Vitamin D metabolites influence expression of genes concerning cellular viability and function in insulin producing β-cells (INS1E).

Background: Studies have shown that vitamin D can enhance glucose-stimulated insulin secretion (GSIS) and change the expression of genes in pancreatic β-cells. Still the mechanisms linking vitamin D and GSIS are unknown.

Material And Methods: We used an established β-cell line, INS1E.

Proteomic analysis of the INS-1E secretome identify novel vitamin D-regulated proteins.

Background: Experimental evidence indicates that vitamin D may have a beneficial role in pancreatic β-cell function.

Methods: In the present study, stable isotope labelling by amino acids in cell culture (SILAC) in combination with liquid chromatography-tandem mass spectrometry was used to quantitatively assess the impact of the active vitamin D metabolite, 1,25-(OH)2 D3 , on global protein expression in INS-1E cell secretome.

Results: Twenty-one proteins were found up-regulated (≥1.

Discovery of novel vitamin D-regulated proteins in INS-1 cells: a proteomic approach.

Background: Experimental evidence indicates that vitamin D may have a beneficial role in pancreatic β-cell function. Global gene expression studies have shown that the active metabolite 1,25-dihydroxyvitamin D3 [1,25-(OH)2 D3 ] modulates genes involved in ion transport, lipid metabolism and insulin secretion.

Methods: We employed stable isotope labelling by amino acids in cell culture in combination with liquid chromatography-tandem mass spectrometry to quantitatively assess the impact of two vitamin D metabolites, 1,25-(OH)2 D3 and 25-hydroxyvitamin D3 [25-(OH)D3 ], on global protein expression on a model rat β-cell line, insulinoma-derived INS-1 cells.

Pharmacology of neurotransmitter transport into secretory vesicles.

Many neuropsychiatric disorders appear to involve a disturbance of chemical neurotransmission, and the mechanism of available therapeutic agents supports this impression. Postsynaptic receptors have received considerable attention as drug targets, but some of the most successful agents influence presynaptic processes, in particular neurotransmitter reuptake. The pharmacological potential of many other presynaptic elements, and in particular the machinery responsible for loading transmitter into vesicles, has received only limited attention.

The effects of hypoxia-ischemia on neutral amino acid transporters in the developing rat brain.

The neutral amino acid transporters SNAT1-3 and ASCT1 play critical roles in the recycling of glutamine, and subsequently glutamate, via the glutamine-glutamate cycle. Hypoxia-ischemia was induced in rat pups using the Rice-Vannucci model. Brains were harvested at 1 h, 24 h and 7 days after ischemia.