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Plin5, a new regulator of myocardial lipid metabolism, decreases free fatty acid peroxidation by inhibiting the lipolysis of intracellular lipid droplets, thus providing cardioprotection against I/R injury and shedding new light on therapeutic solutions for I/R diseases.
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During catecholamine-stimulated lipolysis, Perilipin 5 is phosphorylated by protein kinase A and forms transcriptional complexes with PGC-1alpha and SIRT1 in the nucleus. Perilipin 5 promotes PGC-1alpha co-activator function by disinhibiting SIRT1 deacetylase activity.
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Changes in lipid metabolism resulting from PLIN5 deletion reduce ER stress in muscle, decrease FGF21 production by muscle and liver, and impair glycemic control.
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The data highlight a key role of PLIN5 in lipid droplets function, first by finely adjusting lipid droplets fatty acids supply to mitochondrial oxidation, and second acting as a protective factor against lipotoxicity in skeletal muscle.
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The results indicated that atorvastatin promoted lipolysis and reduced TG accumulation in the liver by increasing PKA-mediated phosphorylation of Plin5. This new mechanism of lipid-lowering effects of atorvastatin might provide a new strategy for NAFLD treatment.
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mitochondria isolated from hearts deficient in Plin5, have specific functional defects
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Plin5 deficiency alters cardiac lipid metabolism and associates with reduced survival following myocardial ischemia.
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Data show that glucose-6-phosphatase and perilipin-5 (G6PC/PLIN5) are upregulated in notch1 knockout (KO) mice.
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PLIN5 is dispensable for normal substrate metabolism during exercise and is not required to promote mitochondrial biogenesis or enhance the cellular adaptations to endurance exercise training.
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High fat diet-induced liver fibrosis is accompanied by an approximate 75% reduction in Plin5 in hepatic stellate cells (HSC), and spontaneous activation of primary HSC produces temporally coincident loss of Plin5 expression and lipid droplet depletion.
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Here, we identify synthetic ligands that release ABHD5 from PLIN1 or PLIN5 without PKA activation and rapidly activate adipocyte and muscle lipolysis.
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the increase in liver PLIN5 during hepatosteatosis drives further lipid accumulation but does not adversely affect hepatic health or insulin sensitivity.
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upregulating the PLIN5 level in skeletal muscle drives expression of the FGF21 gene in fast-twitch fibers and is metabolically protective.
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the elevation of islet PLIN5 during fasting allows partitioning of fatty acids into lipid droplets that is released upon refeeding to support postprandial insulin secretion in cAMP- and GPR40-dependent manners.
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protein kinase A and perilipin 5 interact to regulate cardiac lipolysis
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found that Plin5 expression was increased in steatotic livers
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Results suggest that Plin5 allows excess triacylglycerol accumulation in the hearts of mice with streptozotocin-induced type 1 diabetes.
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Perilipin 5 as a lipid droplet protein adapted to mitochondrial energy utilization
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Plin5 is a novel direct PPARdelta target in muscle
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Findings strongly suggest that Plin5 functions as a lipolytic barrier to protect the cardiac TG pool from uncontrolled TG mobilization and the excessive release of free FAs.
