Human Biomarkers for Assessing Copper Deficiency

2015-03-26 05:53:23 | BioPortfolio


Copper is an essential nutrient for humans and is cofactor in enzymes that participate in critical body functions. Insufficient copper can lead to hematological and neurological abnormalities that may be irreversible if left untreated. Copper deficiency is believed to be rare in the U.S. population because typical dietary intake is usually sufficient to meet requirements. More recent evidence suggests that specific populations may be susceptible to copper deficiency in cases where copper absorption in the gut is impaired following gastric surgery or in individuals with high intakes of zinc. Preliminary studies by us and others have identified significant levels of moderate and severe symptomatic copper deficiency in patients who have undergone weight loss (bariatric) gastric bypass surgery. Copper deficiency in humans is difficult to recognize and treat because current diagnostic tools rely on measures of plasma concentrations of copper and ceruloplasmin, which are neither sensitive nor specific for copper deficiency, and early warning blood markers (biomarkers) have not been identified. Recent developments indicate that copper chaperone molecules and cuproenzymes such as cytochrome C oxidase and superoxide dismutase may be more sensitive to changes in copper status, but there has been very little work done in humans. The studies outlined here are aimed at assessing copper status using these biomarkers in gastric bypass surgery patients who are at risk for symptomatic copper deficiency. In addition, patients identified to be deficient will be supplemented with copper and this treatment will be evaluated using biomarker concentrations. The findings of these studies should provide insight into the effectiveness of novel biomarkers to identify those at risk and to guide appropriate treatment to prevent serious and permanent morbidity due to copper deficiency.

Study Design

Allocation: Randomized, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Single Group Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Diagnostic


Copper Deficiency


Copper gluconate


Purdue University
West Lafayette
United States




Purdue University

Results (where available)

View Results


Published on BioPortfolio: 2015-03-26T05:53:23-0400

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PubMed Articles [2920 Associated PubMed Articles listed on BioPortfolio]

Chelating principles in Menkes and Wilson diseases: Choosing the right compounds in the right combinations at the right time.

Dysregulation of copper homeostasis in humans is primarily found in two genetic diseases of copper transport, Menkes and Wilson diseases, which show symptoms of copper deficiency or overload, respecti...

Idiopathic Copper Deficiency Myeloneuropathy Resulting in Paraparesis: A Case Report.

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The changes of copper metabolism in rats fed with low- or high-calorie ration.

Copper is an essential micronutrient, because it is a catalytic and structural cofactor of enzymes that control the basic processes in all cells, and moreover it is a participant in signaling pathways...

Alcohol amination catalyzed by copper powder as a self-supported catalyst.

Catalytic alcohol amination is a sustainable reaction for N-alkyl amine synthesis. In the past research, homogeneous and supported copper catalysts have been extensively studied and nice resutls were ...

Regiocontrolled Heptafluoroisopropylation of Aromatic Halides by Copper(I) Carboxylates with Heptafluoroisopropyl-Zinc Reagents.

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Medical and Biotech [MESH] Definitions

Unstable isotopes of copper that decay or disintegrate emitting radiation. Cu atoms with atomic weights 58-62, 64, and 66-68 are radioactive copper isotopes.

P-type ATPases which transport copper ions across membranes in prokaryotic and eukaryotic cells. They possess a conserved CYSTEINE-HISTIDINE-SERINE (CPx) amino acid motif within their transmembrane helices that functions in cation translocation and catalytic activation, and an N-terminal copper-binding CxxC motif that regulates enzyme activity. They play essential roles in intracellular copper homeostasis through regulating the uptake, efflux and storage of copper ions, and in cuproprotein biosynthesis.

Congenital locomotor ataxia of lambs, thought to be associated with copper deficiency. It is characterized clinically by progressive incoordination of the hind limbs and pathologically by disruption of neuron and myelin development in the central nervous system. It is caused by a deficiency of metabolizable copper in the ewe during the last half of her pregnancy. (Dorland, 28th ed; Stedman, 26th ed)

A multi-copper blood FERROXIDASE involved in iron and copper homeostasis and inflammation.

An inherited disorder of copper metabolism transmitted as an X-linked trait and characterized by the infantile onset of HYPOTHERMIA, feeding difficulties, hypotonia, SEIZURES, bony deformities, pili torti (twisted hair), and severely impaired intellectual development. Defective copper transport across plasma and endoplasmic reticulum membranes results in copper being unavailable for the synthesis of several copper containing enzymes, including PROTEIN-LYSINE 6-OXIDASE; CERULOPLASMIN; and SUPEROXIDE DISMUTASE. Pathologic changes include defects in arterial elastin, neuronal loss, and gliosis. (From Menkes, Textbook of Child Neurology, 5th ed, p125)

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