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2. The potential roles of transacylation in intracellular lipolysis and related QSSA approximations

Author

Elias, Jan, Fellner, Klemens, Hofer, Peter, Oberer, Monika, Schreiber, Renate, and Zechner, Rudolf

Subjects
Mathematics - Dynamical Systems, 34C60, 37N25, 92C40, 92C45
Abstract

Fatty acids (FAs) are crucial energy metabolites, signalling molecules, and membrane building blocks for a wide range of organisms. Adipose triglyceride lipase (ATGL) is the first and presumingly most crucial regulator of FA release from triacylglycerols (TGs) stored within cytosolic lipid droplets. However, besides the function of releasing FAs by hydrolysing TGs into diacylglycerols (DGs), ATGL also promotes the transacylation reaction of two DG molecules into one TG and one monoacylglycerol molecule. To date, it is unknown whether DG transacylation is a coincidental byproduct of ATGL-mediated lipolysis or whether it is physiologically relevant. Experimental evidence is scarce since both, hydrolysis and transacylation, rely on the same active site of ATGL and always occur in parallel in an ensemble of molecules. This paper illustrates the potential roles of transacylation. It shows that, depending on the kinetic parameters but also on the state of the hydrolytic machinery, transacylation can increase or decrease downstream products up to 50\% and more. We provide an extensive asymptotic analysis including quasi-steady-state approximations (QSSA) with higher order correction terms and provide numerical simulation. We also argue that when assessing the validity of QSSAs one should include parameter sensitivity derivatives. Our results suggest that the transacylation function of ATGL is of biological relevance by providing feedback options and altogether stability to the lipolytic machinery in adipocytes., Comment: 33 pages, 12 figures

Published
2022

17. Optimizing Scatterplot-Matrices for Decision-Support : An Experimental Eye-Tracking Study Assessing Situational Cognitive Load

Author

Perkhofer, Lisa, Hofer, Peter, Spagnoletti, Paolo, Series Editor, De Marco, Marco, Series Editor, Pouloudi, Nancy, Series Editor, Te'eni, Dov, Series Editor, vom Brocke, Jan, Series Editor, Winter, Robert, Series Editor, Baskerville, Richard, Series Editor, Davis, Fred D., editor, Riedl, René, editor, Léger, Pierre-Majorique, editor, Randolph, Adriane B., editor, and Müller-Putz, Gernot, editor

Published
2021
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19. Unmasking Crucial Residues in Adipose Triglyceride Lipase (ATGL) for Co-Activation with Comparative Gene Identification-58 (CGI-58)

Author

Kulminskaya, Natalia, primary, Rodriguez Gamez, Carlos Francisco, additional, Hofer, Peter, additional, Cerk, Ines Kathrin, additional, Dubey, Noopur, additional, Viertlmayr, Roland, additional, Sagmeister, Theo, additional, Pavkov-Keller, Tea, additional, Zechner, Rudolf, additional, and Oberer, Monika, additional

Published
2023
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21. Skin Barrier Development Depends on CGI-58 Protein Expression during Late-Stage Keratinocyte Differentiation

Author

Grond, Susanne, Radner, Franz PW, Eichmann, Thomas O, Kolb, Dagmar, Grabner, Gernot F, Wolinski, Heimo, Gruber, Robert, Hofer, Peter, Heier, Christoph, Schauer, Silvia, Rülicke, Thomas, Hoefler, Gerald, Schmuth, Matthias, Elias, Peter M, Lass, Achim, Zechner, Rudolf, and Haemmerle, Guenter

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, 2.1 Biological and endogenous factors, Aetiology, Skin, 1-Acylglycerol-3-Phosphate O-Acyltransferase, Animals, Cell Differentiation, Ceramides, Keratinocytes, Lipase, Mice, Triglycerides, Oncology and Carcinogenesis, Dermatology & Venereal Diseases, Clinical sciences
Abstract

Adipose triglyceride lipase (ATGL) and its coactivator comparative gene identification-58 (CGI-58) are limiting in cellular triglyceride catabolism. Although ATGL deficiency is compatible with normal skin development, mice globally lacking CGI-58 die postnatally and exhibit a severe epidermal permeability barrier defect, which may originate from epidermal and/or peripheral changes in lipid and energy metabolism. Here, we show that epidermis-specific disruption of CGI-58 is sufficient to provoke a defect in the formation of a functional corneocyte lipid envelope linked to impaired ω-O-acylceramide synthesis. As a result, epidermis-specific CGI-58-deficient mice show severe skin dysfunction, arguing for a tissue autonomous cause of disease development. Defective skin permeability barrier formation in global CGI-58-deficient mice could be reversed via transgenic restoration of CGI-58 expression in differentiated but not basal keratinocytes suggesting that CGI-58 is essential for lipid metabolism in suprabasal epidermal layers. The compatibility of ATGL deficiency with normal epidermal function indicated that CGI-58 may stimulate an epidermal triglyceride lipase beyond ATGL required for the adequate provision of fatty acids as a substrate for ω-O-acylceramide synthesis. Pharmacological inhibition of ATGL enzyme activity similarly reduced triglyceride-hydrolytic activities in wild-type and CGI-58 overexpressing epidermis implicating that CGI-58 participates in ω-O-acylceramide biogenesis independent of its role as a coactivator of epidermal triglyceride catabolism.

Published
2017

24. Advanced lipodystrophy reverses fatty liver in mice lacking adipocyte hormone-sensitive lipase

Author

Pajed, Laura, Taschler, Ulrike, Tilp, Anna, Hofer, Peter, Kotzbeck, Petra, Kolleritsch, Stephanie, Radner, Franz P. W., Pototschnig, Isabella, Wagner, Carina, Schratter, Margarita, Eder, Sandra, Huetter, Sabrina, Schreiber, Renate, Haemmerle, Guenter, Eichmann, Thomas O., Schweiger, Martina, Hoefler, Gerald, Kershaw, Erin E., Lass, Achim, and Schoiswohl, Gabriele

Published
2021
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