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James F. Collins, PhD

Professor
University of Florida
GAINESVILLE, Florida, United States

I have been studying intestinal nutrient absorption for over 30 years, with a focus on intestinal iron absorption for the past two decades.
My work on iron homeostasis has been continuously funded by NIH since 2004. My first iron-related paper, published in 2005,
identified differentially expressed genes in the duodenum of iron-deficient rats. One of the top candidate genes was divalent metal-iron
transporter 1 (DMT1). Interestingly, DMT1 had been identified just a few years earlier as a transporter of nonheme (or inorganic) iron
(in 1999), and was later identified as the main intestinal iron transporter in laboratory rodents (also in 2005). I also made the discovery
that an intestinal copper transporter was strongly upregulated in response to iron deficiency along with an intracellular coper-binding
protein, metallothionein. This observation led to a series of studies on copper and how it influences iron homeostasis, culminating in 4
papers documenting how high dietary (supplemental) iron can impair copper absorption and lead to classic signs of copper deficiency.
My research focus then shifted to studies on the intestinal iron transporter DMT1. We showed that intestinal DMT1 was required for
iron loading in pre-clinical mouse models of hereditary hemochromatosis and beta-thalassemia intermedia, two genetic conditions in
humans that result in iron overload. It was further demonstrated that in vivo knockdown of DMT1 using ginger-derived, lipid
nanoparticle-delivered siRNAs prevented iron loading in both disorders. Since mutations in DMT1 in humans lead to a very similar
phenotype as in rodent models, it seems likely that blocking intestinal DMT1 could be an effective adjunctive approach to lower body
iron burden in these human disorders. More recent work from my lab has focused on mechanisms of heme-iron absorption. Heme is a
highly available source of dietary iron for humans, being found mainly in hemoglobin and myoglobin of animal foods. However,
details of heme-iron absorption have remained unclear despite over 6 decades of work on this topic. Work on heme-iron absorption
has been largely abandoned in recent years since it has been generally perceived that laboratory rodents are poor models of this
process. We, however successfully established a nutritional paradigm to study heme-iron absorption in rats and mice, whereby we
demonstrated that both species were capable of assimilating iron from dietary heme. This has thus put us in a position to now test the
roles of various intestinal transporters and enzymes in the process of heme-iron absorption. These studies are ongoing. A second,
funded line of research in my laboratory focuses on iron homeostasis in beta-thalassemia pregnancy. We made the novel discovery
that iron-loading of unborn fetuses occurs in dams with thalassemia, which had not been shown before. This ongoing work has
possible implications for women with thalassemia that want to become pregnant, especially since mouse models of this human
disorder have been shown to faithfully recapitulate many aspects of the disease in humans.

Presentation(s):

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