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Endothelial Lipase Is an Alternative Pathway for Fatty Acid Release from Lipoproteins: Evidence from a High Fat Diet Model of Obesity in Rats
Author(s) -
Barchuk Magalí,
Miksztowicz Verónica,
Zago Valeria,
Cevey Agata,
López Graciela,
Goren Nora,
Friedman Silvia,
Gelpi Ricardo Jorge,
Morales Celina,
Fernandez Tomé María del Carmen,
Schreier Laura,
Berg Gabriela
Publication year - 2018
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1002/lipd.12107
Subject(s) - lipoprotein lipase , medicine , endocrinology , adipose tissue , biology , lipidology , peroxisome proliferator activated receptor , clinical chemistry , lipoprotein , adipocyte , lipid metabolism , insulin resistance , cholesterol , receptor , insulin
Lipoprotein lipase (LPL) and endothelial lipase (EL) are involved in lipoprotein metabolism. In insulin‐resistance, their behavior is altered. Peroxisome proliferator‐activated receptors (PPAR) and apoproteins (apo)CII and CIII could be partly responsible for these alterations. To evaluate this response, we assessed Lpl and Lipg expression, protein levels, and enzyme activity in adipose tissue (AT) and heart in an obesity model. Besides, we assessed the role of PPAR and apoC. Male Wistar rats were fed with standard diet (Control, n = 14) or high‐fat diet (HFD, n = 14) for 14 weeks. Glucose and lipoprotein profiles were measured. Histological studies were performed in heart and epididymal AT. Lpl and Lipg were assessed by reverse transcription polymerase chain reaction (RT‐qPCR), protein levels by Western Blot, and activities by radiometric assays. Cardiac and AT PPAR expression were measured by Western Blot and hepatic Apoc2 and Apoc3 mRNA by RT‐qPCR. In HFD, fat deposits were observed in hearts, whereas AT presented a higher adipocyte size. In heart and AT, no differences were found in Lipg mRNA between groups, while AT Lpl mRNA and LPL protein were decreased in HFD, without differences in heart. In both tissues, EL protein levels and activity were increased and inversely associated with decreased LPL activity, being partially responsible for the atherogenic lipoprotein profile in HFD. PPARγ expression in AT was decreased in HFD, without differences in cardiac PPARδ expression and hepatic apoC mRNA. The increase in EL activity could be an alternative pathway for fatty acid release from lipoproteins and uptake in tissues with decreased LPL activity. In AT, PPARγ could be involved in enzyme regulation.