title: Heme, an essential nutrient from dietary proteins, critically impacts diverse physiological and pathological processes.
abstract: Heme constitutes 95% of functional iron in the human body, as well as two-thirds of the average person's iron intake in developed countries. Hence, a wide range of epidemiological studies have focused on examining the association of dietary heme intake, mainly from red meat, with the risks of common diseases. High heme intake is associated with increased risk of several cancers, including colorectal cancer, pancreatic cancer and lung cancer. Likewise, the evidence for increased risks of type-2 diabetes and coronary heart disease associated with high heme intake is compelling. Furthermore, recent comparative metabolic and molecular studies of lung cancer cells showed that cancer cells require increased intracellular heme biosynthesis and uptake to meet the increased demand for oxygen-utilizing hemoproteins. Increased levels of hemoproteins in turn lead to intensified oxygen consumption and cellular energy generation, thereby fueling cancer cell progression. Together, both epidemiological and molecular studies support the idea that heme positively impacts cancer progression. However, it is also worth noting that heme deficiency can cause serious diseases in humans, such as anemia, porphyrias, and Alzheimer's disease. This review attempts to summarize the latest literature in understanding the role of dietary heme intake and heme function in diverse diseases.
authors.affiliation: Department of Molecular and Cell Biology, Center for Systems Biology, University of Texas at Dallas, Richardson, TX 79489, USA. jagmohan.hooda@utdallas.edu.
authors.forename: Jagmohan
authors.initials: J
authors.lastname: Hooda
authors.affiliation: Department of Molecular and Cell Biology, Center for Systems Biology, University of Texas at Dallas, Richardson, TX 79489, USA. ajitnshah@icloud.com.
authors.forename: Ajit
authors.initials: A
authors.lastname: Shah
authors.affiliation: Department of Molecular and Cell Biology, Center for Systems Biology, University of Texas at Dallas, Richardson, TX 79489, USA. li.zhang@utdallas.edu.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
mesh_terms: D003327:Coronary Disease / Q000453:epidemiology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D004044:Dietary Proteins / Q000008:administration & dosage*; D018450:Disease Progression; D006418:Heme / Q000008:administration & dosage / Q000009:adverse effects / Q000172:deficiency; D006420:Hemeproteins / Q000235:genetics / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007421:Intestine, Small / Q000187:drug effects / Q000378:metabolism; D008460:Meat / Q000032:analysis*; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism; D009369:Neoplasms / Q000453:epidemiology; D010101:Oxygen Consumption; D011484:Protein-Arginine N-Methyltransferases / Q000235:genetics / Q000378:metabolism; D011991:Receptors, Virus / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors
chemical_list: D004044:Dietary Proteins; C492690:FLVCR1 protein, human; D006420:Hemeproteins; D026901:Membrane Transport Proteins; D011991:Receptors, Virus; D012097:Repressor Proteins; C546602:SLC48A1 protein, human; D006418:Heme; C099988:PRMT1 protein, human; D011484:Protein-Arginine N-Methyltransferases