In beta-cells, mitochondria integrate and generate metabolic signals controlling insulin secretion
Pancreatic beta-cells are unique neuroendocrine cells displaying the peculiar feature of responding to nutrients, principally glucose, as primary stimulus. This requires translation of a metabolic substrate into intracellular messengers recognized by the exocytotic machinery. Central to this signal...
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| Published in: | The international journal of biochemistry & cell biology Vol. 38; no. 5; pp. 696 - 709 |
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| Main Authors: | , , |
| Format: | Journal Article |
| Language: | English |
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01-01-2006
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| Abstract | Pancreatic beta-cells are unique neuroendocrine cells displaying the peculiar feature of responding to nutrients, principally glucose, as primary stimulus. This requires translation of a metabolic substrate into intracellular messengers recognized by the exocytotic machinery. Central to this signal transduction mechanism, mitochondria integrate and generate metabolic signals, thereby coupling glucose recognition to insulin secretion. In response to a glucose rise, nucleotides and metabolites are generated by mitochondria and participate, together with cytosolic calcium, to the stimulation of insulin exocytosis. This review describes the mitochondrion-dependent pathways of regulated insulin secretion. In particular, importance of cataplerotic and anaplerotic processes is discussed, with special attention to the mitochondrial enzyme glutamate dehydrogenase. Mitochondrial defects, such as mutations and reactive oxygen species production, are presented in the context of beta-cell failure in the course of type 2 diabetes. |
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| AbstractList | Pancreatic beta-cells are unique neuroendocrine cells displaying the peculiar feature of responding to nutrients, principally glucose, as primary stimulus. This requires translation of a metabolic substrate into intracellular messengers recognized by the exocytotic machinery. Central to this signal transduction mechanism, mitochondria integrate and generate metabolic signals, thereby coupling glucose recognition to insulin secretion. In response to a glucose rise, nucleotides and metabolites are generated by mitochondria and participate, together with cytosolic calcium, to the stimulation of insulin exocytosis. This review describes the mitochondrion-dependent pathways of regulated insulin secretion. In particular, importance of cataplerotic and anaplerotic processes is discussed, with special attention to the mitochondrial enzyme glutamate dehydrogenase. Mitochondrial defects, such as mutations and reactive oxygen species production, are presented in the context of beta-cell failure in the course of type 2 diabetes. |
| Author | Rubi, Blanca Maechler, Pierre Carobbio, Stefania |
| Author_xml | – sequence: 1 givenname: Pierre surname: Maechler fullname: Maechler, Pierre email: Pierre.Maechler@medecine.unige.ch – sequence: 2 givenname: Stefania surname: Carobbio fullname: Carobbio, Stefania – sequence: 3 givenname: Blanca surname: Rubi fullname: Rubi, Blanca |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16443386$$D View this record in MEDLINE/PubMed |
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| Keywords | Glutamate dehydrogenase GLP-1 Beta-cell BCH GDH GAD Insulin secretion Mitochondria TCA ROS UCP2 LCPT1 K ATP-channel AGC |
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| SubjectTerms | Adenosine Triphosphate - biosynthesis Animals Beta-cell Diabetes Mellitus, Type 2 - physiopathology Electron Transport Chain Complex Proteins - metabolism Exocytosis - physiology Glutamate dehydrogenase Glutamate Dehydrogenase - metabolism Humans Insulin - metabolism Insulin Secretion Insulin-Secreting Cells - physiology Insulin-Secreting Cells - ultrastructure Mitochondria Mitochondria - metabolism NAD - metabolism Pyruvic Acid - metabolism Signal Transduction - physiology |
| Title | In beta-cells, mitochondria integrate and generate metabolic signals controlling insulin secretion |
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