Pathophysiology of Type 2 Diabetes Mellitus
dc.contributor.author | Galicia García, Unai | |
dc.contributor.author | Benito Vicente, Asier | |
dc.contributor.author | Jebari Benslaiman, Shifa | |
dc.contributor.author | Larrea Sebal, Asier | |
dc.contributor.author | Siddiqi, Haziq | |
dc.contributor.author | Belloso Uribe, Kepa | |
dc.contributor.author | Ostolaza Echabe, Elena Amaya | |
dc.contributor.author | Martín Plágaro, César Augusto | |
dc.date.accessioned | 2020-09-30T08:17:42Z | |
dc.date.available | 2020-09-30T08:17:42Z | |
dc.date.issued | 2020-07-30 | |
dc.identifier.citation | International Journal of Molecular Sciences 21(17) : (2020) // Article ID 6275 | es_ES |
dc.identifier.issn | 1422-0067 | |
dc.identifier.uri | http://hdl.handle.net/10810/46289 | |
dc.description.abstract | Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated. Defects in any of the mechanisms involved in these processes can lead to a metabolic imbalance responsible for the development of the disease. This review analyzes the key aspects of T2DM, as well as the molecular mechanisms and pathways implicated in insulin metabolism leading to T2DM and insulin resistance. For that purpose, we summarize the data gathered up until now, focusing especially on insulin synthesis, insulin release, insulin sensing and on the downstream effects on individual insulin-sensitive organs. The review also covers the pathological conditions perpetuating T2DM such as nutritional factors, physical activity, gut dysbiosis and metabolic memory. Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM. | es_ES |
dc.description.sponsorship | This work was supported by the Basque Government (Grupos Consolidados IT-1264-19). U.G-G. was supported by Fundación Biofísica Bizkaia. A.B.-V. was supported by Programa de especializaci.n de Personal Investigador Doctor en la UPV/EHU (2019) 2019–2020. S.J. and A.L-S. were supported by a grant PIF (2017–2018) and (2019–2020), Gobierno Vasco, respectively. A.L.-S. was partially supported by Fundación Biofísica Bizkaia. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | |
dc.subject | type 2 diabetes mellitus | es_ES |
dc.subject | insulin resistance | es_ES |
dc.subject | β-cell | es_ES |
dc.subject | liver | es_ES |
dc.subject | adipocyte | es_ES |
dc.subject | muscle | es_ES |
dc.subject | cardiovascular disease | es_ES |
dc.subject | pathophysiology | es_ES |
dc.title | Pathophysiology of Type 2 Diabetes Mellitus | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.date.updated | 2020-09-07T13:46:36Z | |
dc.rights.holder | 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). | es_ES |
dc.relation.publisherversion | https://www.mdpi.com/1422-0067/21/17/6275 | es_ES |
dc.identifier.doi | 10.3390/ijms21176275 | |
dc.departamentoes | Bioquímica y biología molecular | |
dc.departamentoeu | Biokimika eta biologia molekularra |
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Except where otherwise noted, this item's license is described as 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).