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E-GEOD-73131

ABSTRACT: Transcription profiling by array of pancreatic islets from Sgpp2 knockout mice after high fat diet

PROVIDER: E-GEOD-73131 | ExpressionAtlas | 2016-11-10

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-73131-analysis-methods.tsv	Tabular
	E-GEOD-73131-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-73131-configuration.xml	Xml
	E-GEOD-73131-percentile-ranks.tsv	Tabular
	E-GEOD-73131.condensed-sdrf.tsv	Tabular

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Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet B-cell Endoplasmic Reticulum Stress and Proliferation

Project description:Sphingosine-1-phosphate (S1P) is a sphingolipid metabolite that regulates basic cell functions through metabolic and signaling pathways. Intracellular metabolism of S1P is controlled, in part, by two homologous S1P phosphatases, 1 and 2, which are encoded by Sgpp1 and Sgpp2, respectively. S1P phosphatase activity is needed for efficient recycling of sphingosine into the sphingolipid synthesis pathway. S1P phosphatase 1 is important for skin homeostasis, but little is known about the functional role of S1P phosphatase 2. To identify the functions of S1P phosphatase 2 in vivo, we studied mice with the Sgpp2 gene deleted. In contrast to Sgpp1-/- mice, Sgpp2-/- mice had normal skin and were viable into adulthood. Unexpectedly, WT mice expressed Sgpp2 mRNA at high levels in pancreatic islets when compared with other tissues. Sgpp2-/- mice had normal blood insulin levels and pancreatic islet size; however, Sgpp2-/- mice treated with a high-fat diet (HFD) had significantly lower blood insulin levels and smaller pancreatic islets compared with WT mice. The smaller islets in the HFD-treated Sgpp2-/- mice had a significantly lower adaptive B-cell proliferation rate in response to the diet compared with HFD-treated WT mice. Importantly, B-cells from Sgpp2-/- mice fed a normal diet showed significantly increased expression of proteins characteristic of the endoplasmic reticulum (ER) stress response compared with B-cells from WT mice. Our results suggest that Sgpp2 deletion causes B-cell ER stress, which is a known cause of B-cell dysfunction, and reveal a novel juncture in the sphingolipid recycling pathway that could impact the development of diabetes. Three replications of Mouse (WT vs KO) that were treated with with Normal and HFD foods.

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Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet β-cell Endoplasmic Reticulum Stress and Proliferation

Project description:Sphingosine-1-phosphate (S1P) is a sphingolipid metabolite that regulates basic cell functions through metabolic and signaling pathways. Intracellular metabolism of S1P is controlled, in part, by two homologous S1P phosphatases, 1 and 2, which are encoded by Sgpp1 and Sgpp2, respectively. S1P phosphatase activity is needed for efficient recycling of sphingosine into the sphingolipid synthesis pathway. S1P phosphatase 1 is important for skin homeostasis, but little is known about the functional role of S1P phosphatase 2. To identify the functions of S1P phosphatase 2 in vivo, we studied mice with the Sgpp2 gene deleted. In contrast to Sgpp1-/- mice, Sgpp2-/- mice had normal skin and were viable into adulthood. Unexpectedly, WT mice expressed Sgpp2 mRNA at high levels in pancreatic islets when compared with other tissues. Sgpp2-/- mice had normal blood insulin levels and pancreatic islet size; however, Sgpp2-/- mice treated with a high-fat diet (HFD) had significantly lower blood insulin levels and smaller pancreatic islets compared with WT mice. The smaller islets in the HFD-treated Sgpp2-/- mice had a significantly lower adaptive β-cell proliferation rate in response to the diet compared with HFD-treated WT mice. Importantly, β-cells from Sgpp2-/- mice fed a normal diet showed significantly increased expression of proteins characteristic of the endoplasmic reticulum (ER) stress response compared with β-cells from WT mice. Our results suggest that Sgpp2 deletion causes β-cell ER stress, which is a known cause of β-cell dysfunction, and reveal a novel juncture in the sphingolipid recycling pathway that could impact the development of diabetes.

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