A 41-year-old woman with a long history of heavy menstrual bleeding comes to the office for follow-up. Two weeks ago, the patient was diagnosed with iron deficiency anemia and was started on oral ferrous sulfate. Today, vital signs and physical examination are unremarkable. Laboratory evaluation shows an appropriate response to the medication with an increase in reticulocyte production. She is instructed to continue iron supplementation. The woman is concerned about iron buildup and damage to vital organs if she continues to take the medication. She is reassured that iron homeostasis is closely regulated; as the body's iron stores increase, a hormone is released and functions in reducing the amount of dietary iron absorbed from the intestines. Which of the following cells is most likely responsible for secreting this hormone?

Question

A 41-year-old woman with a long history of heavy menstrual bleeding comes to the office for follow-up.  Two weeks ago, the patient was diagnosed with iron deficiency anemia and was started on oral ferrous sulfate.  Today, vital signs and physical examination are unremarkable.  Laboratory evaluation shows an appropriate response to the medication with an increase in reticulocyte production.  She is instructed to continue iron supplementation.  The woman is concerned about iron buildup and damage to vital organs if she continues to take the medication.  She is reassured that iron homeostasis is closely regulated; as the body's iron stores increase, a hormone is released and functions in reducing the amount of dietary iron absorbed from the intestines.  Which of the following cells is most likely responsible for secreting this hormone?

Quizplus · Accepted Answer

11ec160b_3ccb_24b4_9249_6579155b4357_MD0001_00 Hepcidin is an acute phase reactant synthesized by hepatic parenchymal cells that acts as the central regulator of iron homeostasis. High iron levels and inflammatory conditions increase the synthesis of hepcidin, while hypoxia and increased erythropoiesis act to lower hepcidin levels. Hepcidin influences body iron storage through its interaction with ferroportin, a transmembrane protein responsible for transferring intracellular iron to the circulation. Upon binding hepcidin, ferroportin is internalized and degraded, decreasing intestinal iron absorption and inhibiting the release of iron by macrophages. Regulation of intestinal iron absorption is crucial for maintaining iron homeostasis, since blood loss is the only way of removing large amounts of iron from the body. Iron absorption from the proximal small intestine is facilitated by the divalent metal transporter-1 (DMT-1). Once inside the intestinal cells, iron may take 1 of 2 paths: Iron may bind to ferritin (a primarily intracellular iron-binding protein) and remain stored within the enterocyte. The stored iron is excreted in the stool as enterocytes slough off and are replaced Iron may enter the circulation through ferroportin, the basolateral iron transporter of the enterocyte. Free iron released into the circulation is transported throughout the body by transferrin (an iron-binding transport protein), which becomes internalized after interacting with transferrin receptors present on all cells (Choices A and B) When senescent red blood cells are destroyed by macrophages, the iron is recycled by the reticuloendothelial system for use in new erythroid precursors. Iron released by macrophages under the governance of hepcidin binds rapidly to transferrin and is delivered to the bone marrow, where erythroid precursors use it to synthesize hemoglobin. This internal iron cycle conserves the body's iron very efficiently, and only small amounts of additional iron are required for daily red cell production in the absence of significant blood loss. (Choice D) Enterocytes store iron for excretion in the feces or transport it into the circulation depending on circulating levels of the polypeptide hormone hepcidin. Lower hepcidin levels favor iron absorption and accumulation in the body. (Choice E) Renal tubular cells play a limited role in iron metabolism by secreting lactoferrin, which binds to free iron in the urine and possibly recovers it for metabolic use. Educational objective: Hepcidin is synthesized by the liver that acts as the central regulator of iron homeostasis. High iron levels and inflammatory conditions increase the synthesis of hepcidin; hypoxia and increased erythropoiesis act to lower hepcidin levels. Low hepcidin levels increase intestinal iron absorption and stimulate iron release by macrophages. __________ References: Regulation of cellular iron metabolism (http://www.ncbi.nlm.nih.gov/pubmed/21348856)

A 41-Year-Old Woman with a Long History of Heavy Menstrual