LeBris S. Quinn, Ph.D.
Research Associate Professor
Research Interests: During normal aging, individuals typically lose about one-third of their muscle tissue, with accompanying losses in strength and endurance. The age-associated decline in muscle tissue is termed “sarcopenia” by geriatricians. Sarcopenia is a major cause of frailty, falls, and loss of independence in the elderly. Research conducted in Dr. Quinn’s laboratory has focused on the underlying cellular and biochemical mechanisms of the age-associated loss of skeletal muscle. An understanding of the biochemical bases of these conditions will enable design of treatments for sarcopenia and frailty in the elderly.
In addition to the loss of skeletal muscle, another important change during normal aging is the increased deposition of adipose tissue. Together with sarcopenia, the increase in fat:lean body composition predisposes the elderly to development of insulin resistance, metabolic syndrome, and type-2 diabetes, major factors in death and disability in the aged population. These, in turn, are risk factors for cardiovascular disease, cancer, and Alzheimer’s disease. Dr. Quinn’s laboratory has recently identified a novel factor which appears to regulate fat:lean body composition and whose expression declines with age. This line of research may lead to development of new pharmacologic strategies to modulate fat:lean body composition and insulin sensitivity during aging.
Sarcopenia and the growth hormone/IGF system: Much of Dr. Quinn’s research to date has concerned the cellular and molecular mechanisms of action of the insulin-like growth factor (IGF) system on skeletal muscle. IGF is the effector of growth hormone (GH) action, a master hormone which declines with age. The ultimate goal of this research is to delineate molecular or biochemical strategies to mimic the trophic action of IGF on muscle without the negative effects of IGF and growth hormone on other functions. One recent project has demonstrated that overexpression of the type-1 IGF receptor (IGF-1R) using a skeletal muscle-specific promoter can induce muscle hypertrophy and resistance to muscle atrophy in cultured muscle cells, without stimulating cell proliferation, the basis of many of the undesirable effects of systemic GH or IGF administration. Future work will extend these observations to in vivo systems using laboratory rodents.
Increases in fat:lean body composition and insulin resistance with age: Recently, Dr. Quinn’s laboratory has identified a novel factor, interleukin-15 (IL-15), which appears to regulate fat:lean body composition and insulin sensitivity. Importantly, IL-15 has been shown to stimulate production of the insulin-sensitizing hormone adiponectin. Dr. Quinn’s laboratory has developed several strains of transgenic mice whose muscles produce increased amounts of IL-15, and are currently engaged in characterizing the body composition, aging patterns, and susceptibility to developing insulin resistance of these mice and their normal littermates. Preliminary data indicate IL-15 production declines with age, which may play a role in the increases in fat:lean body composition and decreases in insulin sensitivity with age. Modulation of this novel pathway may represent a new strategy to prevent or treat changes in body composition leading to insulin resistance in the elderly population.
College: 1976, Swarthmore College
Graduate School: 1982, Ph.D., Biological Structure, University of Washington
Postdoctoral Training: 1983-1986, University of Washington
Publications: Go to PubMed.
Community of Science: Click to go to Dr. Quinn's Community of Science page.
General Information: Email Dr. Quinn.