Biography

Professor Karen Lam is Chair Professor in Medicine, Clinical Director of the State Key Lab of Pharmaceutical & Biotechnology, Academic Lead of the Clinical Trial Centre and Director of Clinical Operations, HKU Health System, at the University of Hong Kong. She was the Chief of Endocrinology and Metabolism at the University Department of Medicine and founded the KK Leung Diabetes Centre, Queen Mary Hospital in 1994 as the first comprehensive management and education centre for people with diabetes in Hong Kong. She was the Founding President of Diabetes Hongkong (Honorary President since 2014); a past President of the Hong Kong Society of Endocrine, Metabolism and Reproduction; and a past Chairman of two specialty boards of the HK College of Physicians – Advanced Internal Medicine and Endocrinology, Diabetes & Metabolism as well as the Working Party on Diabetes Care of the Hospital Authority. She is currently the associate editor/editorial board member of several international peer-reviewed journals in diabetes and endocrinology.

Research Profile

Professor Lam has published extensively on clinical, basic and translational research in diabetes and endocrinology, including publications in Diabetes, Diabetes Care, JCEM, ATVB, Circulation, Cell Metabolism, PNAS, JCI , Nat Commun, Nat Genet, and others. Heading an integrated research team with strengths and platforms ranging from cell and animal based research to epidemiological, genetic and clinic-based studies, her current research focuses on the pathogenetic and therapeutic significance of adipokines in diabetes and other obesity-related cardiometabolic disorders. She led the Hong Kong Cardiovascular Risk Factor Prevalence Study (CRISPS; 1995-2018), a population-based cohort study on cardiovascular (CV) risk factors and diseases with the longest follow-up in China, which charted the rise in obesity and metabolic syndrome in Southern China. Together with the Hong Kong West Diabetes Registry (HKWDR) established since 2008, it has provided the database and biobank for investigating the interaction of environmental and genetic factors underlying obesity, diabetes and CV diseases in Chinese (JCEM 2010; Nat Commun 2015, Diabetologia 2017; Nat Genet 2017). The above platforms, database and biobanks have allowed her team to identity novel biomarkers of cardiometabolic diseases and demonstrate their clinical significance, notable examples being the adipocyte fatty acid binding protein (A-FABP) and fibroblast growth factor 21 (FGF21), which have inspired numerous follow-up studies in the field, from the international community.

Her team was the first to demonstrate that serum levels of A-FABP, a proinflammatory adipokine associated with insulin resistance, are raised in obesity and predict the development of the metabolic syndrome and type 2 diabetes (T2DM) (Clin Chem 2006; Circulation 2007; Diabetes Care 2007). She and her collaborators have subsequently confirmed its clinical significance in diabetic nephropathy (Diabetes Care 2009), stroke (Neurology 2011) and other CV diseases (ATVB 2007; EHJ 2008; JAHA 2013), fatty liver diseases (Hepatology 2009), and obstructive sleep apnoea (ERJ 2009). In preclinical studies, they elucidated its regulation by the C-Jun NH2-terminal kinase (JNK) inflammatory signaling (JBC 2010; Diabetes 2011), highlighted its role in mediating the adipo-vascular inter-talk in obesity through fat transplant studies (Clin Sci 2016) and demonstrated the effectiveness of a small molecule A-FABP inhibitor in treating fatty liver diseases (J Hepatol 2013). More recently, they also demonstrated, in the HKWDR cohort, that A-FABP also predicted renal events and multiple mortality outcomes (Clin Chem 2018; Diabetologia 2019). For FGF21, a hormone previously considered as largely a hepatokine, her paper in Diabetes 2008 provided the first evidence for its markedly increased expression in the adipocytes in obesity, leading to raised circulating levels. She subsequently showed that high FGF21 levels could predict the development of T2DM (Diabetes Care 2011) and distinguish T2DM from autoimmune diabetes (JCEM 2012). As beneficial metabolic effects of FGF21 and its analog are observed in animals and humans, respectively, this paradoxical increase in FGF21 levels suggests that obesity is associated with FGF21 resistance, which likely contributes to the clinical findings by her group and others, that elevated FGF21 levels are associated with atherosclerosis (ATVB 2013) and progressive cardiorenal diseases (JCEM 2015; JAHA 2017). In preclinical studies, her group has also demonstrated that FGF21 mediates a liver-brain cross-talk in glucose metabolism (Diabetes 2014) and that it participates in the body’s response against acute liver injury (Hepatology 2014). Their identification on exome-chip analysis of a functional variant of GCKR that regulates FGF21 levels (Diabetes 2017) further supports the physiological relevance of FGF21 in humans.