| Clinical Research Branch |
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| Chee W. Chia, M.D., Staff Clinician Translational Research and Medical Services Section |
 Dr. Chia received her bachelor's degree and master's degree from the Massachusetts Institute of Technology and her medical degree from Northwestern University School of Medicine. After completing her internal medicine training at the University of Texas - Houston Medical School, she obtained her fellowship in endocrinology and metabolism at Johns Hopkins University School of Medicine. She joined the Translational Research and Medical Services Section at the National Institute on Aging in September 2004.Research Interests: Dr. Chia's research interests focus on 1) endocrinology of aging, more specifically on how the age-related decline in immune and metabolic functions is associated with changes in endocrine hormones and functions, and whether hormonal interventions can reverse these changes; 2) the physiology of various enteroendocrine hormones such as glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), ghrelin, etc., in relation to aging as well as different metabolic states; 3) translational research in the development of GLP-1 and GIP analogs for treatment of type 2 diabetes mellitus. |
| Thymic involution begins early in life, as young as one year of age, and continues throughout life. There has been considerable interest in developing means to either restore T cell production in the involuted thymus or delay its rate of decline. The link between the immune and endocrine systems was first proposed 75 years ago when thymic atrophy was observed in rats after hypophysectomies. A number of studies have supported a role for growth hormone (GH) on immune function and thymic growth. Early studies by Dr. Dan L. Longo and colleagues have shown GH to be a potential thymopoietic factor in Snell-Bagg (DW/J) mice by inducing thymic hyperplasia. GH has been shown to stimulate thymopoiesis in aged rodents by increasing both thymic size and cellularity. While the precise mechanism(s) involved in the thymotrophic effects of GH remains to be defined, several theories have suggested that GH increases the number of thymic progenitors recruited from the bone marrow to the thymus, hence promoting thymopoiesis. Despite a number of studies focusing on the effects of GH on thymic activity in rodents, little to no data currently exists on its effects in humans. We are interested in studying whether recombinant human GH (rhGH) can in fact stimulate thymic and immune functions in human. If so, the potential implication of using GH in treating people with diminished immune capacity such as the elderly is substantial. |
| It is well established that the pathogenesis of type 2 diabetes mellitus (DM) involves insulin resistance and impaired insulin secretion. During the progression from normal glucose tolerance (NGT) to impaired glucose tolerance (IGT) to DM, insulin levels are first elevated to compensate for insulin resistance but are reduced when frank diabetes develops due to b-cell failure. However, it is still unclear how these abnormalities arise. Many factors influence insulin action and secretion from b-cells besides glucose. These factors may be derived from the brain, liver, muscle, fat, gut, and other still unknown sources. Enteroendocrine peptides such as GLP-1, GIP, and ghrelin as well as adipokines such as leptin and adiponectin are just a few examples. We are interested in studying the underlying physiology of various enteroendocrine hormones such as GLP-1, GIP, and ghrelin in relation to aging as well as different metabolic states so that we can better understand the progression from NGT to DM and learn more about why insulin resistance develops and insulin secretion decompensates. |
| As stated before, type 2 diabetes is characterized by insulin resistance and insulin deficiency. After a meal, b-cells of the pancreas sense the rise in plasma glucose and secrete insulin to metabolize the glucose and to reset the plasma glucose level back to the pre-fed state. Insulin is also regulated by two enteroendocrine hormones, GLP-1 and GIP, both of which have very potent insulinotropic effect. GLP-1 is synthesized by the enteroendocrine L-cells in the gut which sense glucose and fat levels in digested food. GIP is synthesized by the enteroendocrine K-cells in the gut and also modulates glucose-dependent insulin release. In human, both GLP-1 and GIP are rapidly inactivated by an enzyme dipeptidyl peptide (DPP IV). In collaboration with Dr. Egan from the Laboratory of Clinical Investigation, we are conducting clinical trials on GIP and GLP-1 analogs which have longer half-lives for potential treatment of Type 2 diabetes. |
| Contact Information: Clinical Research Branch Harbor Hospital 3001 Hanover Street Baltimore, MD 21225 Phone 410-350-7376 E mail chiac@grc.nia.nih.gov For more information about the Branch: http://www.grc.nia.nih.gov/branches/crb/crb.htm |
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