Age-related impairment in insulin release: The essential role of β 2-adrenergic receptor (848 views)
Diabetesdiabetes (ISSN: 0012-1797), 2012; 61(3): 692-701.
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Paper type: Journal Article,
Impact factor: 7.895, 5-year impact factor: 8.611
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84857393446&partnerID=40&md5=21bfc25ba07cf3af5c626629ad5d0da8
Keywords: Beta 2 Adrenergic Receptor, Glucose Transporter 2, Peroxisome Proliferator Activated Receptor Gamma, Transcription Factor Pdx 1, Adenovirus, Aging, Animal Cell, Animal Cell Culture, Animal Experiment, Animal Model, Animal Tissue, Article, Assay, Controlled Study, Ex Vivo Study, Gene Transfer, Glucose Homeostasis, Glucose Intolerance, Glucose Metabolism, In Vivo Study, Insulin Release, Insulinoma, Mouse, Nonhuman, Pancreas Islet Beta Cell, Phenotype, Priority Journal, Protein Expression, Wild Type, Age Factors, Glucose Tolerance Test, Glucose Transporter Type 2, Homeodomain Proteins, Mice, Inbred C57bl, Ppar Gamma, Trans-Activators,
Affiliations:
*** IBB - CNR ***
Department of Clinical Medicine, Cardiovascular and Immunologic Sciences, Federico II University of Naples, Naples, Italy
Columbia-Presbyterian Medical Center, College of Physicians and Surgeons, Columbia University, New York, NY, United States
Columbia University Medical Center, Columbia University, New York, NY, United States
Department of Cellular and Molecular Biology and Pathology, Institute of Experimental Endocrinology and Oncology Gaetano Salvatore, Federico II University of Naples, Naples, Italy
School of Medicine, University of Salerno, Salerno, Italy
References:
Not available.
Diabetesdiabetes (ISSN: 0012-1797), 2012; 61(3): 692-701.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 7.895, 5-year impact factor: 8.611
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84857393446&partnerID=40&md5=21bfc25ba07cf3af5c626629ad5d0da8
Keywords: Beta 2 Adrenergic Receptor, Glucose Transporter 2, Peroxisome Proliferator Activated Receptor Gamma, Transcription Factor Pdx 1, Adenovirus, Aging, Animal Cell, Animal Cell Culture, Animal Experiment, Animal Model, Animal Tissue, Article, Assay, Controlled Study, Ex Vivo Study, Gene Transfer, Glucose Homeostasis, Glucose Intolerance, Glucose Metabolism, In Vivo Study, Insulin Release, Insulinoma, Mouse, Nonhuman, Pancreas Islet Beta Cell, Phenotype, Priority Journal, Protein Expression, Wild Type, Age Factors, Glucose Tolerance Test, Glucose Transporter Type 2, Homeodomain Proteins, Mice, Inbred C57bl, Ppar Gamma, Trans-Activators,
Affiliations:
*** IBB - CNR ***
Department of Clinical Medicine, Cardiovascular and Immunologic Sciences, Federico II University of Naples, Naples, Italy
Columbia-Presbyterian Medical Center, College of Physicians and Surgeons, Columbia University, New York, NY, United States
Columbia University Medical Center, Columbia University, New York, NY, United States
Department of Cellular and Molecular Biology and Pathology, Institute of Experimental Endocrinology and Oncology Gaetano Salvatore, Federico II University of Naples, Naples, Italy
School of Medicine, University of Salerno, Salerno, Italy
References:
Not available.
Age-related impairment in insulin release: The essential role of β 2-adrenergic receptor
In this study, we investigated the significance of β 2- adrenergic receptor (β 2AR) in age-related impaired insulin secretion and glucose homeostasis. We characterized the metabolic phenotype of β 2AR-null C57Bl/6N mice (β 2AR -/-) by performing in vivo and ex vivo experiments. In vitro assays in cultured INS-1E β-cells were carried out in order to clarify the mechanism by which β 2AR deficiency affects glucose metabolism. Adult β 2AR -/- mice featured glucose intolerance, and pancreatic islets isolated from these animals displayed impaired glucose-induced insulin release, accompanied by reduced expression of peroxisome proliferator-activated receptor (PPAR)γ, pancreatic duodenal homeobox-1 (PDX-1), and GLUT2. Adenovirus-mediated gene transfer of human β 2AR rescued these defects. Consistent effects were evoked in vitro both upon β 2AR knockdown and pharmacologic treatment. Interestingly, with aging, wild-type (β 2AR +/+) littermates developed impaired insulin secretion and glucose tolerance. Moreover, islets from 20-month-old β 2AR +/+ mice exhibited reduced density of β 2AR compared with those from younger animals, paralleled by decreased levels of PPARγ, PDX-1, and GLUT2. Overexpression of β 2AR in aged mice rescued glucose intolerance and insulin release both in vivo and ex vivo, restoring PPARγ/PDX-1/GLUT2 levels. Our data indicate that reduced β 2AR expression contributes to the age-related decline of glucose tolerance in mice. © 2012 by the American Diabetes Association.
In this study, we investigated the significance of β 2- adrenergic receptor (β 2AR) in age-related impaired insulin secretion and glucose homeostasis. We characterized the metabolic phenotype of β 2AR-null C57Bl/6N mice (β 2AR -/-) by performing in vivo and ex vivo experiments. In vitro assays in cultured INS-1E β-cells were carried out in order to clarify the mechanism by which β 2AR deficiency affects glucose metabolism. Adult β 2AR -/- mice featured glucose intolerance, and pancreatic islets isolated from these animals displayed impaired glucose-induced insulin release, accompanied by reduced expression of peroxisome proliferator-activated receptor (PPAR)γ, pancreatic duodenal homeobox-1 (PDX-1), and GLUT2. Adenovirus-mediated gene transfer of human β 2AR rescued these defects. Consistent effects were evoked in vitro both upon β 2AR knockdown and pharmacologic treatment. Interestingly, with aging, wild-type (β 2AR +/+) littermates developed impaired insulin secretion and glucose tolerance. Moreover, islets from 20-month-old β 2AR +/+ mice exhibited reduced density of β 2AR compared with those from younger animals, paralleled by decreased levels of PPARγ, PDX-1, and GLUT2. Overexpression of β 2AR in aged mice rescued glucose intolerance and insulin release both in vivo and ex vivo, restoring PPARγ/PDX-1/GLUT2 levels. Our data indicate that reduced β 2AR expression contributes to the age-related decline of glucose tolerance in mice. © 2012 by the American Diabetes Association.
Age-related impairment in insulin release: The essential role of β 2-adrenergic receptor
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Age-related impairment in insulin release: The essential role of β 2-adrenergic receptor
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View Export to BibTeX Export to EndNote
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View Export to BibTeX Export to EndNote
22 Records (21 excluding Abstracts).
Total impact factor: 144.087 (139.736 excluding Abstracts).
Total 5 year impact factor: 140.876 (136.493 excluding Abstracts).
Total impact factor: 144.087 (139.736 excluding Abstracts).
Total 5 year impact factor: 140.876 (136.493 excluding Abstracts).
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