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17 results on '"Iepsen, Eva W."'

1. 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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2. SAT032 Circulating Neprilysin Activity Is Increased In Type 2 Diabetes And Fatty Liver Disease, And Reduces Following Bariatric Surgery And Liraglutide Therapy

Author

Sampson Kjeldsen, Sasha Alexandra, primary, Lotte Gluud, Lise, additional, Werge, Mikkel, additional, Steen Pedersen, Julie, additional, Bendtsen, Flemming, additional, Alexiadou, Kleopatra, additional, Tan, Tricia, additional, Torekov, Signe S, additional, Iepsen, Eva W, additional, Jensen, Nicole J, additional, Richter, Michael, additional, Hartmann, Bolette, additional, Holst, Jens J, additional, Holst, Birgitte, additional, Holt, Joachim, additional, Madsbad, Sten, additional, Svane, Maria S, additional, Bojsen-Møller, Kirstine N, additional, and Wewer Albrechtsen, Nicolai J, additional

Published
2023
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3. Neprilysin activity is increased in MASLD and normalizes after bariatric surgery or GLP-1 therapy

Author

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

Published
2023
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6. A Gut-Intrinsic Melanocortin Signaling Complex Augments L-Cell Secretion in Humans

Author

Sun, Emily W., primary, Iepsen, Eva W., additional, Pezos, Nektaria, additional, Lumsden, Amanda L., additional, Martin, Alyce M., additional, Schober, Gudrun, additional, Isaacs, Nichole J., additional, Rayner, Christopher K., additional, Nguyen, Nam Q., additional, de Fontgalland, Dayan, additional, Rabbitt, Philippa, additional, Hollington, Paul, additional, Wattchow, David A., additional, Hansen, Torben, additional, Holm, Jens-Christian, additional, Liou, Alice P., additional, Jackson, V. Margaret, additional, Torekov, Signe S., additional, Young, Richard L., additional, and Keating, Damien J., additional

Published
2021
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11. Patients With Long-QT Syndrome Caused by Impaired hERG -Encoded K v 11.1 Potassium Channel Have Exaggerated Endocrine Pancreatic and Incretin Function Associated With Reactive Hypoglycemia

Author

Hyltén-Cavallius, Louise, primary, Iepsen, Eva W., additional, Wewer Albrechtsen, Nicolai J., additional, Svendstrup, Mathilde, additional, Lubberding, Anniek F., additional, Hartmann, Bolette, additional, Jespersen, Thomas, additional, Linneberg, Allan, additional, Christiansen, Michael, additional, Vestergaard, Henrik, additional, Pedersen, Oluf, additional, Holst, Jens J., additional, Kanters, Jørgen K., additional, Hansen, Torben, additional, and Torekov, Signe S., additional

Published
2017
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14. Patients With Long-QT Syndrome Caused by Impaired -Encoded Kv11.1 Potassium Channel Have Exaggerated Endocrine Pancreatic and Incretin Function Associated With Reactive Hypoglycemia.

Author

Hyltén-Cavallius, Louise, Iepsen, Eva W., Albrechtsen, Nicolai J. Wewer, Svendstrup, Mathilde, Lubberding, Anniek F., Hartmann, Bolette, Jespersen, Thomas, Linneberg, Allan, Christiansen, Michael, Vestergaard, Henrik, Pedersen, Oluf, Holst, Jens J., Kanters, Jørgen K., Hansen, Torben, Torekov, Signe S., and Wewer Albrechtsen, Nicolai J

Subjects
*HYPOGLYCEMIA, *POTASSIUM channels, *ISLANDS of Langerhans, *INCRETINS, *GENETIC mutation, *LONG QT syndrome diagnosis, *ACTION potentials, *BLOOD sugar, *C-peptide, *CELL lines, *DISEASE susceptibility, *ELECTROCARDIOGRAPHY, *GENES, *GENETIC techniques, *GLUCAGON, *GLUCOSE tolerance tests, *HEART conduction system, *INSULIN, *TIME, *PHENOTYPES, *GLUCAGON-like peptide 1, *LONG QT syndrome, *CASE-control method, *POTASSIUM antagonists, *PHARMACODYNAMICS, *DIAGNOSIS
Abstract

Background: Loss-of-function mutations in hERG (encoding the Kv11.1 voltage-gated potassium channel) cause long-QT syndrome type 2 (LQT2) because of prolonged cardiac repolarization. However, Kv11.1 is also present in pancreatic α and β cells and intestinal L and K cells, secreting glucagon, insulin, and the incretins glucagon-like peptide-1 (GLP-1) and GIP (glucose-dependent insulinotropic polypeptide), respectively. These hormones are crucial for glucose regulation, and long-QT syndrome may cause disturbed glucose regulation. We measured secretion of these hormones and cardiac repolarization in response to glucose ingestion in LQT2 patients with functional mutations in hERG and matched healthy participants, testing the hypothesis that LQT2 patients have increased incretin and β-cell function and decreased α-cell function, and thus lower glucose levels.Methods: Eleven patients with LQT2 and 22 sex-, age-, and body mass index-matched control participants underwent a 6-hour 75-g oral glucose tolerance test with ECG recording and blood sampling for measurements of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP.Results: In comparison with matched control participants, LQT2 patients had 56% to 78% increased serum insulin, serum C-peptide, plasma GLP-1, and plasma GIP responses (P=0.03-0.001) and decreased plasma glucose levels after glucose ingestion (P=0.02) with more symptoms of hypoglycemia (P=0.04). Sixty-three percent of LQT2 patients developed hypoglycemic plasma glucose levels (<70 mg/dL) versus 36% control participants (P=0.16), and 18% patients developed serious hypoglycemia (<50 mg/dL) versus none of the controls. LQT2 patients had defective glucagon responses to low glucose, P=0.008. β-Cell function (Insulin Secretion Sensitivity Index-2) was 2-fold higher in LQT2 patients than in controls (4398 [95% confidence interval, 2259-8562] versus 2156 [1961-3201], P=0.03). Pharmacological Kv11.1 blockade (dofetilide) in rats had similar effect, and small interfering RNA inhibition of hERG in β and L cells increased insulin and GLP-1 secretion up to 50%. Glucose ingestion caused cardiac repolarization disturbances with increased QTc intervals in both patients and controls, but with a 122% greater increase in QTcF interval in LQT2 patients (P=0.004).Conclusions: Besides a prolonged cardiac repolarization phase, LQT2 patients display increased GLP-1, GIP, and insulin secretion and defective glucagon secretion, causing decreased plasma glucose and thus increased risk of hypoglycemia. Furthermore, glucose ingestion increased QT interval and aggravated the cardiac repolarization disturbances in LQT2 patients.Clinical Trial Registration: URL: http://clinicaltrials.gov. Unique identifier: NCT02775513. [ABSTRACT FROM AUTHOR]

Published
2017
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16. Patients With Long-QT Syndrome Caused by Impaired hERG-Encoded Kv11.1 Potassium Channel Have Exaggerated Endocrine Pancreatic and Incretin Function Associated With Reactive Hypoglycemia

Author

Hyltén-Cavallius, Louise, Iepsen, Eva W., Wewer Albrechtsen, Nicolai J., Svendstrup, Mathilde, Lubberding, Anniek F., Hartmann, Bolette, Jespersen, Thomas, Linneberg, Allan, Christiansen, Michael, Vestergaard, Henrik, Pedersen, Oluf, Holst, Jens J., Kanters, Jørgen K., Hansen, Torben, and Torekov, Signe S.

Abstract

Supplemental Digital Content is available in the text.

Published
2017
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17. A gut-intrinsic melanocortin signaling complex augments L-cell secretion in humans

Author

Philippa Rabbitt, Torben Hansen, Alyce M. Martin, Eva W. Iepsen, Nichole J. Isaacs, Nektaria Pezos, Richard L. Young, Gudrun Schober, Nam Q. Nguyen, Amanda L. Lumsden, Paul Hollington, Alice P. Liou, V. Margaret Jackson, Dayan de Fontgalland, Jens-Christian Holm, Christopher K. Rayner, Signe S. Torekov, David A. Wattchow, Damien J. Keating, Emily W. Sun, Sun, Emily W, Iepsen, Eva W, Pezos, Nektaria, Lumsden, Amanda L, Martin, Alyce M, Schober, Gudrun, Isaacs, Nicole J, Rayner, Christopher K, Nguyen, Nam Q, de Fontgalland, Dayan, Rabbitt, Philippa, Hollington, Paul, Wattchow, David A, Hansen, Torben, Holm, Jens-Christian, Liou, Alice P, Jackson, V Margaret, Torekov, Signe S, Young, Richard L, and Keating, Damien J

Subjects
Blood Glucose, medicine.medical_specialty, endocrine system, Pro-Opiomelanocortin, Time Factors, gut hormones, Enteroendocrine Cells, enteroendocrine, 030209 endocrinology & metabolism, Enteroendocrine cell, MC4R, 03 medical and health sciences, Paracrine signalling, 0302 clinical medicine, Glucagon-Like Peptide 1, Loss of Function Mutation, Internal medicine, Paracrine Communication, medicine, Humans, Secretion, Peptide YY, Intestinal Mucosa, Receptor, Autocrine signalling, 030304 developmental biology, 2. Zero hunger, 0303 health sciences, Secretory Pathway, Hepatology, PYY, Chemistry, digestive, oral, and skin physiology, Gastroenterology, Glucose Tolerance Test, Glucagon-like peptide-1, Melanocortin 4 receptor, Autocrine Communication, Endocrinology, Glucose, alpha-MSH, Case-Control Studies, Receptor, Melanocortin, Type 4, Melanocortin, GLP-1, hormones, hormone substitutes, and hormone antagonists, Signal Transduction
Abstract

Objective: Hypothalamic melanocortin 4 receptors (MC4R) are a key regulator of energy homeostasis. Brain-penetrant MC4R agonists have failed, as concentrations required to suppress food intake also increase blood pressure. However, peripherally located MC4R may also mediate metabolic benefits of MC4R activation. Mc4r transcript is enriched in mouse enteroendocrine L cells and peripheral administration of the endogenous MC4R agonist, α-melanocyte stimulating hormone (α-MSH), triggers the release of the anorectic hormones Glucagon-like peptide-1 (GLP-1) and peptide tyrosine tyrosine (PYY) in mice. This study aimed to determine whether pathways linking MC4R and L-cell secretion exist in humans. Design: GLP-1 and PYY levels were assessed in body mass index–matched individuals with or without loss-of-function MC4R mutations following an oral glucose tolerance test. Immunohistochemistry was performed on human intestinal sections to characterize the mucosal MC4R system. Static incubations with MC4R agonists were carried out on human intestinal epithelia, GLP-1 and PYY contents of secretion supernatants were assayed. Results: Fasting PYY levels and oral glucose-induced GLP-1 secretion were reduced in humans carrying a total loss-of-function MC4R mutation. MC4R was localized to L cells and regulates GLP-1 and PYY secretion from ex vivo human intestine. α-MSH immunoreactivity in the human intestinal epithelia was predominantly localized to L cells. Glucose-sensitive mucosal pro-opiomelanocortin cells provide a local source of α-MSH that is essential for glucose-induced GLP-1 secretion in small intestine. Conclusion: Our findings describe a previously unidentified signaling nexus in the human gastrointestinal tract involving α-MSH release and MC4R activation on L cells in an autocrine and paracrine fashion. Outcomes from this study have direct implications for targeting mucosal MC4R to treat human metabolic disorders. Refereed/Peer-reviewed

Published
2021

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