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3. Proteomic profiling reveals diagnostic signatures and pathogenic insights in multisystem inflammatory syndrome in children

Author

Nygaard, Ulrikka, Nielsen, Annelaura Bach, Dungu, Kia Hee Schultz, Drici, Lylia, Holm, Mette, Ottenheijm, Maud Eline, Nielsen, Allan Bybeck, Glenthøj, Jonathan Peter, Schmidt, Lisbeth Samsø, Cortes, Dina, Jørgensen, Inger Merete, Mogensen, Trine Hyrup, Schmiegelow, Kjeld, Mann, Matthias, Vissing, Nadja Hawwa, and Wewer Albrechtsen, Nicolai J.

Published
2024
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6. The impact of short-term eucaloric low- and high-carbohydrate diets on liver triacylglycerol content in males with overweight and obesity: a randomized crossover study

Author

London, Amalie, Richter, Michael M, Sjøberg, Kim Anker, Wewer Albrechtsen, Nicolai J, Považan, Michal, Drici, Lylia, Schaufuss, Amanda, Madsen, Lise, Øyen, Jannike, Madsbad, Sten, Holst, Jens Juul, van Hall, Gerrit, Siebner, Hartwig Roman, Richter, Erik A, Kiens, Bente, Lundsgaard, Annemarie, and Bojsen-Møller, Kirstine Nyvold

Published
2024
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7. Glucagon augments the secretion of FGF21 and GDF15 in MASLD by indirect mechanisms

Author

Richter, Michael M., Kemp, Ida M., Heebøll, Sara, Winther-Sørensen, Marie, Kjeldsen, Sasha A.S., Jensen, Nicole J., Nybing, Janus D., Linden, Frederik H., Høgh-Schmidt, Erik, Boesen, Mikael P., Madsbad, Sten, Schiødt, Frank Vinholt, Nørgaard, Kirsten, Schmidt, Signe, Gluud, Lise Lotte, Haugaard, Steen B., Holst, Jens J., Nielsen, Søren, Rungby, Jørgen, and Wewer Albrechtsen, Nicolai J.

Published
2024
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9. 100 years of glucagon and 100 more

Author

Wewer Albrechtsen, Nicolai J., Holst, Jens J., Cherrington, Alan D., Finan, Brian, Gluud, Lise Lotte, Dean, E. Danielle, Campbell, Jonathan E., Bloom, Stephen R., Tan, Tricia M.-M., Knop, Filip K., and Müller, Timo D.

Published
2023
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10. Effects of 3 months of 10-h per-day time-restricted eating and 3 months of follow-up on bodyweight and cardiometabolic health in Danish individuals at high risk of type 2 diabetes: the RESET single-centre, parallel, superiority, open-label, randomised controlled trial

Author

Quist, Jonas Salling, Pedersen, Hanne Enghoff, Jensen, Marie Møller, Clemmensen, Kim Katrine Bjerring, Bjerre, Natasja, Ekblond, Trine Spragge, Uldal, Sarah, Størling, Joachim, Wewer Albrechtsen, Nicolai J, Holst, Jens Juul, Torekov, Signe Sørensen, Nyeland, Martin Erik, Vistisen, Dorte, Jørgensen, Marit Eika, Panda, Satchidananda, Brock, Christina, Finlayson, Graham, Blond, Martin Bæk, and Færch, Kristine

Published
2024
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12. Neprilysin activity is increased in metabolic dysfunction-associated steatotic liver disease and normalizes after bariatric surgery or GLP-1 therapy

Author

Kjeldsen, Sasha A.S., Gluud, Lise L., Werge, Mikkel P., Pedersen, Julie S., Bendtsen, Flemming, Alexiadou, Kleopatra, Tan, Tricia, Torekov, Signe S., Iepsen, Eva W., Jensen, Nicole J., Richter, Michael M., Goetze, Jens P., Rungby, Jørgen, Hartmann, Bolette, Holst, Jens J., Holst, Birgitte, Holt, Joachim, Gustafsson, Finn, Madsbad, Sten, Svane, Maria S., Bojsen-Møller, Kirstine N., and Wewer Albrechtsen, Nicolai J.

Published
2023
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13. Four weeks treatment with the GLP-1 receptor analogue liraglutide lowers liver fat and concomitantly circulating glucagon in individuals with overweight

Author

Svane, Maria S., Johannesen, Helle H., Hansen, Adam E., Martinussen, Christoffer, Bojsen-Møller, Kirstine N., Hansen, Martin Lundsgaard, Deacon, Carolyn F., Keller, Sune H., Klausen, Thomas L., Loft, Annika, Kjaer, Andreas, Löfgren, Johan, Madsbad, Sten, Holst, Jens J., and Wewer Albrechtsen, Nicolai J.

Published
2022
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16. Glucagon, Metabolic Dysfunction-Associated Steatotic Liver Disease and Amino Acids in Humans and Animals without Diabetes Mellitus—An Evidence Map.

Author

Maruszczak, Katharina, Koren, Pia, Radzikowski, Konrad, Pixner, Thomas, Suppli, Malte Palm, Wewer Albrechtsen, Nicolai J., Weghuber, Daniel, and Torbahn, Gabriel

Subjects
EVIDENCE gaps, GLUCOSE tolerance tests, PANCREATIC beta cells, GLUCOSE clamp technique, CHILDHOOD obesity
Abstract

Introduction: Health systems are confronted with not only the growing worldwide childhood obesity epidemic but also associated comorbidities. These subsequently cause variations in distinct metabolic pathways, leading to metabolic dysfunction-associated steatotic liver disease (MASLD). The aim of this evidence map is to systematically evaluate the evidence and to identify research gaps on glucagon-induced amino acid (AA) turnover and its metabolic interaction with MASLD. Methodology: A systematic literature search was conducted up to April 2023 in three electronic databases. Studies were required to include at least two of the main research areas, glucagon, AA metabolism and MASLD. Two independent reviewers screened titles and abstracts according to prespecified eligibility criteria, as well as full-text articles. Results are summarized in tables stratified by human and animal studies and study population age. Results: Thirty-four references were ultimately included. The publication years dated back to 1965 showed a great increase from 2012 to 2023. In total, there were 19 animal studies and 15 human studies. Among the human studies, except for two studies in adolescents, all the studies were conducted in adults. In human studies, the methods used to evaluate metabolic changes differed among hyperinsulinemic-euglycemic clamp and oral glucose tolerance tests. Thirteen studies focused on the metabolic effects of MASLD, while only two studies explored the interaction between MASLD, glucagon and AA metabolism in humans. The other 19 studies focused on metabolomics, beta cell function or just one topic of a research area and not on interactions between one another. Conclusion: Research on the interaction between MASLD, glucagon and AA metabolism in humans is sparse and complete lacking in pediatrics. Furthermore, longitudinal studies with a focus on hyperglucagonemia independent of diabetes but related to MASLD present an unambiguous research gap. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Impairments of insulin and glucagon sensitivity in Chinese women with gestational diabetes mellitus.

Author

Zhang, Dan, Zhu, Jianan, Wewer Albrechtsen, Nicolai J., Rayner, Christopher K., Saffery, Richard, Zhang, Hua, Chen, Chang, and Wu, Tongzhi

Subjects
PATHOLOGICAL physiology, GLUCOSE tolerance tests, FATTY liver, BLOOD sugar, CHINESE people, INSULIN sensitivity, GESTATIONAL diabetes, INSULIN
Abstract

Aim: To evaluate insulin and glucagon sensitivity in Han Chinese women with and without gestational diabetes mellitus (GDM). Methods: In total, 81 women with GDM and 81 age‐matched healthy controls were evaluated with a 75 g oral glucose tolerance test (OGTT) at gestational weeks 24‐28. Plasma glucose concentrations were measured at fasting and 1 h and 2 h post‐OGTT. Fasting plasma insulin, glucagon and amino acids were also measured. Insulin and glucagon sensitivity were assessed by the homeostatic model assessment of insulin resistance (HOMA‐IR) and glucagon‐alanine index, respectively. Results: As expected, plasma glucose concentrations were higher at fasting and 1 h and 2 h post‐OGTT in GDM participants (p <.001 each). Both the HOMA‐IR and the glucagon‐alanine index were higher in GDM participants. There was a weak positive correlation between HOMA‐IR and glucagon‐alanine index (r = 0.24, p =.0024). Combining the HOMA‐IR and the glucagon‐alanine index yielded better capacity (area under the curve = 0.878) than either alone (area under the curve = 0.828 for HOMA‐IR and 0.751 for glucagon‐alanine index, respectively) in differentiating GDM from healthy participants. While the majority of GDM participants (64%) exhibited both reduced insulin and glucagon sensitivity, a third of them presented either reduced insulin (20%) or glucagon (14%) sensitivity alone. HOMA‐IR and glucagon‐alanine index correlated differentially with fasting glucose, triglycerides, low‐density lipoprotein cholesterol, sum of amino acids and hepatic steatosis index. Conclusions: Impairments of both insulin and glucagon sensitivity occur frequently in Chinese women with GDM, which may, individually or together, drive metabolic derangements in GDM. These observations provide new insights into the pathophysiology of GDM and support the need to target insulin or glucagon resistance, or both, in the management of GDM. [ABSTRACT FROM AUTHOR]

Published
2024
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18. Glucagon receptor antagonism impairs and glucagon receptor agonism enhances triglycerides metabolism in mice

Author

Galsgaard, Katrine D., Elmelund, Emilie, Johansen, Christian D., Bomholt, Anna B., Kizilkaya, Hüsün S., Ceutz, Frederik, Hunt, Jenna E., Kissow, Hannelouise, Winther-Sørensen, Marie, Sørensen, Charlotte M., Kruse, Thomas, Lau, Jesper F., Rosenkilde, Mette M., Ørskov, Cathrine, Christoffersen, Christina, Holst, Jens J., and Wewer Albrechtsen, Nicolai J.

Published
2022
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20. Glucagon acutely regulates hepatic amino acid catabolism and the effect may be disturbed by steatosis

Author

Winther-Sørensen, Marie, Galsgaard, Katrine D., Santos, Alberto, Trammell, Samuel A.J., Sulek, Karolina, Kuhre, Rune E., Pedersen, Jens, Andersen, Daniel B., Hassing, Anna S., Dall, Morten, Treebak, Jonas T., Gillum, Matthew P., Torekov, Signe S., Windeløv, Johanne A., Hunt, Jenna E., Kjeldsen, Sasha A.S., Jepsen, Sara L., Vasilopoulou, Catherine G., Knop, Filip K., Ørskov, Cathrine, Werge, Mikkel P., Bisgaard, Hanne Cathrine, Eriksen, Peter Lykke, Vilstrup, Hendrik, Gluud, Lise Lotte, Holst, Jens J., and Wewer Albrechtsen, Nicolai J.

Published
2020
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30. Secretin release after Roux-en-Y gastric bypass reveals a population of glucose-sensitive S cells in distal small intestine

Author

Modvig, Ida M., Andersen, Daniel B., Grunddal, Kaare V., Kuhre, Rune E., Martinussen, Christoffer, Christiansen, Charlotte B., Ørskov, Cathrine, Larraufie, Pierre, Kay, Richard G., Reimann, Frank, Gribble, Fiona M., Hartmann, Bolette, Bojsen-Møller, Kirstine N., Madsbad, Sten, Wewer Albrechtsen, Nicolai J., and Holst, Jens J.

Published
2020
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38. No direct effect of SGLT2 activity on glucagon secretion

Author

Kuhre, Rune E., Ghiasi, Seyed M., Adriaenssens, Alice E., Wewer Albrechtsen, Nicolai J., Andersen, Daniel B., Aivazidis, Alexander, Chen, Lihua, Mandrup-Poulsen, Thomas, Ørskov, Cathrine, Gribble, Fiona M., Reimann, Frank, Wierup, Nils, Tyrberg, Björn, and Holst, Jens J.

Published
2019
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39. Preanalytical impact on the accuracy of measurements of glucagon, GLP-1 and GIP in clinical trials.

Author

Rasmussen, Christine, Richter, Michael M., Jensen, Nicole J., Heinz, Niklas, Hartmann, Bolette, Holst, Jens J., Kjeldsen, Sasha A. S., and Wewer Albrechtsen, Nicolai J.

Subjects
GLUCAGON, CLINICAL trials, INTRAVENOUS therapy, KALLIKREIN, PROTEASE inhibitors
Abstract

Plasma concentrations of glucagon, GLP-1 and GIP are reported in numerous clinical trials as outcome measures but preanalytical guidelines are lacking. We addressed the impact of commonly used blood containers in metabolic research on measurements of glucagon, GLP-1 and GIP in humans. Seventeen overweight individuals were subjected to an overnight fast followed by an intravenous infusion of amino acids to stimulate hormonal secretion. Blood was sampled into five containers: EDTA-coated tubes supplemented with DMSO (control), a neprilysin inhibitor, aprotinin (a kallikrein inhibitor) or a DPP-4 inhibitor, and P800 tubes. Plasma was kept on ice before and after centrifugation and stored at −80 Celsius until batch analysis using validated sandwich ELISAs or radioimmunoassays (RIA). Measures of fasting plasma glucagon did not depend on sampling containers, whether measured by ELISA or RIA. Amino acid-induced hyperglucagonemia was numerically higher when blood was collected into P800 tubes or tubes with aprotinin. The use of p800 tubes resulted in higher concentrations of GLP-1 by RIA compared to control tubes but not for measurements with sandwich ELISA. Plasma concentrations of GIP measured by ELISA were higher in control tubes and negatively affected by P800 and the addition of aprotinin. The choice of blood containers impacts on measurements of plasma concentrations of glucagon, GLP-1 and GIP, and based on this study, we recommend using EDTA-coated tubes without protease inhibitors or P800 tubes for measurements of glucagon, GLP-1 and GIP in clinical trials. [ABSTRACT FROM AUTHOR]

Published
2023
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40. Evidence of a liver–alpha cell axis in humans: hepatic insulin resistance attenuates relationship between fasting plasma glucagon and glucagonotropic amino acids

Author

Wewer Albrechtsen, Nicolai J., Færch, Kristine, Jensen, Troels M., Witte, Daniel R., Pedersen, Jens, Mahendran, Yuvaraj, Jonsson, Anna E., Galsgaard, Katrine D., Winther-Sørensen, Marie, Torekov, Signe S., Lauritzen, Torsten, Pedersen, Oluf, Knop, Filip K., Hansen, Torben, Jørgensen, Marit E., Vistisen, Dorte, and Holst, Jens J.

Published
2018
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43. Autoimmune liver diseases and diabetes: A propensity score matched analysis and a proportional meta‐analysis.

Author

Jensen, Anne‐Sofie H., Winther‐Sørensen, Marie, Burisch, Johan, Bergquist, Annika, Ytting, Henriette, Gluud, Lise L., and Wewer Albrechtsen, Nicolai J.

Subjects
LIVER diseases, PROPENSITY score matching, AUTOIMMUNE diseases, AUTOIMMUNE hepatitis, TYPE 1 diabetes
Abstract

Background and Aims: Patients with some chronic liver diseases have increased risk of diabetes. Whether this is also the case for patients with autoimmune liver diseases is unknown. The study aimed to calculate risk and worldwide prevalence of diabetes in patients with autoimmune hepatitis (AIH), primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). Methods: We performed a case–control study using data from the United Kingdom Biobank (UKB) and compared frequency of type 1 diabetes (T1D) and type 2 diabetes (T2D) in AIH and PBC with age‐, sex‐, BMI‐ and ethnicity‐matched controls. Next, we performed a systematic review and proportional meta‐analysis searching PubMed, Embase, Cochrane Library and Web of Science (inception to 1 May 2022 [AIH]; 20 August 2022 [PBC]; 11 November 2022 [PSC]). The pooled prevalence of diabetes was calculated using an inverse method random effects model. Results: Three hundred twenty‐eight AIH patients and 345 PBC patients were identified in UKB and risk of T1D and T2D significantly increased compared with matched controls. Our systematic search identified 6914 records including the UKB study. Of these, 77 studies were eligible for inclusion comprising 36 467, 39 924 and 4877 individuals with AIH, PBC and PSC, respectively. The pooled prevalence of T1D was 3.8% (2.6%–5.7%), 1.7% (0.9%–3.1%), 3.1% (1.9%–4.8%) and of T2D 14.8% (11.1%–19.5%), 18.1% (14.6%–22.2%), 6.3% (2.8%–13.3%) in patients with AIH, PBC and PSC, respectively. Conclusions: Patients with autoimmune liver diseases have increased risk of diabetes. Increased awareness of diabetes risk in patients with autoimmune liver diseases is warranted. [ABSTRACT FROM AUTHOR]

Published
2023
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47. Postprandial dysfunction in fatty liver disease.

Author

Grandt, Josephine, Jensen, Anne‐Sofie H., Werge, Mikkel P., Rashu, Elias B., Møller, Andreas, Junker, Anders E., Hobolth, Lise, Mortensen, Christian, Johansen, Christian D., Vyberg, Mogens, Serizawa, Reza Rafiolsadat, Møller, Søren, Gluud, Lise Lotte, and Wewer Albrechtsen, Nicolai J.

Subjects
FATTY liver, NON-alcoholic fatty liver disease, FIBROBLAST growth factors, BLOOD sugar, LIVER biopsy
Abstract

Fatty liver disease has mainly been characterized under fasting conditions. However, as the liver is essential for postprandial homeostasis, identifying postprandial disturbances may be important. Here, we investigated postprandial changes in markers of metabolic dysfunction between healthy individuals, obese individuals with non‐alcoholic fatty liver disease (NAFLD) and patients with cirrhosis. We included individuals with biopsy‐proven NAFLD (n = 9, mean age 50 years, mean BMI 35 kg/m2, no/mild fibrosis), cirrhosis with hepatic steatosis (n = 10, age 62 years, BMI 32 kg/m2, CHILD A/B) and healthy controls (n = 10, age 23, BMI 25 kg/m2), randomized 1:1 to fasting or standardized mixed meal test (postprandial). None of the patients randomized to mixed meal test had type 2 diabetes (T2D). Peripheral blood was collected for 120 min. After 60 min, a transjugular liver biopsy and liver vein blood was taken. Plasma levels of glucose, insulin, C‐peptide, glucagon, and fibroblast growth factor 21 (FGF21) were measured. Postprandial peak glucose and C‐peptide were significantly increased in NAFLD, and cirrhosis compared with healthy. Patients with NAFLD and cirrhosis had hyperglucagonemia as a potential sign of glucagon resistance. FGF21 was increased in NAFLD and cirrhosis independent of sampling from the liver vein versus peripheral blood. Glucagon levels were higher in the liver vein compared with peripheral blood. Patients with NAFLD and cirrhosis without T2D showed impaired glucose tolerance, hyperinsulinemia, and hyperglucagonemia after a meal compared to healthy individual. Postprandial characterization of patients with NAFLD may be important to capture their metabolic health. [ABSTRACT FROM AUTHOR]

Published
2023
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