UC Davis

Iron-deficiency (ID) is the most common cause of iron deficiency anemia (IDA). Infants, children, and females of child-bearing age are at an increased risk of ID and IDA. Within the past 20 years, the prevalence of IDA in the United States has been increasing at an alarming rate. Early-life ID and IDA has been associated with irreparable consequences in cognitive, neurological, and immunological function, as well as metabolic development. Coincidentally, early-life ID can exaggerate the immunological response to infection, thereby increasing the likelihood of antibiotic exposure. Exposure to antibiotics within the first 1000 days has not yet been examined in the context of ID and IDA, perhaps causing an organ-specific shift in metabolism. A 6-week piglet model was used because like human infants, ID and IDA can be acquired naturally without dietary intervention, and pigs are similar anatomically and biologically to humans relative to other animal models. The focus of this thesis is to first characterize the impact of iron deficiency within the liver and skeletal muscle on the metabolomes of 6-week-old piglets, and second to characterize the impact of antibiotic exposure on top of iron deficiency. Iron deficiency resulted in metabolic dysfunction that was reflected in the skeletal muscle and liver metabolomes that was exaggerated when antibiotics were administered. Metabolic characteristics of ID indicated perturbed lipid metabolism, and energy status, as well as altered glucose-utilization. These results underline the importance of ensuring adequate iron status in children, and in particular highlight the need for further study of the impact of antibiotics in the face of nutrient deficiencies.