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The dependence of lipid monolayer lipolysis on surface pressure.

ABSTRACT: Brönsted-Bjerrum theory [Brönsted (1922) Z. Phys. Chem. 102, 169-207; (1925) Z. Phys. Chem. 115, 337-364; Bjerrum (1924) Z. Phys. Chem. 108, 82-100] as applied to reactions at interfaces is used to interpret published data on the lipolysis of dinonanoyl phosphatidylcholine monolayers by pancreatic phospholipase A2. Reasonable quantitative agreement between theoretical and experimental results occurs when the reported effects of surface pressure on the amount of adsorbed enzyme are used together with the assumption that the Langmuir-Syskowski [Lange (1967) Nonionic Surfactants (Schick, M., ed.), chap. 4, Marcel Dekker, London and New York] isotherm describes the adsorption of lipid. The equations of Mass Action kinetics are less successful. Equivalent data on the lipolysis of didodecanoyl phosphatidylglycerol by pancreatic lipase can also be interpreted by arguing that the adsorbed enzyme forms significant amounts of enzyme substrate complex which reacts to give products in accordance with the well-known Briggs-Haldane [Lehninger (1975) Biochemistry, 2nd edn., chap. 8, Worth, New York] mechanism. The positions of the observed maxima in rate versus surface pressure plots suggests that the adsorption of an enzyme molecule displaces less lipid than one expects from the pronounced differences in molecular sizes of the two adsorbed species.

SUBMITTER: Hall DG

PROVIDER: S-EPMC1133125 | biostudies-other | 1992 Oct

REPOSITORIES: biostudies-other

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Project description:BackgroundElucidation of lipid metabolism and accumulation mechanisms is of paramount importance to understanding obesity and unveiling therapeutic targets. In vitro cell models have been extensively used for these purposes, yet, they do not entirely reflect the in vivo setup. Conventional lipomas, characterized by the presence of mature adipocytes and increased adipogenesis, could overcome the drawbacks of cell cultures. Also, they have the unique advantage of easily accessible matched controls in the form of subcutaneous adipose tissue (SAT) from the same individual. We aimed to determine whether lipomas are a good model to understand lipid accumulation.MethodsWe histologically compared lipomas and control SAT, followed by assessment of the lipidome using high-resolution 1H NMR spectroscopy and ESI-IT mass spectrometry. RNA-sequencing was used to obtain the transcriptome of lipomas and the matched SAT.ResultsWe found a significant increase of small-size (maximal axis?<?70?µm) and very big (maximal axis?>?150?µm) adipocytes within lipomas. This suggests both enhanced adipocyte proliferation and increased lipid accumulation. We further show that there is no significant change in the lipid composition compared to matched SAT. To better delineate the pathophysiology of lipid accumulation, we considered two groups with different genetic backgrounds: (1) lipomas with HMGA2 fusions and (2) without gene fusions. To reduce the search space for genes that are relevant for lipid pathophysiology, we focused on the overlapping differentially expressed (DE) genes between the two groups. Gene Ontology analysis revealed that DE genes are enriched in pathways related to lipid accumulation.ConclusionsWe show that the common shared lipid accumulation mechanism in lipoma is a reduction in lipolysis, with most gene dysregulations leading to a reduced cAMP in the adipocyte. Superficial lipomas could thus be used as a model for lipid accumulation through altered lipolysis as found in obese patients.

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The dependence of lipid monolayer lipolysis on surface pressure.

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