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Article: Vignette diagnostique de l’étudiant. Ne pas négliger le syndrome métabolique.

Scheen, André / Luyckx, Françoise / Esser, Nathalie / Paquot, Nicolas

2024 Volume 79, Issue 3, Page(s) 191–194

Abstract: The concept of «metabolic syndrome» was brought to the forefront in the early 2000s in international literature, but this interest seems to have faded somewhat in recent years. However, this constellation of cardiovascular risk factors should not be ... ...

Title translation	Don't neglect metabolic syndrome.
Abstract	The concept of «metabolic syndrome» was brought to the forefront in the early 2000s in international literature, but this interest seems to have faded somewhat in recent years. However, this constellation of cardiovascular risk factors should not be neglected. Taken individually, they hardly seem problematic, but when they are present within the same individual, they significantly increase the risk of cardiovascular morbidity and mortality. This clinical vignette aims to draw attention to the usefulness of the search for metabolic syndrome in clinical practic.
MeSH term(s)	Humans ; Metabolic Syndrome/complications ; Metabolic Syndrome/diagnosis ; Metabolic Syndrome/metabolism ; Risk Factors ; Cardiovascular Diseases/etiology ; Diabetes Mellitus, Type 2/complications
Language	French
Publishing date	2024-03-15
Publishing country	Belgium
Document type	English Abstract ; Practice Guideline
ZDB-ID	414001-1
ISSN	0370-629X ; 0035-3663
ISSN	0370-629X ; 0035-3663
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Zs.A 597: Show issues

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Article: Actualisation des recommandations nutritionnelles dans le traitement du diabète de type 2.

Esser, Nathalie / Paquot, Nicolas

Revue medicale suisse

2022 Volume 19, Issue 838, Page(s) 1486–1490

Abstract: Dietary management of type 2 diabetes is essential to improve glycaemic control et reduce risk of diabetes complications. Key recommendations for people with diabetes are largely similar to those for the general population. Overweight or obese diabetic ... ...

Title translation	Update of nutritional recommendations in the treatment of type 2 diabetes.
Abstract	Dietary management of type 2 diabetes is essential to improve glycaemic control et reduce risk of diabetes complications. Key recommendations for people with diabetes are largely similar to those for the general population. Overweight or obese diabetic persons should be supported with evidence-based treatments to achieve and maintain weight loss. A wide range of carbohydrate intakes are acceptable and diets with a low glycaemic index or low glycaemic load may be recommended, provided their composition is consistent with overall diet recommendations for dietary fibers, sugars, saturated fats and proteins. It is also important to consume minimally processed plant foods, such as whole grains, vegetables, whole fruits, legumes, while reducing the consumption of red and processed meats, sodium and sugar-sweetened beverages.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/therapy ; Vegetables ; Food, Processed ; Fruit ; Meat
Language	French
Publishing date	2022-10-18
Publishing country	Switzerland
Document type	English Abstract ; Journal Article
ZDB-ID	2177010-4
ISSN	1660-9379
ISSN	1660-9379
DOI	10.53738/REVMED.2023.19.838.1486
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Zs.A 5998: Show issues

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Article: Neprilysin Inhibitors and Angiotensin(1-7) in COVID-19.

Esser, Nathalie / Zraika, Sakeneh

The British journal of cardiology

2020 Volume 27, Issue 4, Page(s) 109–111

Language	English
Publishing date	2020-10-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1354589-9
ISSN	0969-6113
ISSN	0969-6113
DOI	10.5837/bjc.2020.031
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Zs.A 4578: Show issues

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Article: Intérêt de la combinaison sacubitril/valsartan dans le diabète de type 2.

Esser, Nathalie / Paquot, Nicolas

Revue medicale suisse

2021 Volume 17, Issue 747, Page(s) 1418–1422

Abstract: Sacubitril/valsartan, a first-in-class angiotensin receptor-neprilysin inhibitor (ARNI), is indicated for the treatment of heart failure with reduced ejection fraction. It has demonstrated benefits in terms of cardiovascular morbidity and mortality ... ...

Title translation	Potential role of sacubitril/valsartan combination in type 2 diabetes.
Abstract	Sacubitril/valsartan, a first-in-class angiotensin receptor-neprilysin inhibitor (ARNI), is indicated for the treatment of heart failure with reduced ejection fraction. It has demonstrated benefits in terms of cardiovascular morbidity and mortality reduction in this population. Recently, this drug association has also been shown to improve glycemic control and insulin sensitivity in patients with obesity and/or type 2 diabetes. Furthermore, some studies suggest a protective role of this new drug class in diabetic nephropathy. Altogether, these data raise the question about the potential place of ARNI in prevention and treatment of type 2 diabetes, a condition closely associated with heart failure.
MeSH term(s)	Aminobutyrates ; Angiotensin Receptor Antagonists/therapeutic use ; Biphenyl Compounds ; Diabetes Mellitus, Type 2/drug therapy ; Drug Combinations ; Humans ; Neprilysin ; Valsartan
Chemical Substances	Aminobutyrates ; Angiotensin Receptor Antagonists ; Biphenyl Compounds ; Drug Combinations ; Valsartan (80M03YXJ7I) ; Neprilysin (EC 3.4.24.11) ; sacubitril and valsartan sodium hydrate drug combination (WB8FT61183)
Language	French
Publishing date	2021-08-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2177010-4
ISSN	1660-9379
ISSN	1660-9379
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Article ; Online: Acute Inhibition of Intestinal Neprilysin Enhances Insulin Secretion via GLP-1 Receptor Signaling in Male Mice.

Esser, Nathalie / Mundinger, Thomas O / Barrow, Breanne M / Zraika, Sakeneh

Endocrinology

2023 Volume 164, Issue 5

Abstract: The peptidase neprilysin modulates glucose homeostasis by cleaving and inactivating insulinotropic peptides, including some produced in the intestine such as glucagon-like peptide-1 (GLP-1). Under diabetic conditions, systemic or islet-selective ... ...

Abstract	The peptidase neprilysin modulates glucose homeostasis by cleaving and inactivating insulinotropic peptides, including some produced in the intestine such as glucagon-like peptide-1 (GLP-1). Under diabetic conditions, systemic or islet-selective inhibition of neprilysin enhances beta-cell function through GLP-1 receptor (GLP-1R) signaling. While neprilysin is expressed in intestine, its local contribution to modulation of beta-cell function remains unknown. We sought to determine whether acute selective pharmacological inhibition of intestinal neprilysin enhanced glucose-stimulated insulin secretion under physiological conditions, and whether this effect was mediated through GLP-1R. Lean chow-fed Glp1r+/+ and Glp1r-/- mice received a single oral low dose of the neprilysin inhibitor thiorphan or vehicle. To confirm selective intestinal neprilysin inhibition, neprilysin activity in plasma and intestine (ileum and colon) was assessed 40 minutes after thiorphan or vehicle administration. In a separate cohort of mice, an oral glucose tolerance test was performed 30 minutes after thiorphan or vehicle administration to assess glucose-stimulated insulin secretion. Systemic active GLP-1 levels were measured in plasma collected 10 minutes after glucose administration. In both Glp1r+/+ and Glp1r-/- mice, thiorphan inhibited neprilysin activity in ileum and colon without altering plasma neprilysin activity or active GLP-1 levels. Further, thiorphan significantly increased insulin secretion in Glp1r+/+ mice, whereas it did not change insulin secretion in Glp1r-/- mice. In conclusion, under physiological conditions, acute pharmacological inhibition of intestinal neprilysin increases glucose-stimulated insulin secretion in a GLP-1R-dependent manner. Since intestinal neprilysin modulates beta-cell function, strategies to inhibit its activity specifically in the intestine may improve beta-cell dysfunction in type 2 diabetes.
MeSH term(s)	Animals ; Male ; Mice ; Diabetes Mellitus, Type 2 ; Glucagon-Like Peptide 1 ; Glucagon-Like Peptide-1 Receptor/metabolism ; Glucose ; Insulin/metabolism ; Insulin Secretion ; Intestines ; Mice, Inbred C57BL ; Neprilysin/genetics ; Neprilysin/metabolism ; Thiorphan/pharmacology
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon-Like Peptide-1 Receptor ; Glucose (IY9XDZ35W2) ; Insulin ; Neprilysin (EC 3.4.24.11) ; Thiorphan (B79L7B5X3Z)
Language	English
Publishing date	2023-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqad055
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Article ; Online: On the causal relationships between hyperinsulinaemia, insulin resistance, obesity and dysglycaemia in type 2 diabetes: Reply to Johnson JD [letter].

Esser, Nathalie / Utzschneider, Kristina M / Kahn, Steven E

Diabetologia

2021 Volume 64, Issue 10, Page(s) 2345–2347

MeSH term(s)	Diabetes Mellitus, Type 2/complications ; Humans ; Hyperinsulinism ; Insulin Resistance ; Obesity/complications
Language	English
Publishing date	2021-07-29
Publishing country	Germany
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-021-05511-6
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Zs.A 279: Show issues

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Article ; Online: Neprilysin deficiency reduces hepatic gluconeogenesis in high fat-fed mice.

Esser, Nathalie / Mongovin, Stephen M / Mundinger, Thomas O / Barrow, Breanne M / Zraika, Sakeneh

Peptides

2023 Volume 168, Page(s) 171076

Abstract: Neprilysin is a peptidase that cleaves glucoregulatory peptides, including glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK). Some studies suggest that its inhibition in diabetes and/or obesity improves glycemia, and that this is associated with ... ...

Abstract	Neprilysin is a peptidase that cleaves glucoregulatory peptides, including glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK). Some studies suggest that its inhibition in diabetes and/or obesity improves glycemia, and that this is associated with enhanced insulin secretion, glucose tolerance and insulin sensitivity. Whether reduced neprilysin activity also improves hepatic glucose metabolism has not been explored. We sought to determine whether genetic deletion of neprilysin suppresses hepatic glucose production (HGP) in high fat-fed mice. Nep
MeSH term(s)	Mice ; Animals ; Gluconeogenesis/genetics ; Neprilysin ; Diabetes Mellitus, Type 2/metabolism ; Liver Glycogen/metabolism ; Glucose/metabolism ; Liver/metabolism ; Glucagon-Like Peptide 1/metabolism ; Obesity/metabolism ; Insulin/metabolism ; Blood Glucose/metabolism
Chemical Substances	Neprilysin (EC 3.4.24.11) ; Liver Glycogen ; Glucose (IY9XDZ35W2) ; Glucagon-Like Peptide 1 (89750-14-1) ; Insulin ; Blood Glucose
Language	English
Publishing date	2023-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2023.171076
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Zs.A 1649: Show issues

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Article ; Online: Neprilysin inhibition: a new therapeutic option for type 2 diabetes?

Esser, Nathalie / Zraika, Sakeneh

Diabetologia

2019 Volume 62, Issue 7, Page(s) 1113–1122

Abstract: Neprilysin is a widely expressed peptidase with broad substrate specificity that preferentially hydrolyses oligopeptide substrates, many of which regulate the cardiovascular, nervous and immune systems. Emerging evidence suggests that neprilysin also ... ...

Abstract	Neprilysin is a widely expressed peptidase with broad substrate specificity that preferentially hydrolyses oligopeptide substrates, many of which regulate the cardiovascular, nervous and immune systems. Emerging evidence suggests that neprilysin also hydrolyses peptides that play an important role in glucose metabolism. In recent studies in humans, a dual angiotensin receptor-neprilysin inhibitor (ARNi) improved glycaemic control and insulin sensitivity in individuals with type 2 diabetes and/or obesity. Moreover, preclinical studies have also reported that neprilysin inhibition, alone or in combination with renin-angiotensin system blockers, elicits beneficial effects on glucose homeostasis. Since neprilysin inhibitors have been approved for the treatment of heart failure, their repurposing for treating type 2 diabetes would provide a novel therapeutic strategy. In this review, we evaluate existing evidence from preclinical and clinical studies in which neprilysin is deleted/inhibited, we highlight potential mechanisms underlying the beneficial glycaemic effects of neprilysin inhibition, and discuss possible deleterious effects that may limit the efficacy and safety of neprilysin inhibitors in the clinic. We also review the favourable impact neprilysin inhibition can have on diabetic complications, in addition to glucose control. Finally, we conclude that neprilysin inhibitors may be a useful therapeutic option for treating type 2 diabetes; however, their combination with angiotensin II receptor blockers is needed to circumvent deleterious consequences of neprilysin inhibition alone.
MeSH term(s)	Angiotensin Receptor Antagonists/therapeutic use ; Animals ; Antihypertensive Agents/therapeutic use ; Antineoplastic Agents/therapeutic use ; Blood Glucose/drug effects ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/therapeutic use ; Humans ; Neprilysin/antagonists & inhibitors ; Neprilysin/metabolism ; Renin-Angiotensin System/drug effects
Chemical Substances	Angiotensin Receptor Antagonists ; Antihypertensive Agents ; Antineoplastic Agents ; Blood Glucose ; Dipeptidyl-Peptidase IV Inhibitors ; Neprilysin (EC 3.4.24.11)
Language	English
Publishing date	2019-05-14
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-019-4889-y
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Article ; Online: Early beta cell dysfunction vs insulin hypersecretion as the primary event in the pathogenesis of dysglycaemia.

Esser, Nathalie / Utzschneider, Kristina M / Kahn, Steven E

Diabetologia

2020 Volume 63, Issue 10, Page(s) 2007–2021

Abstract: Obesity and insulin resistance are associated with the development of type 2 diabetes. It is well accepted that beta cell dysfunction is required for hyperglycaemia to occur. The prevailing view is that, in the presence of insulin resistance, beta cell ... ...

Abstract	Obesity and insulin resistance are associated with the development of type 2 diabetes. It is well accepted that beta cell dysfunction is required for hyperglycaemia to occur. The prevailing view is that, in the presence of insulin resistance, beta cell dysfunction that occurs early in the course of the disease process is the critical abnormality. An alternative model has been proposed in which primary beta cell overstimulation results in insulin hypersecretion that then leads to the development of obesity and insulin resistance, and ultimately to beta cell exhaustion. In this review, data from preclinical and clinical studies, including intervention studies, are discussed in the context of these models. The preponderance of the data supports the view that an early beta cell functional defect is the more likely mechanism underlying the pathogenesis of hyperglycaemia in the majority of individuals who develop type 2 diabetes. Graphical abstract.
MeSH term(s)	Diabetes Mellitus, Type 2/metabolism ; Humans ; Hyperglycemia/metabolism ; Hyperinsulinism/metabolism ; Insulin Resistance ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Obesity/metabolism
Language	English
Publishing date	2020-09-07
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-020-05245-x
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Article ; Online: RIPK3 promotes islet amyloid-induced β-cell loss and glucose intolerance in a humanized mouse model of type 2 diabetes.

Mukherjee, Noyonika / Contreras, Christopher J / Lin, Li / Colglazier, Kaitlyn A / Mather, Egan G / Kalwat, Michael A / Esser, Nathalie / Kahn, Steven E / Templin, Andrew T

Molecular metabolism

2024 Volume 80, Page(s) 101877

Abstract: Objective: Aggregation of human islet amyloid polypeptide (hIAPP), a β-cell secretory product, leads to islet amyloid deposition, islet inflammation and β-cell loss in type 2 diabetes (T2D), but the mechanisms that underlie this process are incompletely ...

Abstract	Objective: Aggregation of human islet amyloid polypeptide (hIAPP), a β-cell secretory product, leads to islet amyloid deposition, islet inflammation and β-cell loss in type 2 diabetes (T2D), but the mechanisms that underlie this process are incompletely understood. Receptor interacting protein kinase 3 (RIPK3) is a pro-death signaling molecule that has recently been implicated in amyloid-associated brain pathology and β-cell cytotoxicity. Here, we evaluated the role of RIPK3 in amyloid-induced β-cell loss using a humanized mouse model of T2D that expresses hIAPP and is prone to islet amyloid formation. Methods: We quantified amyloid deposition, cell death and caspase 3/7 activity in islets isolated from WT, Ripk3 Results: We found that amyloid-prone hIAPP mouse islets exhibited increased cell death and caspase 3/7 activity compared to amyloid-free WT islets in vitro, and this was associated with increased RIPK3 expression. hIAPP; Ripk3 Conclusions: In conclusion, loss of RIPK3 protects from amyloid-induced inflammation and islet cell death in vitro and amyloid-induced β-cell loss and glucose intolerance in vivo. We propose that therapies targeting RIPK3 may reduce islet inflammation and β-cell loss and improve glucose homeostasis in the pathogenesis of T2D.
MeSH term(s)	Animals ; Humans ; Mice ; Amyloid/metabolism ; Amyloid beta-Peptides/metabolism ; Caspase 3/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Glucose ; Glucose Intolerance ; Inflammation ; Islet Amyloid Polypeptide/genetics ; Islet Amyloid Polypeptide/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics
Chemical Substances	Amyloid ; Amyloid beta-Peptides ; Caspase 3 (EC 3.4.22.-) ; Glucose (IY9XDZ35W2) ; Islet Amyloid Polypeptide ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2024-01-11
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2024.101877
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