Abstract
Iron deficiency (ID) is particularly frequent in obese patients due to increased circulating levels of acute-phase reactant hepcidin and adiposity-associated inflammation. Inflammation in obese subjects is closely related to ID. It induces reduced iron absorption correlated to the inhibition of duodenal ferroportin expression, parallel to the increased concentrations of hepcidin. Obese subjects often get decreased inflammatory response after bariatric surgery, accompanied by decreased serum hepcidin and therefore improved iron absorption. Bariatric surgery can induce the mitigation or resolution of obesity-associated complications, such as hypertension, insulin resistance, diabetes mellitus, and hyperlipidemia, adjusting many parameters in the metabolism. However, gastric bypass surgery and sleeve gastrectomy can induce malabsorption and may accentuate ID. The present review explores the burden and characteristics of ID and anemia in obese patients after bariatric surgery, accounting for gastric bypass technique (Roux-en-Y gastric bypass—RYGB) and sleeve gastrectomy (SG). After bariatric surgery, obese subjects’ iron status should be monitored, and they should be motivated to use adequate and recommended iron supplementation.
Highlights
Iron (Fe) is one of about 20 essential trace elements bearing crucial functions in the human organism and almost all living systems [1,2,3]
The Hep-Fpn-1 complex is located in cells that have an essential role in degrading and internalizing the Fpn-1, and the complex represses the Fe efflux from enterocytes, macrophages, and hepatocytes, reducing the Fe released into the circulation [42]
There is evidence of erythroferrone as suppressor a Hep suppressor in anemias to loss, hemolysis, and hereditary anemias with ineffective erythropoiesis. This ability may be useful for treating anemias with increased hepcidin expression, including anemias in inflammatory diseases, chronic kidney diseases, and iron-deficiency anemias resistant to treatment with iron medications [49]
Summary
Iron (Fe) is one of about 20 essential trace elements bearing crucial functions in the human organism and almost all living systems [1,2,3]. The inflammatory component of obesity leading to excessive production of Hep (and lipocalin 2) is considered one of the potential mechanisms of hypoferremia in obesity The overproduction of these proteins is associated with the sequestration of iron in the cells of the reticuloendothelial system. Tumor necrosis factor α (TNFα), a key mediator of different inflammatory disorders, including inflammatory bowel disease (IBD), can inhibit Hep expression, and treatment with anti-TNFα antibodies improved anemia status in patients with IBD. Low-grade chronic inflammation is common in obesity, and recent research offered some insights into the intracellular pathways of obesity-associated inflammation Such overfeeding is the starting point of inflammation, which originates from cells and tissues involved in metabolism, i.e., adipocytes and hepatic macrophages that trigger the inflammatory response. The present review explores the burden and characteristics of ID and iron-deficiency anemia in obese patients and after bariatric surgery (especially RYGB and SG)
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