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Article ; Online: The GLP-1 journey: from discovery science to therapeutic impact.

Drucker, Daniel J

2024 Volume 134, Issue 2

MeSH term(s)	Humans ; Glucagon-Like Peptide 1 ; Diabetes Mellitus, Type 2/drug therapy ; Glucagon-Like Peptide-1 Receptor
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon-Like Peptide-1 Receptor
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI175634
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Article ; Online: Transforming type 1 diabetes: the next wave of innovation.

Drucker, Daniel J

Diabetologia

2021 Volume 64, Issue 5, Page(s) 1059–1065

Abstract: The discovery of insulin in 1921 enabled pharmaceutical production of animal insulins for the treatment of people with type 1 diabetes by 1922. The last several decades have witnessed enormous scientific progress in the therapy of type 1 diabetes, yet ... ...

Abstract	The discovery of insulin in 1921 enabled pharmaceutical production of animal insulins for the treatment of people with type 1 diabetes by 1922. The last several decades have witnessed enormous scientific progress in the therapy of type 1 diabetes, yet some developments have been incremental, and insulin is not a cure. Herein, I highlight key scientific advances potentially poised to improve the quality of life and treatment outcomes in type 1 diabetes. These innovations range from newer insulin analogues to the development of smart insulins, oral and weekly insulins, glucose sensors and closed-loop insulin-delivery devices, as well as strategies for durable human beta cell replacement coupled with selective immune manipulation to preserve beta cell function. Finally, progress in the prediction and prevention of type 1 diabetes highlights the ongoing challenges and potential for altering the natural history of the disease or eliminating type 1 diabetes altogether.
MeSH term(s)	Blood Glucose/analysis ; Blood Glucose/metabolism ; Blood Glucose Self-Monitoring/instrumentation ; Blood Glucose Self-Monitoring/trends ; Diabetes Mellitus, Type 1/blood ; Diabetes Mellitus, Type 1/epidemiology ; Diabetes Mellitus, Type 1/therapy ; Humans ; Insulin/administration & dosage ; Insulin Infusion Systems/trends ; Inventions/trends ; Pancreas, Artificial/trends ; Treatment Outcome
Chemical Substances	Blood Glucose ; Insulin
Language	English
Publishing date	2021-02-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-021-05396-5
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Article ; Online: Diabetes, obesity, metabolism, and SARS-CoV-2 infection: the end of the beginning.

Drucker, Daniel J

Cell metabolism

2021 Volume 33, Issue 3, Page(s) 479–498

Abstract: The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update ... ...

Abstract	The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population.
MeSH term(s)	Angiotensin-Converting Enzyme 2/metabolism ; Blood Glucose/analysis ; COVID-19/epidemiology ; COVID-19/pathology ; Cholesterol/metabolism ; Comorbidity ; Diabetes Mellitus/pathology ; Genetic Predisposition to Disease/genetics ; Glucose/metabolism ; Heart Disease Risk Factors ; Humans ; Hyperglycemia/pathology ; Metabolic Diseases/pathology ; Obesity/pathology ; SARS-CoV-2 ; COVID-19 Drug Treatment
Chemical Substances	Blood Glucose ; Cholesterol (97C5T2UQ7J) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2021.01.016
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Article ; Online: GLP-1 physiology informs the pharmacotherapy of obesity.

Drucker, Daniel J

Molecular metabolism

2021 Volume 57, Page(s) 101351

Abstract: Background: Glucagon-like peptide-1 receptor agonists (GLP1RA) augment glucose-dependent insulin release and reduce glucagon secretion and gastric emptying, enabling their successful development for the treatment of type 2 diabetes (T2D). These agents ... ...

Abstract	Background: Glucagon-like peptide-1 receptor agonists (GLP1RA) augment glucose-dependent insulin release and reduce glucagon secretion and gastric emptying, enabling their successful development for the treatment of type 2 diabetes (T2D). These agents also inhibit food intake and reduce body weight, fostering investigation of GLP1RA for the treatment of obesity. Scope of review: Here I discuss the physiology of Glucagon-like peptide-1 (GLP-1) action in the control of food intake in animals and humans, highlighting the importance of gut vs. brain-derived GLP-1 for the control of feeding and body weight. The widespread distribution and function of multiple GLP-1 receptor (GLP1R) populations in the central and autonomic nervous system are outlined, and the importance of pathways controlling energy expenditure in preclinical studies vs. reduction of food intake in both animals and humans is highlighted. The relative contributions of vagal afferent pathways vs. GLP1R+ populations in the central nervous system for the physiological reduction of food intake and the anorectic response to GLP1RA are compared and reviewed. Key data enabling the development of two GLP1RA for obesity therapy (liraglutide 3 mg daily and semaglutide 2.4 mg once weekly) are discussed. Finally, emerging data potentially supporting the combination of GLP-1 with additional peptide epitopes in unimolecular multi-agonists, as well as in fixed-dose combination therapies, are highlighted. Major conclusions: The actions of GLP-1 to reduce food intake and body weight are highly conserved in obese animals and humans, in both adolescents and adults. The well-defined mechanisms of GLP-1 action through a single G protein-coupled receptor, together with the extensive safety database of GLP1RA in people with T2D, provide reassurance surrounding the long-term use of these agents in people with obesity and multiple co-morbidities. GLP1RA may also be effective in conditions associated with obesity, such as cardiovascular disease and non-alcoholic steatohepatitis (NASH). Progressive improvements in the efficacy of GLP1RA suggest that GLP-1-based therapies may soon rival bariatric surgery as viable options for the treatment of obesity and its complications.
MeSH term(s)	Adolescent ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/metabolism ; Humans ; Liraglutide/therapeutic use ; Obesity/drug therapy ; Obesity/metabolism
Chemical Substances	Glucagon-Like Peptide-1 Receptor ; Liraglutide (839I73S42A) ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2021-10-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2021.101351
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Article ; Online: The expanding incretin universe: from basic biology to clinical translation.

Drucker, Daniel J / Holst, Jens J

Diabetologia

2023 Volume 66, Issue 10, Page(s) 1765–1779

Abstract: Incretin hormones, principally glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1(GLP-1), potentiate meal-stimulated insulin secretion through direct (GIP + GLP-1) and indirect (GLP-1) actions on islet β-cells. GIP and GLP-1 ... ...

Abstract	Incretin hormones, principally glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1(GLP-1), potentiate meal-stimulated insulin secretion through direct (GIP + GLP-1) and indirect (GLP-1) actions on islet β-cells. GIP and GLP-1 also regulate glucagon secretion, through direct and indirect pathways. The incretin hormone receptors (GIPR and GLP-1R) are widely distributed beyond the pancreas, principally in the brain, cardiovascular and immune systems, gut and kidney, consistent with a broad array of extrapancreatic incretin actions. Notably, the glucoregulatory and anorectic activities of GIP and GLP-1 have supported development of incretin-based therapies for the treatment of type 2 diabetes and obesity. Here we review evolving concepts of incretin action, focusing predominantly on GLP-1, from discovery, to clinical proof of concept, to therapeutic outcomes. We identify established vs uncertain mechanisms of action, highlighting biology conserved across species, while illuminating areas of active investigation and uncertainty that require additional clarification.
MeSH term(s)	Humans ; Incretins/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Glucagon-Like Peptide 1/metabolism ; Gastric Inhibitory Polypeptide/metabolism ; Biology
Chemical Substances	Incretins ; Glucagon-Like Peptide 1 (89750-14-1) ; Gastric Inhibitory Polypeptide (59392-49-3)
Language	English
Publishing date	2023-03-28
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-023-05906-7
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Article ; Online: Parathyroid hormone-like peptide.

Drucker, Daniel J

Endocrine pathology

2020 Volume 2, Issue 1, Page(s) 4–11

Language	English
Publishing date	2020-03-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1033267-4
ISSN	1559-0097 ; 1046-3976
ISSN (online)	1559-0097
ISSN	1046-3976
DOI	10.1007/BF02915320
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Zs.A 2956: Show issues

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Article ; Online: Glucagon-like peptide 1 receptor agonists: cardiovascular benefits and mechanisms of action.

Ussher, John R / Drucker, Daniel J

Nature reviews. Cardiology

2023 Volume 20, Issue 7, Page(s) 463–474

Abstract: Type 2 diabetes mellitus (T2DM) and obesity are metabolic disorders characterized by excess cardiovascular risk. Glucagon-like peptide 1 (GLP1) receptor (GLP1R) agonists reduce body weight, glycaemia, blood pressure, postprandial lipaemia and ... ...

Abstract	Type 2 diabetes mellitus (T2DM) and obesity are metabolic disorders characterized by excess cardiovascular risk. Glucagon-like peptide 1 (GLP1) receptor (GLP1R) agonists reduce body weight, glycaemia, blood pressure, postprandial lipaemia and inflammation - actions that could contribute to the reduction of cardiovascular events. Cardiovascular outcome trials (CVOTs) have demonstrated that GLP1R agonists reduce the rates of major adverse cardiovascular events in patients with T2DM. Separate phase III CVOTs of GLP1R agonists are currently being conducted in people living with heart failure with preserved ejection fraction and in those with obesity. Mechanistically, GLP1R is expressed at low levels in the heart and vasculature, raising the possibility that GLP1 might have both direct and indirect actions on the cardiovascular system. In this Review, we summarize the data from CVOTs of GLP1R agonists in patients with T2DM and describe the actions of GLP1R agonists on the heart and blood vessels. We also assess the potential mechanisms that contribute to the reduction in major adverse cardiovascular events in individuals treated with GLP1R agonists and highlight the emerging cardiovascular biology of novel GLP1-based multi-agonists currently in development. Understanding how GLP1R signalling protects the heart and blood vessels will optimize the therapeutic use and development of next-generation GLP1-based therapies with improved cardiovascular safety.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Hypoglycemic Agents/adverse effects ; Glucagon-Like Peptide 1 ; Glucagon-Like Peptide-1 Receptor/agonists ; Obesity ; Cardiovascular System/metabolism ; Cardiovascular Diseases/prevention & control ; Cardiovascular Diseases/drug therapy
Chemical Substances	Hypoglycemic Agents ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon-Like Peptide-1 Receptor
Language	English
Publishing date	2023-03-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490375-9
ISSN	1759-5010 ; 1759-5002
ISSN (online)	1759-5010
ISSN	1759-5002
DOI	10.1038/s41569-023-00849-3
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Article ; Online: Coronavirus Infections and Type 2 Diabetes-Shared Pathways with Therapeutic Implications.

Drucker, Daniel J

Endocrine reviews

2020 Volume 41, Issue 3

Abstract: Individuals with diabetes are at increased risk for bacterial, mycotic, parasitic, and viral infections. The severe acute respiratory syndrome (SARS)-CoV-2 (also referred to as COVID-19) coronavirus pandemic highlights the importance of understanding ... ...

Abstract	Individuals with diabetes are at increased risk for bacterial, mycotic, parasitic, and viral infections. The severe acute respiratory syndrome (SARS)-CoV-2 (also referred to as COVID-19) coronavirus pandemic highlights the importance of understanding shared disease pathophysiology potentially informing therapeutic choices in individuals with type 2 diabetes (T2D). Two coronavirus receptor proteins, angiotensin-converting enzyme 2 (ACE2) and dipeptidyl peptidase-4 (DPP4) are also established transducers of metabolic signals and pathways regulating inflammation, renal and cardiovascular physiology, and glucose homeostasis. Moreover, glucose-lowering agents such as the DPP4 inhibitors, widely used in subjects with T2D, are known to modify the biological activities of multiple immunomodulatory substrates. Here, we review the basic and clinical science spanning the intersections of diabetes, coronavirus infections, ACE2, and DPP4 biology, highlighting clinical relevance and evolving areas of uncertainty underlying the pathophysiology and treatment of T2D in the context of coronavirus infection.
MeSH term(s)	Angiotensin-Converting Enzyme 2 ; Animals ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications ; Coronavirus Infections/metabolism ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Dipeptidyl Peptidase 4/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Dipeptidyl-Peptidase IV Inhibitors/therapeutic use ; Gastrointestinal Tract/metabolism ; Humans ; Insulin/therapeutic use ; Lung/metabolism ; Obesity/complications ; Obesity/metabolism ; Pandemics ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/complications ; Pneumonia, Viral/metabolism ; Receptors, Coronavirus ; Receptors, Virus/metabolism ; Risk Factors ; SARS-CoV-2 ; Serine Endopeptidases/metabolism
Chemical Substances	Dipeptidyl-Peptidase IV Inhibitors ; Insulin ; Receptors, Coronavirus ; Receptors, Virus ; DPP4 protein, human (EC 3.4.14.5) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Serine Endopeptidases (EC 3.4.21.-) ; TMPRSS2 protein, human (EC 3.4.21.-)
Keywords	covid19
Language	English
Publishing date	2020-04-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/endrev/bnaa011
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Article ; Online: GLP-1 physiology informs the pharmacotherapy of obesity

Daniel J. Drucker

Molecular Metabolism, Vol 57, Iss , Pp 101351- (2022)

2022

Abstract	Background: Glucagon-like peptide-1 receptor agonists (GLP1RA) augment glucose-dependent insulin release and reduce glucagon secretion and gastric emptying, enabling their successful development for the treatment of type 2 diabetes (T2D). These agents also inhibit food intake and reduce body weight, fostering investigation of GLP1RA for the treatment of obesity. Scope of review: Here I discuss the physiology of Glucagon-like peptide-1 (GLP-1) action in the control of food intake in animals and humans, highlighting the importance of gut vs. brain-derived GLP-1 for the control of feeding and body weight. The widespread distribution and function of multiple GLP-1 receptor (GLP1R) populations in the central and autonomic nervous system are outlined, and the importance of pathways controlling energy expenditure in preclinical studies vs. reduction of food intake in both animals and humans is highlighted. The relative contributions of vagal afferent pathways vs. GLP1R+ populations in the central nervous system for the physiological reduction of food intake and the anorectic response to GLP1RA are compared and reviewed. Key data enabling the development of two GLP1RA for obesity therapy (liraglutide 3 mg daily and semaglutide 2.4 mg once weekly) are discussed. Finally, emerging data potentially supporting the combination of GLP-1 with additional peptide epitopes in unimolecular multi-agonists, as well as in fixed-dose combination therapies, are highlighted. Major conclusions: The actions of GLP-1 to reduce food intake and body weight are highly conserved in obese animals and humans, in both adolescents and adults. The well-defined mechanisms of GLP-1 action through a single G protein-coupled receptor, together with the extensive safety database of GLP1RA in people with T2D, provide reassurance surrounding the long-term use of these agents in people with obesity and multiple co-morbidities. GLP1RA may also be effective in conditions associated with obesity, such as cardiovascular disease and non-alcoholic steatohepatitis (NASH). Progressive improvements in the efficacy of GLP1RA suggest that GLP-1-based therapies may soon rival bariatric surgery as viable options for the treatment of obesity and its complications.
Keywords	Weight loss ; Hunger ; Diabetes ; Obesity ; Brain ; G protein-coupled receptor ; Internal medicine ; RC31-1245
Subject code	630
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Beyond the pancreas: contrasting cardiometabolic actions of GIP and GLP1.

Hammoud, Rola / Drucker, Daniel J

Nature reviews. Endocrinology

2022 Volume 19, Issue 4, Page(s) 201–216

Abstract: Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP1) exhibit incretin activity, meaning that they potentiate glucose-dependent insulin secretion. The emergence of GIP receptor (GIPR)-GLP1 receptor (GLP1R) co-agonists has ... ...

Abstract	Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP1) exhibit incretin activity, meaning that they potentiate glucose-dependent insulin secretion. The emergence of GIP receptor (GIPR)-GLP1 receptor (GLP1R) co-agonists has fostered growing interest in the actions of GIP and GLP1 in metabolically relevant tissues. Here, we update concepts of how these hormones act beyond the pancreas. The actions of GIP and GLP1 on liver, muscle and adipose tissue, in the control of glucose and lipid homeostasis, are discussed in the context of plausible mechanisms of action. Both the GIPR and GLP1R are expressed in the central nervous system, wherein receptor activation produces anorectic effects enabling weight loss. In preclinical studies, GIP and GLP1 reduce atherosclerosis. Furthermore, GIPR and GLP1R are expressed within the heart and immune system, and GLP1R within the kidney, revealing putative mechanisms linking GIP and GLP1R agonism to cardiorenal protection. We interpret the clinical and mechanistic data obtained for different agents that enable weight loss and glucose control for the treatment of obesity and type 2 diabetes mellitus, respectively, by activating or blocking GIPR signalling, including the GIPR-GLP1R co-agonist tirzepatide, as well as the GIPR antagonist-GLP1R agonist AMG-133. Collectively, we update translational concepts of GIP and GLP1 action, while highlighting gaps, areas of uncertainty and controversies meriting ongoing investigation.
MeSH term(s)	Humans ; Glucagon-Like Peptide 1/therapeutic use ; Diabetes Mellitus, Type 2/drug therapy ; Gastric Inhibitory Polypeptide/pharmacology ; Gastric Inhibitory Polypeptide/physiology ; Gastric Inhibitory Polypeptide/therapeutic use ; Pancreas ; Glucose ; Receptors, G-Protein-Coupled ; Weight Loss ; Cardiovascular Diseases
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1) ; gastric inhibitory polypeptide receptor (D6H00MV7K8) ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucose (IY9XDZ35W2) ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2022-12-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-022-00783-3
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