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Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β -Cells

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ABSTRACT

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.

No MeSH data available.


The involvement of 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 apoptosis induction by saturated fatty acids (FAs) in pancreatic β-cells. Solid lines represent relationships with a reasonable probability where bold solid line means more important relationship. Dashed lines represent possible, but less certain, relationships.
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ijms-17-01400-f001: The involvement of 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 apoptosis induction by saturated fatty acids (FAs) in pancreatic β-cells. Solid lines represent relationships with a reasonable probability where bold solid line means more important relationship. Dashed lines represent possible, but less certain, relationships.

Mentions: To conclude, it has been documented that saturated FAs activate JNK kinase in pancreatic β-cells mainly via ER stress. However, other mechanisms cannot be excluded. It seems that JNK activation mediates apoptosis induction by saturated FAs. Nevertheless, the amount of available data is insufficient to say that this is conclusive. In addition to the process of apoptosis induction, JNK is probably also involved in fatty acid-induced autophagy [47] in pancreatic β-cells. The pro-apoptotic role of JNK has also been documented in osteoblasts and hepatocytes treated with saturated FAs [48,49,50]. JNK seems to be one of the most important kinases in the process of apoptosis induction by FAs in pancreatic β-cells, mainly via ER stress induction (Figure 1).


Kinase Signaling in Apoptosis Induced by Saturated Fatty Acids in Pancreatic β -Cells
The involvement of 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 apoptosis induction by saturated fatty acids (FAs) in pancreatic β-cells. Solid lines represent relationships with a reasonable probability where bold solid line means more important relationship. Dashed lines represent possible, but less certain, relationships.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037680&req=5

ijms-17-01400-f001: The involvement of 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 apoptosis induction by saturated fatty acids (FAs) in pancreatic β-cells. Solid lines represent relationships with a reasonable probability where bold solid line means more important relationship. Dashed lines represent possible, but less certain, relationships.
Mentions: To conclude, it has been documented that saturated FAs activate JNK kinase in pancreatic β-cells mainly via ER stress. However, other mechanisms cannot be excluded. It seems that JNK activation mediates apoptosis induction by saturated FAs. Nevertheless, the amount of available data is insufficient to say that this is conclusive. In addition to the process of apoptosis induction, JNK is probably also involved in fatty acid-induced autophagy [47] in pancreatic β-cells. The pro-apoptotic role of JNK has also been documented in osteoblasts and hepatocytes treated with saturated FAs [48,49,50]. JNK seems to be one of the most important kinases in the process of apoptosis induction by FAs in pancreatic β-cells, mainly via ER stress induction (Figure 1).

View Article: PubMed Central - PubMed

ABSTRACT

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.

No MeSH data available.