSIONSIron is increasingly recognized to influence glucose metabolism at multiple levels. Body iron stores should be considered as a potential target for therapy in subjects with T2D or those at risk for developing T2D. Further research is warranted.Iron levels help to modulate the clinical manifestations of numerous systemic diseases. The importance of adequate amounts of iron for health and well-being in humans is well known. Iron is involved in binding and transporting oxygen and regulating cell growth and differentiation, as well as electron transport, DNA synthesis, and many important metabolic processes (1).From a clinical standpoint, assessing serum ferritin concentrations is a useful measure of iron storage. Ferritin is also an acute-phase reactant and, as such, is

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Section: Iron Status May Influence the Release Of Adipokines From Adimentioning

confidence: 99%

Mechanisms Linking Glucose Homeostasis and Iron Metabolism Toward the Onset and Progression of Type 2 Diabetes

2015

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“…16,17 Although a physiological explanation has not been provided yet, in the cohort of our patients visfatin was positively related to TSAT. Others did not detect such an association between visfatin and markers of iron metabolism in HD patients, although an almost statistically significant correlation was detected with prohepcidin.…”

Section: 2mentioning

confidence: 96%

“…15 In patients with altered glucose tolerance serum visfatin is related to serum soluble transferrin receptors and with prohepcidin, 16 whereas in patients with gestational diabetes mellitus serum visfatin is associated with serum ferritin. 17 In the light of the above findings, the level of this multifactorial peptide in HD patients, and its associations with markers of iron metabolism, as well as with inflammation and situations characterized by insulin resistance were evaluated.…”

Section: Introductionmentioning

confidence: 99%

Increased visfatin in hemodialysis patients is associated with decreased demands for recombinant human erythropoietin

et al. 2013

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“…Furthermore, excess iron the diet may be routed to visceral adipose tissue and change the expression of adipokines, as demonstrated for resistin [101] Adipokines represent a diverse group of hormones which mediate the metabolic effects of diseased adipose tissue to organs and tissues. Associations have been observed bet ween retinolbinding protein 4 (RBP4) and visfatin serum concentrations and parameters of iron meta bolism [102,103] . However, these reports may reflect the coincidence of elevated iron stores with surrogate markers of IR and do not prove causality [93] .…”

Section: How Does Iron Lead To Disease Progression In Nafld?mentioning

confidence: 99%

Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver

Aigner

Weiss

Datz

2014

WJH

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Elevated iron stores as indicated by hyperferritinemia with normal or mildly elevated transferrin saturation and mostly mild hepatic iron deposition are a characteristic finding in subjects with non-alcoholic fatty liver disease (NAFLD). Excess iron is observed in approximately one third of NAFLD patients and is commonly referred to as the "dysmetabolic iron overload syndrome". Clinical evidence suggests that elevated body iron stores aggravate the clinical course of NAFLD with regard to liver-related and extrahepatic disease complications which relates to the fact that excess iron catalyses the formation of toxic hydroxylradicals subsequently resulting in cellular damage. Iron removal improves insulin sensitivity, delays the onset of type 2 diabetes mellitus, improves pathologic liver function tests and likewise ameliorates NAFLD histology. Several mechanisms contribute to pathologic iron accumulation in NAFLD. These include impaired iron export from hepatocytes and mesenchymal Kupffer cells as a consequence of imbalances in the concentrations of iron regulatory factors, such as hepcidin, cytokines, copper or other dietary factors. This review summarizes the knowledge about iron homeostasis in NAFLD and the rationale for its therapeutic implications.

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Circulating Visfatin Is Associated With Parameters of Iron Metabolism in Subjects With Altered Glucose Tolerance

Cited by 49 publications

References 37 publications

Mechanisms Linking Glucose Homeostasis and Iron Metabolism Toward the Onset and Progression of Type 2 Diabetes

Mechanisms Linking Glucose Homeostasis and Iron Metabolism Toward the Onset and Progression of Type 2 Diabetes

Increased visfatin in hemodialysis patients is associated with decreased demands for recombinant human erythropoietin

Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver

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