期刊
CELLS
卷 9, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/cells9071682
关键词
Sphingosine-1-phosphate; obesity; type 2 diabetes; insulin resistance; pancreatic beta cell fate; hypothalamus
类别
资金
- Centre National de la Recherche Scientifique (CNRS)
- Institut National de la Recherche Medicale (INSERM)
- Sorbonne Universite
- Universite Paris Saclay
- Fondation de France
- Societe Francophone de Diabetologie (SFD)
- French Research Ministry/University Paris Saclay
Obesity is a pathophysiological condition where excess free fatty acids (FFA) target and promote the dysfunctioning of insulin sensitive tissues and of pancreatic beta cells. This leads to the dysregulation of glucose homeostasis, which culminates in the onset of type 2 diabetes (T2D). FFA, which accumulate in these tissues, are metabolized as lipid derivatives such as ceramide, and the ectopic accumulation of the latter has been shown to lead to lipotoxicity. Ceramide is an active lipid that inhibits the insulin signaling pathway as well as inducing pancreatic beta cell death. In mammals, ceramide is a key lipid intermediate for sphingolipid metabolism as is sphingosine-1-phosphate (S1P). S1P levels have also been associated with the development of obesity and T2D. In this review, the current knowledge on S1P metabolism in regulating insulin signaling in pancreatic beta cell fate and in the regulation of feeding by the hypothalamus in the context of obesity and T2D is summarized. It demonstrates that S1P can display opposite effects on insulin sensitive tissues and pancreatic beta cells, which depends on its origin or its degradation pathway.
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