Perilipin‐1 in Hemodialyzed Patients: Association With History of Coronary Heart Disease and Lipid Profile

Abstract

Perilipin-1 surrounds lipid droplets in both adipocytes and in atheroma plaque foam cells and controls access of lipases to the lipid core. In hemodialysis (HD) patients, dyslipidemia, malnutrition, inflammation and atherosclerosis are common. Thirty-six HD patients and 28 healthy volunteers were enrolled into the study. Ten HD patients suffered from coronary heart disease (CHD). Perilipin-1, triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), body mass index, albumin, geriatric nutritional risk index, normalized protein catabolic rate, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured. Perilipin-1 did not differ between HD patients and healthy volunteers. IL-6 and TNF-α were higher in HD patients. The evaluated nutritional markers and the markers of inflammation did not differ between HD patients with high perilipin-1 levels and HD patients with low perilipin-1 levels. Regarding the lipid profile, only HDL-C differed between HD patients with high perilipin-1 levels and HD patients with low perilipin-1 levels, and it was higher in the first subgroup. Perilipin-1 was significantly higher in HD patients without CHD. Perilipin-1 is detectable in the serum of HD patients and it is associated with increased HDL-C and decreased incidence of CHD.

Pathways linking aging and atheroprotection in Mif‐deficient atherosclerotic mice

“…Plin1 and Il34 have previously been shown to be higher in patients with coronary heart disease with a hemodialysis and heart failure background, respectively, indicating they may have roles in atherogenic diseases. Furthermore, Plin1 enhances CD36 expression and inhibits cholesterol ester hydrolysis inside macrophages promoting foam cell formation, while systemic or myeloid Plin1 ‐deficient mice exhibited an attenuation of plaque size in aortic root; IL‐34 also enhances foam cell formation via upregulating CD36 expression on macrophages and promoting oxLDL uptake 64,68–70 . To this end, it is interesting to note that the Luminex data showed that Mif deficiency led to a down‐regulation of circulating M‐CSF, although no aging/HFD‐dependent difference was observed.…”

“…Furthermore, Plin1 enhances CD36 expression and inhibits cholesterol ester hydrolysis inside macrophages promoting foam cell formation, while systemic or myeloid Plin1-deficient mice exhibited an attenuation of plaque size in aortic root; IL-34 also enhances foam cell formation via upregulating CD36 expression on macrophages and promoting oxLDL uptake. 64,[68][69][70] To this end, it is interesting to note that the Luminex data showed that Mif deficiency led to a down-regulation of circulating M-CSF, although no aging/HFD-dependent difference was observed. Furthermore, the observed enrichment of the TP53-regulated cell death gene pathway in the 24-week HFD Mif-deficient group provides further links to foam cells and inflammation.…”

Perilipin1 Expression as a Prognostic Factor in Patients with Squamous Cell Carcinoma of the Lung

“…PLIN1 has also been studied in coronary artery disease and nonalcoholic fatty liver disease, which are major diseases associated with obesity. Eleftheriadis et al measured serum PLIN1 in hemodialysis patients with frequent dyslipidemia, malnutrition, inflammation and atherosclerosis, and found an association between increased high-density lipoprotein cholesterol and reduced incidence of coronary artery disease [18]. The lipid metabolism association of PLIN1 also has great potential for use in the diagnosis and treatment of nonalcoholic fatty liver disease [19,20].…”