Marja-Riitta Taskinen is Emerita Professor of Medicine and her team is a member of the Research Program Unit, Diabetes & Obesity Research program at the University of Helsinki. Her research team at Biomedicum Helsinki focuses on lipoprotein kinetics in health and metabolic disorders including diabetes and dyslipidaemias, as well as the genetics of familial dyslipidemias.
Professor Taskinen’s outstanding achievements have been recognized by several international associations. These include the Claude Bernard Award (European Association for Study of Diabetes [EASD] 2002), Edwin Bierman Award (American Diabetes Association 2004), Novartis Award (2006), the Pohjola and Suomi Mutual Medical Award by the Finnish Medical Foundation (2012), and the Jean Vague/Per Björntorp Award by the International Chair on Cardiometabolic Risk (May, 2017). In November this year, Professor Taskinen was awarded the prestigious Robert Levy Memorial lecture at the 2017 American Heart Association Scientific Sessions, Anaheim, California, USA.
Professor Taskinen has been extensively involved in the activities of the European Atherosclerosis Society (President of EAS 2006-2008), International Atherosclerosis Society, EASD and International Diabetes Federation. Professor Taskinen is a member of the European Society of Cardiology/EAS Guidelines Committee on Management of Dyslipidaemias and is also a member of EAS Consensus Panel. She has published extensively in high-impact journals (H-index 85).
Disturbances in hepatic and lipoprotein metabolism is the hallmark of atherogenic dyslipidaemia
Atherogenic dyslipidaemia is characterized by elevated plasma concentrations of both fasting and postprandial triglyceride-rich lipoproteins (TRLs), small dense low-density lipoprotein (LDL) and low plasma concentration of high-density lipoprotein (HDL) cholesterol. This dyslipidaemia is a major driver of cardiovascular risk in individuals who are obese and/or have type 2 diabetes. The different components of diabetic dyslipidemia are not isolated abnormalities but closely linked to each other metabolically.
Elevated circulating TRLs, which reflect an imbalance between the synthesis and removal of the largest of the TRLs, very low-density lipoproteins (VLDL1), are pivotal to the development of atherogenic dyslipidaemia. Two key metabolic defects contribute: hepatic overproduction and delayed clearance of VLDL1. Increased deposition of fat in the liver (steatosis) and visceral adiposity are linked with increased secretion of VLDL1, whereas increased levels of apolipoprotein C-III (apoC-III), which regulates the metabolism of TRLs via direct effects on lipoprotein lipase and indirect mechanisms, such as promoting secretion of TRLs, is implicated in the reduced clearance of TRLs. Of the two defects, kinetic studies have shown that the increase in apoC-III is a more important contributor to plasma triglycerides. Together with evidence from studies showing a link between higher apoCIII levels in VLDL and LDL and increased cardiovascular risk, as well as recent genetic insights, these findings reinforce the relevance of apoC-III as a proatherogenic apolipoprotein.
Understanding the metabolic defects in hepatic and lipoprotein metabolism that underpin the development of atherogenic dyslipidaemia in abdominal obesity offers the opportunity for the development of novel therapeutic approaches, notably those targeting apoC-III. Ultimately these strategies may result in improvements in the prevention, diagnosis and management of atherogenic dyslipidaemia.
Taskinen MR, Söderlund S, Bogl LH, Hakkarainen A, Matikainen N, Pietiläinen KH, Räsänen S, Lundbom N, Björnson E, Eliasson B, Mancina RM, Romeo S, Alméras N, Pepa GD, Vetrani C, Prinster A, Annuzzi G, Rivellese A, Després JP, Borén J. Adverse effects of fructose on cardiometabolic risk factors and hepatic lipid metabolism in subjects with abdominal obesity. J Intern Med 2017;282:187-201.
Björnson E, Adiels M, Taskinen MR, Borén J. Kinetics of plasma triglycerides in abdominal obesity. Curr Opin Lipidol 2017;28:11-18.
Taskinen MR, Borén J. Why is apolipoprotein CIII emerging as a novel therapeutic target to reduce the burden of cardiovascular disease? Curr Atheroscler Rep 2016;18:59.