An NCI-designated Comprehensive Cancer Center

Ken C Chiu, F.A.C.E., M.D.

Clinical Expertise
Research Focus
  • Diabetes
  • Vit D, metabolism, Epigenetics
Professor of Clinical Diabetes, Endocrinology & Metabolism; Site Director, Endocrinology Fellowship Training Program
Other Languages Spoken
  • Mandarin
Ken C. Chiu, M.D., F.A.C.E. is a board certified endocrinologist and joined the City of Hope in July 2005 as the site director of Endocrinology Fellowship Training Program. He has been very actively involved in fostering the next generation of endocrinologists since he completed the NIH sponsored Endocrinology Fellowship Training Program at the Washington University Medical Center/Barnes Hospital in St. Louis. Formerly, he served as the associate director of the Endocrinology Fellowship Training Program at the UCLA Medical Center, Los Angeles, California.
His research endeavors have been focused on the identification of the factors that may affect the development of type 2 diabetes through genetic and epidemiological approaches. In addition to his expertise in diabetes, he also provides general endocrinology service, including thyroid disorders and thyroid cancer, bone/osteoporosis, hirsutism/polycystic ovarian syndrome, pituitary and adrenal disorders. In 2010, he was an ad hoc reviewer of NIDDK/NIH's "Special Emphasis Panel: NIDDK Multi-Center Clinical Study Implementation Planning Grants (U34)"
Research Interests: Type 2 diabetes mellitus (T2DM) is a multi-factorial disease, influenced by both genetic and non-genetic factors. We are interested in factors that could potentially influence the development of T2DM, other than unhealthy dietary habit and physical inactivity. Identification of these factors could potentially provide new approaches in prevention and treatment of diabetes. We take several approaches to tackle this issue. With the candidate gene approach, we identified glucokinase as the first gene in T2DM (Lancet 1992) in my mentor's laboratory (M. Alan Permutt, MD). Mutated glucokianse caused MODY2 (maturity onset diabetes of the young 2). We also demonstrated the role of glucoskinase in T2DM (Diabetes 1992). Through the genome-wide systemic mapping, the locus of infantile nesidioblastosis was mapped to chromosome 11p14-15.1 (Nature Genetics 1994), which was also showed to play an important role in T2DM.
With the candidate gene approach, we also demonstrated the association of various genes with the intermediate phenotypes of T2DM, notably: angiotensin I converting enzyme (Metabolism 1997), Peroxisome proliferator activated receptor gamma (Metabolism 2000), hepatic nuclear factor-1alpha (the gene of MODY3, JCEM 2000; Diabetic Medicine 2003), vitamin D receptor (BMC Medical Genetics 2001), leptin receptor (European Journal of Endocrinology 2004), and APOA5 (Diabetic Medicine 2005). Transcription Factor7- like 2 (TCF7L2) was identified through the genome-wide association study, we also demonstrated that TCF7L2 played an important role in a Taiwanese population with a population attributable risk fraction of 18.7% (Diabetes 2007) and was associated with insulin resistance phenotype (JCEM 2009). Identification of genetic causes could provide a better intervention strategy and lead to new drug discovery.  
Our work of vitamin D in diabetes stems from the genetic study of vitamin D receptor. We demonstrated that low serum vitamin D level was associated with insulin resistance and metabolic syndrome (American Journal of Clinical Nutrition 2004). We also reported the association of low serum vitamin D level with beta cell dysfunction (Pancreas 2012). Although significant association with insulin resistance and beta cell dysfunction were noted, the contribution of vitamin D on these two traits was relatively small, 6.1% and 4.76% respectively. The association with insulin resistance is more significant in obese subjects than lean subjects (European Journal of Clinical Investigation 2011). Thus, hypovitaminosis D could play more significant role in the development of T2DM in obsess subjects than lean subjects.  
Through the epidemiological approaches, we also quantified the relative contribution of various factors in T2DM. We found that insulin sensitivity differed among different ethnic groups with a compensatory response in beta cell function (Diabetes Care 2000; JCEM 2001). We observed that beta cell function declined as aging but not insulin sensitivity and age accounted for 3.2-5.1% of the variation in beta cell function (Clinical Endocrinology 2000; 2005). We also reported that insulin resistance was not an essential component for metabolic syndrome (Endocrine 2013). We are currently defining the aging process in other intermediate phenotypes of T2DM. These studies will help us in the quantification of the contributing factors in the pathogenesis of T2DM.


City of Hope Comprehensive Cancer Center, 1500 East Duarte Road

Duarte, CA 91010

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