Functional genetics reveals the contribution of delta opioid receptor to type 2 diabetes and beta-cell function

Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 an...

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Published inNature communications Vol. 15; no. 1; pp. 6627 - 12
Main Authors Meulebrouck, Sarah, Merrheim, Judith, Queniat, Gurvan, Bourouh, Cyril, Derhourhi, Mehdi, Boissel, Mathilde, Yi, Xiaoyan, Badreddine, Alaa, Boutry, Raphaël, Leloire, Audrey, Toussaint, Bénédicte, Amanzougarene, Souhila, Vaillant, Emmanuel, Durand, Emmanuelle, Loiselle, Hélène, Huyvaert, Marlène, Dechaume, Aurélie, Scherrer, Victoria, Marchetti, Piero, Balkau, Beverley, Charpentier, Guillaume, Franc, Sylvia, Marre, Michel, Roussel, Ronan, Scharfmann, Raphaël, Cnop, Miriam, Canouil, Mickaël, Baron, Morgane, Froguel, Philippe, Bonnefond, Amélie
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 05.08.2024
Nature Publishing Group
Nature Portfolio
Subjects
14/1
49/23
49/47
49/91
631/208/191
692/163/2743
692/308/2056
96/44
96/95
Addicts
Adipose tissue
Adult
Beta cells
Biochemistry, Molecular Biology
Circadian rhythms
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Drug abuse
Endocrinology and metabolism
Female
Gene expression
Gene sequencing
Genetics
Genomics
Growth factors
Health risks
Homeostasis
Human genetics
Human health and pathology
Humanities and Social Sciences
Humans
Hyperglycemia
Insulin - metabolism
Insulin secretion
Insulin Secretion - drug effects
Insulin Secretion - genetics
Insulin-Secreting Cells - metabolism
Life Sciences
Male
Metabolic disorders
Metabolism
Middle Aged
multidisciplinary
Narcotics
Nerve growth factor
Opioid receptors (type delta)
Oprd1 gene
Receptors
Receptors, Opioid, delta - genetics
Receptors, Opioid, delta - metabolism
Risk analysis
Science
Science (multidisciplinary)
Therapeutic targets
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-024-51004-6

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Abstract Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes. Opioid use impacts metabolic homeostasis, although the mechanisms remain elusive. Here, the authors explore the OPRD1 gene (encoding the delta opioid receptor, DOP) to understand its impact on type 2 diabetes and highlight DOP as a key player between opioids and metabolic homeostasis.
AbstractList Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes.Opioid use impacts metabolic homeostasis, although the mechanisms remain elusive. Here, the authors explore the OPRD1 gene (encoding the delta opioid receptor, DOP) to understand its impact on type 2 diabetes and highlight DOP as a key player between opioids and metabolic homeostasis.
Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes. Opioid use impacts metabolic homeostasis, although the mechanisms remain elusive. Here, the authors explore the OPRD1 gene (encoding the delta opioid receptor, DOP) to understand its impact on type 2 diabetes and highlight DOP as a key player between opioids and metabolic homeostasis.
Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes.
Abstract Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes.
Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes.Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we explore the OPRD1 gene (encoding delta opioid receptor, DOP) to understand its impact on type 2 diabetes. Large-scale sequencing of OPRD1 and in vitro analysis reveal that loss-of-function variants are associated with higher adiposity and lower hyperglycemia risk, whereas gain-of-function variants are associated with lower adiposity and higher type 2 diabetes risk. These findings align with studies of opium addicts. OPRD1 is expressed in human islets and beta cells, with decreased expression under type 2 diabetes conditions. DOP inhibition by an antagonist enhances insulin secretion from human beta cells and islets. RNA-sequencing identifies pathways regulated by DOP antagonism, including nerve growth factor, circadian clock, and nuclear receptor pathways. Our study highlights DOP as a key player between opioids and metabolic homeostasis, suggesting its potential as a therapeutic target for type 2 diabetes.
ArticleNumber 6627
Author Meulebrouck, Sarah
Loiselle, Hélène
Yi, Xiaoyan
Vaillant, Emmanuel
Boutry, Raphaël
Charpentier, Guillaume
Baron, Morgane
Bonnefond, Amélie
Marchetti, Piero
Franc, Sylvia
Dechaume, Aurélie
Badreddine, Alaa
Cnop, Miriam
Amanzougarene, Souhila
Balkau, Beverley
Roussel, Ronan
Merrheim, Judith
Bourouh, Cyril
Huyvaert, Marlène
Scharfmann, Raphaël
Scherrer, Victoria
Canouil, Mickaël
Leloire, Audrey
Marre, Michel
Durand, Emmanuelle
Derhourhi, Mehdi
Boissel, Mathilde
Toussaint, Bénédicte
Froguel, Philippe
Queniat, Gurvan
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GrantInformation_xml – fundername: This study was funded by the French National Research Agency (ANR-10-LABX-46 [European Genomics Institute for Diabetes] to PF and AB), the French National Research Agency (ANR-10-EQPX-07-01 [LIGAN-PM] to PF and AB), the European Research Council (ERC Reg-Seq – 715575 and ERC OpiO – 101043671, to AB), the EFSD New Targets for Diabetes or Obesity-related Metabolic Diseases Programme supported by an educational research grant from MSD (to AB) and the National Center for Precision Diabetic Medicine – PreciDIAB, which is jointly supported by the French National Agency for Research (ANR-18-IBHU-0001), by the European Union (FEDER), by the Hauts-de-France Regional Council and by the European Metropolis of Lille (MEL). The study was also supported by "France Génomique" consortium (ANR-10-INBS-009). XY was supported by the Fondation ULB and the China Scholarship Council. MCnop acknowledges support by the Walloon Region SPW-EER (Win2Wal project BetaSource), the Fonds National de la Recherche Scientifique (FRS-FNRS) and the Francophone Foundation for Diabetes Research (FFRD, that is sponsored by the French Diabetes Federation, Abbott, Eli Lilly, Merck Sharp & Dohme and Novo Nordisk).
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Snippet Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive. Here, we...
Abstract Functional genetics has identified drug targets for metabolic disorders. Opioid use impacts metabolic homeostasis, although mechanisms remain elusive....
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SubjectTerms 14/1
49/23
49/47
49/91
631/208/191
692/163/2743
692/308/2056
96/44
96/95
Addicts
Adipose tissue
Adult
Beta cells
Biochemistry, Molecular Biology
Circadian rhythms
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Drug abuse
Endocrinology and metabolism
Female
Gene expression
Gene sequencing
Genetics
Genomics
Growth factors
Health risks
Homeostasis
Human genetics
Human health and pathology
Humanities and Social Sciences
Humans
Hyperglycemia
Insulin - metabolism
Insulin secretion
Insulin Secretion - drug effects
Insulin Secretion - genetics
Insulin-Secreting Cells - metabolism
Life Sciences
Male
Metabolic disorders
Metabolism
Middle Aged
multidisciplinary
Narcotics
Nerve growth factor
Opioid receptors (type delta)
Oprd1 gene
Receptors
Receptors, Opioid, delta - genetics
Receptors, Opioid, delta - metabolism
Risk analysis
Science
Science (multidisciplinary)
Therapeutic targets
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Title Functional genetics reveals the contribution of delta opioid receptor to type 2 diabetes and beta-cell function
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Volume 15
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