ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism
Diabetes (DM), especially type 2 diabetes (T2DM) has become one of the major diseases severely threatening public health worldwide. Islet beta cell dysfunctions and peripheral insulin resistance including liver and muscle metabolic disorder play decisive roles in the pathogenesis of T2DM. Particular...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-06-01
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| Series: | Frontiers in Physiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2022.918042/full |
| _version_ | 1811242646662807552 |
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| author | Jing Li Han Yan Rui Xiang Weili Yang Jingjing Ye Jingjing Ye Ruili Yin Jichun Yang Yujing Chi |
| author_facet | Jing Li Han Yan Rui Xiang Weili Yang Jingjing Ye Jingjing Ye Ruili Yin Jichun Yang Yujing Chi |
| author_sort | Jing Li |
| collection | DOAJ |
| description | Diabetes (DM), especially type 2 diabetes (T2DM) has become one of the major diseases severely threatening public health worldwide. Islet beta cell dysfunctions and peripheral insulin resistance including liver and muscle metabolic disorder play decisive roles in the pathogenesis of T2DM. Particularly, increased hepatic gluconeogenesis due to insulin deficiency or resistance is the central event in the development of fasting hyperglycemia. To maintain or restore the functions of islet beta cells and suppress hepatic gluconeogenesis is crucial for delaying or even stopping the progression of T2DM and diabetic complications. As the key energy outcome of mitochondrial oxidative phosphorylation, adenosine triphosphate (ATP) plays vital roles in the process of almost all the biological activities including metabolic regulation. Cellular adenosine triphosphate participates intracellular energy transfer in all forms of life. Recently, it had also been revealed that ATP can be released by islet beta cells and hepatocytes, and the released ATP and its degraded products including ADP, AMP and adenosine act as important signaling molecules to regulate islet beta cell functions and hepatic glycolipid metabolism via the activation of P2 receptors (ATP receptors). In this review, the latest findings regarding the roles and mechanisms of intracellular and extracellular ATP in regulating islet functions and hepatic glycolipid metabolism would be briefly summarized and discussed. |
| first_indexed | 2024-04-12T13:54:15Z |
| format | Article |
| id | doaj.art-7933ced78d6a419fa53deceaf455956d |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-04-12T13:54:15Z |
| publishDate | 2022-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Physiology |
| spelling | doaj.art-7933ced78d6a419fa53deceaf455956d2022-12-22T03:30:25ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2022-06-011310.3389/fphys.2022.918042918042ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid MetabolismJing Li0Han Yan1Rui Xiang2Weili Yang3Jingjing Ye4Jingjing Ye5Ruili Yin6Jichun Yang7Yujing Chi8Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, ChinaKey Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, ChinaBeijing Key Laboratory of Diabetes Research and Care, Beijing Tongren Hospital, Capital Medical University, Beijing, ChinaDepartment of Central Laboratory and Institute of Clinical Molecular Biology, Peking University People’s Hospital, Beijing, ChinaKey Laboratory of Trauma and Neural Regeneration (Peking University), National Center for Trauma Medicine, Trauma Medicine Center, Peking University People’s Hospital, Beijing, ChinaBeijing Key Laboratory of Diabetes Prevention and Research, Center for Endocrine Metabolic and Immune Disease, Beijing Luhe Hospital, Capital Medical University, Beijing, ChinaKey Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, ChinaDepartment of Central Laboratory and Institute of Clinical Molecular Biology, Peking University People’s Hospital, Beijing, ChinaDiabetes (DM), especially type 2 diabetes (T2DM) has become one of the major diseases severely threatening public health worldwide. Islet beta cell dysfunctions and peripheral insulin resistance including liver and muscle metabolic disorder play decisive roles in the pathogenesis of T2DM. Particularly, increased hepatic gluconeogenesis due to insulin deficiency or resistance is the central event in the development of fasting hyperglycemia. To maintain or restore the functions of islet beta cells and suppress hepatic gluconeogenesis is crucial for delaying or even stopping the progression of T2DM and diabetic complications. As the key energy outcome of mitochondrial oxidative phosphorylation, adenosine triphosphate (ATP) plays vital roles in the process of almost all the biological activities including metabolic regulation. Cellular adenosine triphosphate participates intracellular energy transfer in all forms of life. Recently, it had also been revealed that ATP can be released by islet beta cells and hepatocytes, and the released ATP and its degraded products including ADP, AMP and adenosine act as important signaling molecules to regulate islet beta cell functions and hepatic glycolipid metabolism via the activation of P2 receptors (ATP receptors). In this review, the latest findings regarding the roles and mechanisms of intracellular and extracellular ATP in regulating islet functions and hepatic glycolipid metabolism would be briefly summarized and discussed.https://www.frontiersin.org/articles/10.3389/fphys.2022.918042/fullATPpurinergic P2 receptorinsulin secretionglucolipid metabolismmitochondrial dysfunction |
| spellingShingle | Jing Li Han Yan Rui Xiang Weili Yang Jingjing Ye Jingjing Ye Ruili Yin Jichun Yang Yujing Chi ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism Frontiers in Physiology ATP purinergic P2 receptor insulin secretion glucolipid metabolism mitochondrial dysfunction |
| title | ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism |
| title_full | ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism |
| title_fullStr | ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism |
| title_full_unstemmed | ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism |
| title_short | ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism |
| title_sort | atp secretion and metabolism in regulating pancreatic beta cell functions and hepatic glycolipid metabolism |
| topic | ATP purinergic P2 receptor insulin secretion glucolipid metabolism mitochondrial dysfunction |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2022.918042/full |
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