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Overexpressed PLIN1 in macrophages had a protected role against atheroma progression in ApoeKO in the absence of changes in gonadal fat mass or plasma lipid levels, presumably due to modification of the stability and/or inflammatory profile of macrophages.
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Hypertension in Plin1-/- mice might occur as a deleterious consequence of perivascular adipose tissue dysfunction.
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Plin1 is required to restrain fat loss and pro-inflammatory responses in adipose tissue by reducing futile lipolysis to maintain metabolic homeostasis.
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This mouse model might mimic and explain the pathogenesis of hepatosteatosis occurring in two typical disorders of adipose tissue dysfunction, obesity and lipodystrophy, particularly in lipodystrophic patients with Plin1 mutation.
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IP6K1 is a novel regulator of PLIN1 mediated lipolysis
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ex vivo studies in human primary adipocytes, demonstrate that perilipin 1 binds to AQP7, and that catecholamine activated protein kinase A phosphorylates the N-terminus of AQP7, thereby reducing complex formation
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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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Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis.
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Plin1 deficiency in bone marrow-derived cells may be responsible for reduced atherosclerotic lesions in the mice
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Perilipin+ embryonic preadipocytes actively proliferate along growing vasculatures for adipose expansion.
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Data suggest cardiotrophin-1 up-regulates lipolysis in adipocytes via 1) induction of Plin1, 2) activation of hormone sensitive lipase (via phosphorylation by PKA), and 3) inactivation of adipose triglyceride lipase (via up-regulation of G0S2).
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Adipocytes of Plin1/ mice showed robust basal lipolysis and fatty acid efflux to the plasma. Such adipose tissue dysfunctions accounted for the ectopic lipid accumulation and enhanced fatty acid transport and oxidation in Plin1/ hearts.
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QRFP-43 attenuates lipolysis by preventing the formation of an active complex between perilipin A, caveolin-1, the catalytic subunit of protein kinase and hormone-sensitive lipase on lipid droplets.
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ESR1 regulates ATGL and perilipin-mediated lipid metabolism and droplet size in femurs from mice.
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Collectively these data suggest that whereas perilipin 1 potently suppresses basal lipolysis in adipocytes, perilipins 2 and 3 facilitate higher rates of basal lipolysis
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these findings indicated that PLIN1 disruption leads to the increase of round spermatid-containing seminiferous tubules at the meiotic stage of the first wave of spermatogenesis through regulating spermatogenic related genes.
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Data indicate that perilipin (plin) deficiency suppresses sterol regulatory element-binding protein-1 (SREBP-1) activation in white adipose tissue (WAT).
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Perilipin1 (Plin1), another adipocyte-specific lipid droplet-associated protein, is an Fsp27 activator.
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FSP27 acts to constitutively limit the lipid droplet presence of ATGL, perilipin 1 plays an essential role in mediating the response of ATGL action to beta-adrenergic hormones.
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the reduction of perilipin1 in white adipose tissues may at least in part contribute to conjugated linoleic acid -mediated alternation of lipolysis of white adipose tissues.