Welcome to the Hjelt Foundations

"The three Hjelt Foundations, Spina Bifida, Diabetes and Art were created because of very important events that have considerably influenced my life."

 Bo Hjelt

News

By The Diabetes Foundation 11 Oct, 2023
The Diabetes Foundation: The application period for next year’s research grants is 11 October to 15 December. Research grants are awarded to applicants at the Medical Faculties of Lund University, Sweden and Geneva University, Switzerland. Read more/apply
By The Diabetes Foundation 05 Sep, 2023
Jiangming Sun, Emma Ahlqvist and Sabrina Ruhrmann have each been awarded a project grant of 47,500 euro by the Hjelt Diabetes Foundation.
By The Art Foundation 17 May, 2023
Allan and Bo Hjelt Art Foundation had the great honour to welcome Mr. Leonardo Ferragamo, Chairman of Nautor Swan, to give an inspirational design talk on Finnish-Italian collaboration in Helsinki in March.
By The Diabetes Foundation 19 Oct, 2022
The Diabetes Foundation: The application period for next year’s research grants is 19 October to 15 December. Research grants are awarded to applicants at the Medical Faculties of Lund University, Sweden and Geneva University, Switzerland. Read more/apply
By The Diabetes Foundation 08 Sep, 2022
Today, three of our grant holders in the Diabetes foundation for 2022 are presented in an article on the Lund University Diabetes Center website. Read more at the LUDC web site .
By The Art Foundation 31 Mar, 2022
Sir John Stuttard: "Pre-War Rolls-Royce Motor Cars with a Finnish connection" Time: Wed, April 27th 2022 at 5 pm Venue: Handelsgilletin juhlasali, Kasarminkatu 40, 2. krs., Helsinki Lecture in English. Due to limited seats available, pre-registration is required to art@hjeltfoundations.org. Welcome!
By The Diabetes Foundation 04 Mar, 2022
We are pleased to announce that four scientists have been awarded the Hjelt Research Grant for 2022: Luis Rodrigo Cataldo Bascunan, Anja Schmidt-Christensen and Sebastian Kalamajski, Lund University Diabetes Centre, and Monika Gjorgijeva Ducros, University of Geneva Faculty of Medicine Diabetes Centre.
By The Art Foundation 05 Nov, 2021
The biography "Allan Hjelt – Entreprenör i brytningstider", published in Swedish in 2020, is now available in Finnish. In this biography, written by Maria Ekman, we meet a man who built an empire, lost almost everything, – and started all over again. It tells the story of a successful Finland-Swedish entrepreneur, patron of the arts, honorary consul and Finland’s trade negotiator for military equipment and support in the midst of World War II. ”Allan Hjelt - murrosvaiheiden liikemies” is translated into Finnish by writer and editor Marjo Uusikylä. It is available in bookstores in Helsinki, and in your online bookstore. Publisher: Mistake Media. ISBN 9789527188194 A tribute to his late father The half-hour documentary of Allan Hjelt premiered on Finnish AlfaTV on 27 October 2021. It is shown as a part of the series ”Merkit” (Brands) that explores the history, present, values and future of brands . In the documentary, Bo Hjelt, the son of Allan Hjelt, tells about his childhood memories of his father and how the biography has brought new information of A  llan Hjelt to the fore. Maria Ekman, the writer of Allan Hjelt’s biography, presents important places for Consul Hjelt in Helsinki, such as Villa Hjelt and Keskuskatu, the street that transformed the city centre of Helsinki hundred years ago in the 1920’s . View the episode: Merkit , Kausi 2: 3/10 Producer: Mistake Media. (in Finnish)
By The Diabetes Foundation 19 Oct, 2021
The Diabetes Foundation: The application period for next year’s research grants is 19 October to 15 December. Research grants are awarded to applicants at the Medical Faculties of Lund University, Sweden and Geneva University, Switzerland. Read more/apply
Lund University.
By The Diabetes Foundation 12 Oct, 2021
Lund University presents three Hjelt researchers. Ola Hansson, Karl Bacos and Malin Fex have been awarded 45 000 euros each for their research projects.
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Spina Bifida Foundation

Having lost a child due to Spina Bifida, a most traumatic experience that no family should have to go through, the Bo Hjelt Foundation for Spina Bifida in memory of Madeleine Hjelt was set up to aid research into its’ prevention.
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Diabetes Foundation

The Bo and Kerstin Hjelt Foundation for research into Diabetes II was set up because, being a diabetic himself, he wanted to contribute to research in this field as it is increasing rapidly worldwide.
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Art Foundation

The Allan and Bo Hjelt Art Foundation was created in honour of Bo Hjelt's parents. He wanted to return to Finland some pieces of art that his Finnish-born father had collected; and to create the Falsterbonaset Open Air Museum in memory of his mother’s happy times in Falsterbo (five bronze statues by the Swedish sculptor Gudmar Olovson).
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Diabetes Foundation: Our Recent Research Projects

07 Mar, 2024
Sebastian Kalamajski, Hjelt Grant Holder 2024, Lund University. Leveraging discordancy between obesity and type 2 diabetes to target insulin resistance
By Hjelt Grant Holder 2023, Sabrina Ruhrmann 21 Mar, 2023
Sabrina Ruhrmann, Hjelt Grant Holder 2023, Lund University. Epigenetic Editing - a way to a personalized treatment approach in type 2diabetes (T2D) The number of people affected by diabetes is rapidly increasing worldwide. Type 2 diabetes (T2D) largely contributes to this increase and individuals with T2D usually face high blood sugar levels. To balance our blood sugar level the hormone Insulin is necessary and Insulin target tissues like muscles need to be able to take up glucose in response to Insulin. Overweight and no physical exercise can lead to insulin resistance (where the uptake of glucose is not any longer possible e.g. in our muscles) and almost all individuals with T2D show Insulin resistance. Our DNA only explains a small proportion of how T2D is passed on from parents to their children (also described as the so called “missing heritability”). Given the crucial role of diet and physical exercise in the development of T2D, mechanisms mediating the interaction of those factors with our genes should be of particular importance when trying to explain how T2D develops. Epigenetic mechanisms fulfil this criterion. Epigenetics is the study of how e.g. the environment and/or our behavior can affect the expression of our genes without changing our DNA. The fact that epigenetic changes do not change our DNA unlike genetic changes gives us the opportunity to “correct“ them. We are here trying to discover epigenetic changes that cause T2D. We will create small molecules called guideRNAs (gRNAs) that will help us to search for those epigenetic changes using the so called inactivated gene scissor system, CRISPR-dCas9. We will further try to also 'correct' these epigenetic changes to explore if epigenetic mechanisms may be targeted for a more patient specific treatment of T2D in the future.
By Hjelt Grant Holder 2022, Monika Gjorgijeva Ducros 04 Mar, 2022
Monika Gjorgijeva Ducros, Hjelt Grant Holder 2022, University of Geneva. Background MicroRNAs (miRNAs) are critical gene expression regulators involved in mRNA decay or translation inhibition. MiRNAs play an important role in various physiological processes and therefore, deregulation of their expression/activity has been associated with the development of metabolic disorders. Obesity and the metabolic syndrome represent key etiological conditions that predispose to the development of insulin resistance (IR), Type 2 Diabetes (T2D) and non-alcoholic fatty liver disease (NAFLD). Increasing evidence indicate that miRNA deregulation contributes to the development of these diseases. In this context, our recent findings highlighted a strong induction of miR-149 in the liver of various models of IR, T2D and NAFLD, suggesting an important role of this miRNA in these metabolic disorders. Hypothesis Based on our preliminary results, we hypothesize that the increase in hepatic mir-149 in IR/T2D/NAFLD conditions can favor these pathologies. We will therefore investigate i) the pathophysiological role and pre-clinical relevance of miR-149 upregulation in IR/T2D/NAFLD and ii) which miR-149 target genes are involved in this process. Methods To investigate the role of miR-149 in IR/T2D/NAFLD, we are using human liver organoids (HLOs). HLOs are obtained by inducing differentiation of human progenitor cells into different hepatic cell types (hepatocytes, Kuppfer cells, stellate cells) that form functional structures. These organoids respond to insulin stimulation in the same manner as human liver. Moreover, they develop hepatic steatosis under high-fat/high sugar conditions and can undergo inflammation when stimulated with cytokines. Finally, HLOs are an extremely relevant experimental model as they allow us to avoid animal experimentation protocols. Therefore, we will modulate the expression of miR-149 in HLOs via synthetic nucleotides and/ or viral vectors and we will analyze the molecular responses in HLO under various metabolic / inflammatory stimuli. We will further identify miR-149 target genes involved in IR/T2D/NAFLD and we will validate their relevance in public human datasets. Results Our preliminary data suggest a pertinent role for miR-149 upregulation in the induction of steatosis in vitro in currently used hepatic cell lines, as well as in HLO. We have also observed that alteration of miR-149 levels has a striking effect on hepatic glucose and lipid metabolism, implying a functional role for this miRNA in IR/T2D/NAFLD. Conclusion This project should allow us to better understand the role of miR-149 in hepatic IR, and more generally in obesity-associated disorders of the hepatic lipid/glucose metabolism. We will identify novel target genes of miR-149 contributing to IR/T2D/NAFLD and the fine-tuning metabolic regulation in the liver in pathophysiological conditions. Our investigations should provide key evidence and proof-of-concept about the potential of miR-149 and its targets as new biomarkers for IR/T2D as well as the therapeutic potential of targeting this miRNA to counteract and/or to alleviate IR/T2D development. Importance Modulation of miR-149 represents a promising therapeutic strategy by targeting numerous genes at once. Therefore, miR-149 modulation could represent a multi-targeting approach relevant and pertinent for multifactorial disorders such as obesity, IR/T2D/NAFLD. A significant and innovative aspect of this proposal is the development and use of genetically engineered functional HLOs in which hepatic steatosis, inflammation and IR can be reproduced. HLOs have the potential of replacing animal experimentation, thereby alleviating important ethical issues related to the use of laboratory mice for pre-clinical research.
By Hjelt Grant Holder 2022, Rodrigo Cataldo 01 Mar, 2022
Rodrigo Cataldo, Hjelt Grant Holder 2022, Lund University. Background The role of beta cells is to sense glucose and response by releasing insulin to maintain glucose homeostasis. Consequently, the loss of beta cell function is the main culprit of type 2 diabetes development. Ependymin-related protein 1 (EPDR1) was recently identified as a protein released by the human brown adipose tissue, where it plays a role in regulating thermogenesis, a protective metabolic process that transform stored fat into heat. It was suggested that EPDR1 may act as a novel hormone regulating whole-body energy metabolism. Apart of this, the biological role of EPDR1 is poorly known. I have identified that human beta cells also produce EPDR1 protein and that its expression is upregulated in pancreatic islets from Type 2 diabetes vs. non diabetic donors and that its expression is associated to beta cell function. Hypothesis Based on the data obtained so far, I believe that EPDR1 expression in beta cells may increase in response to the metabolic stress caused by overfeeding in obese people to, in a compensatory fashion, restore glucose metabolism and maintain beta cell function. Methods I aim to apply a cutting-edge methodology, Metabolic Flux Analysis (MFA), which is based in fueling beta cells with labeled energy substrates and then quantify the rate of different metabolic pathways underlying insulin secretion. With this method we plan to elucidate the mechanism of action for EPDR1 in regulating beta cell function. I also plan to study animals that lack EPDR1, make them obese (to mimic metabolic stress in obese people) and test beta cell function (in vitro) and glucose tolerance (in vivo) to understand the role of EPDR1 in beta cell function and glucose homeostasis. Results I have so far conducted some in vitro experiments and found that treatment of beta cells with EPDR1 protein increases insulin secretion whereas silencing EPDR1 expression reduces insulin secretion. I have performed metabolomics experiments and found that silencing EPDR1 expression in beta cells alter the levels of glucose-derived metabolites in different relevant pathways associated to insulin secretion. Conclusions I have found that EPDR1 is required to maintain normal human beta cell function. EDPR1 regulates glucose metabolism by increasing coupling of glycolysis and mitochondrial function in beta cells. Importance The proposed research project will help to elucidate the role of EPDR1 for beta cell function and glucose homeostasis and to deepen the knowledge of molecular mechanisms of EPDR1 to regulate beta cell metabolism and function. We have also identified genetic variants associated to EPDR1 expression in human beta cells and function and this study will also explore the potential of these genetic variants to make advances of precision medicine in Type 2 diabetes. Finally, if we confirm the positive effects of EPDR1 protein for human beta cell function and glucose homeostasis, EPDR1 could become a target to develop treatments for obese people to prevent progress to T2D.
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