In 1985, Paterson and Bettger found hypoplastic hematopoiesis in severely zinc-deficient rats. Therefore, we investigated plasma erythropoietin concentration in zinc-deficient rats. Forty 4-wk-old male Sprague- Dawley rats were assigned into 4 dietary treatment groups of 10 for the 4-wk study: zinc-deficient group (4.5 mg zinc and 35 mg iron/kg; -Zn), iron-deficient group (30 mg zinc/kg, no supplemental iron; -Fe), zinc/ iron-deficient group (4.5 mg zinc/kg, no supplemental iron; -Zn-Fe), and control group (AIN-93G; Cont). Water intake determined at d 19 was similar among all treatment groups. At d 27-28, bioimpedance was measured. The intracellular water/extracellular water ratio was significantly increased in the -Zn group (p < 0.05). Compared to the Cont, group, the plasma erythropoietin concentration was increased by iron deficiency and decreased by zinc deficiency (p < 0.01). Hematocrit was significantly decreased in both the -Fe and -Zn-Fe groups and was significantly increased in the -Zn group (p < 0.01). Transferrin saturation in the -Fe and -Zn-Fe groups was significantly lower than the Cont group (p < 0.01), and that of the -Zn group was highest among all groups. The low plasma erythropoietin concentration might account for depressed hematopoiesis associated with zinc deficiency.
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http://dx.doi.org/10.1385/BTER:107:3:289 | DOI Listing |
Urolithiasis
December 2024
Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, 1, Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Japan.
The early stages of kidney crystal formation involve inflammation and hypoxia-induced cell injury; however, the role of the hypoxic response in kidney crystal formation remains unclear. This study investigated the effects of a prolyl hydroxylase domain inhibitor (roxadustat) on renal calcium oxalate (CaOx) crystal formation through in vitro and in vivo approaches. In the in vitro experiment, murine renal tubular cells (RTCs) were exposed to varying roxadustat concentrations and CaOx crystals.
View Article and Find Full Text PDFHematology Am Soc Hematol Educ Program
December 2024
Medical and Research Service, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN.
Anemia is a hallmark of chronic kidney disease (CKD), worsens with disease progression, and profoundly affects a patient's well-being. Major pathogenic factors are inadequate kidney erythropoietin (EPO) production and absolute and functional iron deficiency. The 2 mainstays of current anemia treatment are a) replacement therapy with recombinant EPO or 1 of its glycosylated derivatives, administered subcutaneously or intravenously, and b) intravenous (IV) iron injections.
View Article and Find Full Text PDFJ Vet Intern Med
December 2024
College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Republic of Korea.
Background: Nucleated red blood cells (nRBCs) are increased by disease processes and hematopoietic stress.
Objectives: To evaluate the utility of nRBCs as a marker of disease severity and prognosis in dogs with systemic inflammatory response syndrome (SIRS).
Animals: Sixty-two client-owned dogs met the criteria of SIRS without anemia.
Am J Physiol Regul Integr Comp Physiol
January 2025
Institute for Integrative Physiology and Center for Systems Biology of O2 Sensing, Biological Sciences Division, University of Chicago, Chicago, Illinois, United States.
Hypobaric hypoxia (HH) occurring at high altitudes activates the sympathetic nervous system (SNS) and increases circulating erythropoietin (EPO) levels. EPO stimulates red blood cell production (erythropoiesis), enhancing oxygen transport in arterial blood to counteract hypoxemia. The present study tested the hypothesis that SNS contributes to EPO activation by HH through epinephrine (EPI) release from the adrenal medullae.
View Article and Find Full Text PDFLipids Health Dis
November 2024
The Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, Department of Biology, College of Life Sciences, Beijing Normal University, Beijing, 100875, China.
Background: Lysophosphatidic acid (LPA) is a lipid mediator with diverse biological functions through its receptors on the cell membrane. As one of the six LPA receptors, LPA receptor 3 (LPAR3) is highly expressed in mouse kidneys, but its physiological function in the kidney has been poorly explored.
Methods: Wild-type (WT) and Lpar3 mice were used to investigate the renal physiological function of LPAR3 under hypoxia.
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