Regulation of insulin secretion and expression of SUR1 gene by chronic exposure to free fatty acids in rat pancreatic β cells

2004 ◽  
Vol 24 (4) ◽  
pp. 358-360 ◽  
Author(s):  
Yuan Li ◽  
Deng Xiuling ◽  
Chen Lulu ◽  
Zhou Min
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Chronic Exposure ◽  
Β Cells ◽  
Pancreatic Β Cells

Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40

Nature ◽  
2003 ◽  
Vol 422 (6928) ◽  
pp. 173-176 ◽  
Author(s):  
Yasuaki Itoh ◽  
Yuji Kawamata ◽  
Masataka Harada ◽  
Makoto Kobayashi ◽  
Ryo Fujii ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Β Cells ◽  
Pancreatic Β Cells

Free fatty acids stimulate autophagy in pancreatic β-cells via JNK pathway

2010 ◽  
Vol 401 (4) ◽  
pp. 561-567 ◽  
Author(s):  
Koji Komiya ◽  
Toyoyoshi Uchida ◽  
Takashi Ueno ◽  
Masato Koike ◽  
Hiroko Abe ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Jnk Pathway

n-3 polyunsaturated fatty acids and insulin secretion

2014 ◽  
Vol 224 (3) ◽  
pp. R97-R106 ◽  
Author(s):  
Xiaofeng Wang ◽  
Catherine B Chan
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Polyunsaturated Fatty Acids ◽  
Beneficial Effect ◽  
Health Benefits ◽  
Β Cells ◽  
Pancreatic Β Cells

n-3 polyunsaturated fatty acids (PUFAs) are a subgroup of fatty acids with broad health benefits, such as lowering blood triglycerides and decreasing the risk of some types of cancer. A beneficial effect of n-3 PUFAs in diabetes is indicated by results from some studies. Defective insulin secretion is a fundamental pathophysiological change in both types 1 and 2 diabetes. Emerging studies have provided evidence of a connection between n-3 PUFAs and improved insulin secretion from pancreatic β-cells. This review summarizes the recent findings in this regard and discusses the potential mechanisms by which n-3 PUFAs influence insulin secretion from pancreatic β-cells.

scholarly journals Long-chain Saturated Fatty Acid Species Are Not Toxic to Human Pancreatic Β-cells and May Offer Protection Against Pro-inflammatory Cytokine Induced β-cell Death

2020 ◽  
Author(s):  
Patricia Thomas ◽  
Kaiyven A Leslie ◽  
Hannah J Welters ◽  
Noel G Morgan
Keyword(s):  
Fatty Acids ◽  
Cell Death ◽  
Chain Length ◽  
Inflammatory Cytokines ◽  
Chronic Exposure ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Long Chain ◽  
Pro Inflammatory Cytokines

Abstract Obesity is a major risk factor for type 2 diabetes (T2D) although the causal links remain unclear. A feature shared by both conditions however is systemic inflammation and raised levels of circulating fatty acids (FFA). It is widely believed that in obese individuals genetically prone to T2D, elevated levels of plasma FFA may contribute towards the death and dysfunction of insulin-producing pancreatic β-cells in a process of (gluco)lipotoxicity. In support of this, in vitro studies have shown consistently that long-chain saturated fatty acids (LC-SFA) are toxic to rodent β-cells during chronic exposure (>24h). Conversely, shorter chain SFA and unsaturated species are well tolerated, suggesting that toxicity is dependent on carbon chain length and/or double bond configuration. Despite the wealth of evidence implicating lipotoxicity as a means of β-cell death in rodents, the evidence that a similar process occurs in humans is much less substantial. Therefore, the present study has evaluated the effects of chronic exposure to fatty acids of varying chain length and degree of saturation, on the viability of human β-cells in culture. We have also studied the effects of a combination of fatty acids and pro-inflammatory cytokines. Strikingly, we find that LC-FFA do not readily promote the demise of human β-cells and that they may even offer a measure of protection against the toxic effects of pro-inflammatory cytokines. Therefore, these findings imply that a model in which elevated circulating LC-FFA play a direct role in mediating β-cell dysfunction and death in humans, may be overly simplistic.

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