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Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells
Pancreatic β-cell failure and death is considered to be one of the main factors responsible for type 2 diabetes. It is caused by, in addition to hyperglycemia, chronic exposure to increased concentrations of fatty acids, mainly saturated fatty acids. Molecular mechanisms of apoptosis induction by sa...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037680/ https://www.ncbi.nlm.nih.gov/pubmed/27626409 http://dx.doi.org/10.3390/ijms17091400 |
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author | Šrámek, Jan Němcová-Fürstová, Vlasta Kovář, Jan |
author_facet | Šrámek, Jan Němcová-Fürstová, Vlasta Kovář, Jan |
author_sort | Šrámek, Jan |
collection | PubMed |
description | Pancreatic β-cell failure and death is considered to be one of the main factors responsible for type 2 diabetes. It is caused by, in addition to hyperglycemia, chronic exposure to increased concentrations of fatty acids, mainly saturated fatty acids. Molecular mechanisms of apoptosis induction by saturated fatty acids in β-cells are not completely clear. It has been proposed that kinase signaling could be involved, particularly, c-Jun N-terminal kinase (JNK), protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt kinases and their pathways. In this review, we discuss these kinases and their signaling pathways with respect to their possible role in apoptosis induction by saturated fatty acids in pancreatic β-cells. |
format | Online Article Text |
id | pubmed-5037680 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-50376802016-09-29 Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells Šrámek, Jan Němcová-Fürstová, Vlasta Kovář, Jan Int J Mol Sci Review Pancreatic β-cell failure and death is considered to be one of the main factors responsible for type 2 diabetes. It is caused by, in addition to hyperglycemia, chronic exposure to increased concentrations of fatty acids, mainly saturated fatty acids. Molecular mechanisms of apoptosis induction by saturated fatty acids in β-cells are not completely clear. It has been proposed that kinase signaling could be involved, particularly, c-Jun N-terminal kinase (JNK), protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt kinases and their pathways. In this review, we discuss these kinases and their signaling pathways with respect to their possible role in apoptosis induction by saturated fatty acids in pancreatic β-cells. MDPI 2016-09-12 /pmc/articles/PMC5037680/ /pubmed/27626409 http://dx.doi.org/10.3390/ijms17091400 Text en © 2016 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/). |
spellingShingle | Review Šrámek, Jan Němcová-Fürstová, Vlasta Kovář, Jan Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells |
title | Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells |
title_full | Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells |
title_fullStr | Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells |
title_full_unstemmed | Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells |
title_short | Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β-Cells |
title_sort | kinase signaling in apoptosis induced by saturated fatty acids in pancreatic β-cells |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037680/ https://www.ncbi.nlm.nih.gov/pubmed/27626409 http://dx.doi.org/10.3390/ijms17091400 |
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