Thesis Abstract

Abstract
Copper is an essential trace element that plays a crucial role in various physiological processes in the human body. This review article aims to provide an in-depth understanding of the metabolism of copper in the human body, including its absorption, distribution, and excretion mechanisms. Copper is primarily absorbed in the small intestine through a combination of active transport and passive diffusion processes. Once absorbed, copper is transported in the bloodstream bound to ceruloplasmin, albumin, and other carrier proteins. The liver serves as the central organ for copper metabolism, where excess copper is stored, incorporated into ceruloplasmin, or excreted into bile. Within cells, copper is utilized as a cofactor for numerous enzymes involved in critical biochemical reactions, including antioxidant defense, energy production, iron metabolism, and connective tissue synthesis. Copper homeostasis is tightly regulated by a complex network of transporters, chaperone proteins, and regulatory factors to maintain optimal intracellular levels and prevent toxicity. Genetic disorders affecting copper metabolism, such as Menkes disease and Wilson disease, result in severe copper imbalances leading to neurological dysfunction, connective tissue abnormalities, and hepatic damage. Understanding the molecular mechanisms underlying these disorders has provided valuable insights into the importance of copper homeostasis for human health. The excretion of copper mainly occurs through bile secretion, with a minor fraction being eliminated in urine. Hepatocytes regulate copper excretion by transporting excess copper into the bile via ATP7B transporters, which are defective in Wilson disease. Dietary sources of copper include organ meats, shellfish, nuts, seeds, whole grains, and legumes. Copper deficiency is rare but can occur in individuals with malabsorption disorders, excessive zinc intake, or inadequate dietary copper intake. Symptoms of copper deficiency include anemia, neutropenia, and neurological abnormalities. In conclusion, copper metabolism is a tightly regulated process essential for human health and well-being. Disruption of copper homeostasis can lead to severe health consequences, highlighting the importance of maintaining optimal copper levels through a balanced diet and proper medical management of copper-related disorders. Further research into copper metabolism may uncover novel therapeutic strategies for managing conditions associated with copper dysregulation.

Thesis Overview