Lipolysis of serum-activated triacylglycerol at the surface of J774.1 macrophages

Abstract

Cultured mouse (J774.1) macrophages accumulated triacylglycerol, but no cholesteryl ester or cholesterol, when incubated in albumin-poor medium with serum-activated lipid particles containing 84 mol% trioleoylglycerol and 9 mol% cholesteryl oleate. Accumulation of triacylglycerol by cells was associated with hydrolysis of particulate triacylglycerol to fatty acid and glycerol. Both acyl and glyceryl moieties of particulate triacylglycerol were recovered in cellular triacylglycerol with a molar ratio of 3.6. The cells also accumulated fatty acid and monoacylglycerol. Whether acylglycerol was taken up as a single molecular species, such as monoacylglycerol, or as several species can not be determined by the present findings. Macrophages incubated with lipid particles for 24 h had many lipid particles attached to cell surfaces and numerous intracellular lipid droplets. The surface film of attached particles was continuous with the outer leaflet of plasma membrane of the cells. Particles partially depleted of core triacylglycerol and collapsed surface films were found attached to surfaces of macrophages. There was no morphological evidence that lipid particles were taken up intact by cells, through endocytosis or phagocytosis. Macrophages incubated with lipid particles also contained intracellular lamellar structures. They varied in size and shape, and were located in the periphery of cells, sometimes near lipid droplets and endoplasmic reticulum. Only 3% of the lamellar structures were associated with lysosomes, indicating they probably were not of lysosomal origin. Lipid particles attached to cells decreased in size and number, and lamellar structures developed at the surface of particles, or replaced the particles, when glutaraldehyde-fixed specimens were incubated at 25 degrees C, demonstrating lipolytic activity at the surface of macrophages. Our findings suggest that particulate triacylglycerol was hydrolyzed by lipoprotein lipase at the surface of macrophages, and that fatty acid and monoacylglycerol formed by lipolysis were transported directly into the cells to be reesterified. When lipolytic products were taken up faster than they could be utilized, they accumulated as lamellar structures in the cells.

Lipoprotein lipase expression exclusively in liver. A mouse model for metabolism in the neonatal period and during cachexia.

“…The fact that LPL0/A-I-LPL(L) mice survived without a dramatic decrease in triglyceride levels compared with neonatal LPL0 mice was somewhat unexpected. Neonatal death in LPL0 mice and another mutant mouse deficient in LPL activity, the cld mouse, had been thought to be due to extremely high triglyceride levels causing pulmonary capillary obstruction and microinfarcts of other organs (15,27,28). The survival of the LPL0/A-I-LPL(L) mice suggests an alternative explanation.…”

Power transmission along biological membranes

“…The authors mentioned that there is only one (inner) mitochondrial membrane between a fat droplet and the matrix as if the droplet were localized in the intermembrane space of a mitochondrion. Urgent mobilization of neutral lipids in brown fat at cold-induced stress was found to be accompanied by such a massive release of free fatty acids that they seem to form a continuum extending from a fat droplet to the inner mitochondrial membrane (Blanchette-Mackie & Scow, 1982).…”

Autopsy case of Gaucher disease type I in a patient on enzyme replacement therapy. Comments on the dynamics of persistent storage process

“…It should be stressed that the persisting GCs in other sites did not exhibit any TAG accumulation and the adipose tissue in many of the available samples did not exhibit either alteration or association with GCs. The relationship of GCs and bone marrow adipocytes should be investigated in future studies of GD pathology as experimental ex vivo studies focused on resorption of TAG by macrophages point to potentially interesting mechanisms (Blanchette-Mackie et al 1986). …”