We are analyzing https://link.springer.com/article/10.1007/s11010-010-0520-8.

Title:
Activation of PPARδ promotes mitochondrial energy metabolism and decreases basal insulin secretion in palmitate-treated β-cells | Molecular and Cellular Biochemistry
Description:
The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells.
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article, google, scholar, pubmed, cas, insulin, mitochondrial, secretion, pparδ, metabolism, peroxisome, proliferatoractivated, activation, diabetes, energy, receptor, muscle, expression, role, cells, usa, content, βcells, cell, proc, natl, acad, sci, privacy, cookies, basal, pancreatic, gene, coactivator, pgcα, transcription, protein, uncoupling, fatty, publish, search, cellular, promotes, june, βcell, factor, glucosestimulated, access, metabolic, acid,

Topics {✒️}

qing-guo lü & nan-wei tong peroxisome proliferator-activated receptor 6-dimethoxyisoflavone-7-o-β-d-glucopyranoside peroxisome proliferator-activated receptors palmitate-treated β-cells published month download article/chapter glucose-stimulated insulin secretion nan-wei tong insulin-secreting β-cells fatty acid excess palmitate-treated β-cells diabetic db/db mice katp channel-dependent pathway mitochondrial energy metabolism slow-twitch muscle fibres cell energy metabolism basal insulin secretion activator pgc-1α drives δ promotes reversal anaerobic glucose metabolism insulin secretion capacity attenuates metabolic syndrome multiple metabolic abnormalities full article pdf pancreatic β-cell high-fat diet pancreatic β cells βhc9 cells deficient ppar{delta} pancreatic beta cells privacy choices/manage cookies mitochondrial dna transcription β-cell model lipotoxic β-cells improves insulin sensitivity improved insulin sensitivity energy metabolism glucose-dependent esterification mitochondrial transcription factor concomitant mitochondrial uncoupling abnormal weight control thermogenic coactivator pgc gw501516-induced activation related subjects mitochondrial gene expression glucose metabolism insulin secretion state key laboratory xiao-yü li hit-t15 cells

Questions {❓}

Lameloise N, Muzzin P, Prentki M et al (2001) Uncoupling protein 2: a possible link between fatty acid excess and impaired glucose-induced insulin secretion?

Schema {🗺️}

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         description:The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells.
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