Metabolic and Bariatric Surgery

Biography

Associate Professor Signe Torekov has a strong background in metabolic translational research.

In collaboration with University of California her research has shown that infusion of the natural appetite hormone GLP-1 inhibits appetite and lowers blood glucose (2 first authorships in Diabetes, Obesity and Metabolism (Impact factor (IF) 6.2), 2011 and 2013). During the last three years, her research team has discovered that: 1) obese people have low endogenous GLP-1 response (first author in Diabetes (IF8.4), 2015); 2) weight loss induces a marked increase in GLP-1 response and that this is part of a successful maintenance of weight loss (last author in European Journal of endocrinology (IF4.1), 2016) (major media exposure: front page interview of The Times and live on BBC Today, April 2016 (7 mill listeners), and 3) treatment with GLP-1 analogues facilitate long term weight loss maintenance accompanied by substantial improvement in metabolic health, compared to diet-induced weight loss maintenance (Last author in Journal of Clinical Endocrinology and Metabolism (IF6.4) and International Journal of Obesity (IF5.4), 2015). Furthermore, by synergistically integrating metabolic physiology with novel state of the art mass spectrometry based proteomics and metabolomics, in collaboration with Professor Matthias Mann, Max Planck Institute, they have designed a novel experimental approach for clinical translational metabolism in order to identify new health markers in obesity (2. last author in Molecular Systems Biology, (IF 12.3) and last author in Metabolomics (IF3.7), 2016). In addition, Signe Torekov was awarded Major Discovery 2010-2015 for the her first author paper in Diabetes (IF8.4) 2014 where she, together with the research team, showed that Long QT Syndrome patients with mutations in KCNQ1 besides having prolonged cardiac arrhythmia, also have hyperinsulinemic hypoglycemia. More recently, Signe Torekov has shown that Long QT Syndrome patients with loss of function mutations in hERG display exaggerated incretin and endocrine pancreatic function and thus increased risk of symptomatic reactive hypoglycemia. Pharmacological blockade in rats and inhibition of hERG in β and L- cells had similar effects. Hypoglycemia leads to increased propensity for arrhythmias; hypoglycemia may therefore even further increase the risk of malignant arrhythmia in LQTS patients (published in Circulation (IF17) with Dr. Torekov as last and corresponding author).

Abstract

Abstract : Obesity and GLP-1. Obesity pathophysiology and GLP-1 treatment potential