Michael Henson
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My research in reproductive physiology-endocrinology at the University of Tennessee focused on the roles of microminerals in porcine spermatogenesis, while work at the University of Arkansas focused on steroidogenesis and the neuroendocrine regulation of lactation in bovine and ovine models.

The NIH, CDC, and foundations supported my investigations in humans and nonhuman primates at the University of Maryland and Tulane University Schools of Medicine, with my early work (for review: Henson MC, Human Reproduction Update 4:389-405, 1998) describing estrogen's role in maintaining placental progesterone biosynthesis via the low-density lipoprotein (LDL) receptor, as well as the potential for other cholesterol sources to fuel the progesterone production needed to maintain threatened pregnancies until normal term.

Later investigations centered on leptin, a polypeptide hormone that regulates energy balance and satiety, and promotes conceptus development. Work in my lab defined leptin dynamics with advancing pregnancy and suggested a role for the hormone in regulating fetal lung maturity (for review: MC Henson & VD Castracane, Leptin in pregnancy: an update. Biology of Reproduction 74: 218-229, 2006; and MC Henson & VD Castracane, Leptin as a reproductive hormone. In Reproductive Endocrinology: A Molecular Approach, Springer Publishers, 2009).

An interest in fetal toxicology resulted in identifying cadmium, an industrial pollutant and constituent of tobacco smoke, as an inhibitor of progesterone synthesis that linked maternal exposure to premature labor and miscarriage (for review: MC Henson & JP Chedrese: Experimental Biology and Medicine 229:383-392, 2004; and MC Henson, et al.: Metal toxicity in mammalian reproduction. In Endocrine Toxicology, Informa Publishers, 2010).

To date, my work is illustrated in over 100 peer-reviewed publications and scientific presentations, in research grants, invited lectures and the mentorship of 53 scientific trainees.

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