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Professor Karen Lam is Chair Professor and Head of Medicine, Director of the Research Centre of Heart, Brain, Hormone & Healthy Aging, Chairman of Clinical Trial Centre and Clinical Director of the State Key Laboratory of Pharmaceutical Biotechnology (focusing on diabetes and obesity), at the University of Hong Kong. The Founding President of Diabetes Hongkong, she was also a president of the HK Endocrine Society and Chairman of two specialty boards of the HK College of Physicians – Advanced Internal Medicine and Endocrinology, Diabetes & Metabolism.
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 and Lancet. 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 leads the Hong Kong Cardiovascular Risk Factor Prevalence Study (CRISPS; 1995-2014), a population-based cohort study on cardiovascular (CV) risk factors and diseases with the longest follow-up in China, which serves to chart the rise in obesity and metabolic syndrome in Southern China, as well as providing the database and biobank for investigating the interaction of environmental and genetic factors underlying obesity, diabetes and CV diseases in Chinese. 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); elucidated its regulation by the C-Jun NH2-terminal kinase (JNK) inflammatory signaling (JBC 2010; Diabetes 2011), and demonstrated the effectiveness of a small molecule A-FABP inhibitor in treating fatty liver diseases (J Hepatol 2013). In addition, her study on a transgenic mouse with adipose tissue specific JNK inactivation (Diabetes 2011) highlighted the importance of JNK activation in linking adipose tissue inflammation, dysregulated adipokine secretion and insulin resistance in obesity. For FGF21, a hormone previously considered as largely a hepatokine, her paper in Diabetes 2008 provided the first evidence that the FGF21 expression in the adipocytes is markedly increased in obesity, leading to raised circulating FGF21 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. Her findings have been confirmed by numerous other groups. Subsequent studies conducted by her group and others have also reported elevated FGF21 levels in atherosclerosis (ATVB 2013), fatty liver and other obesity related disorders. The underlying mechanisms of FGF21 resistance, which will impact on the therapeutic use of FGF21, have elucidated by her group (Diabetes 2013) and other researchers. Her work on the genetics of obesity and diabetes, including the first demonstration that obesity susceptibility gene variants identified from GWAS in Caucasians are also clinically relevant to Chinese (JCEM 2010; EJE 2011), has led to invitations of international collaborations (Diabetologia 2012; Diabetes 2013).