Abstract
Sonication of rat fat cells caused an increase in lipolysis in the absence of lipolytic stimulants (basal lipolysis) and loss of epinephrine responsiveness. Sonication of endogenous lipid droplets from fat cells also induced an increase in lipolysis in the presence of hormone-sensitive lipase (HSL) and loss of epinephrine responsiveness in a cell-free system consisting of lipid droplets and HSL. This increase in lipolysis was found not to be due to an increase in the surface area resulting from sonication, but seemed to be due to a decrease in the phosphatidylcholine concentration on the surface of the lipid droplets. Addition of phosphatidylcholine to the sonicated lipid droplets reduced the hydrolysis of triglyceride by HSL in the cell-free system, consisting of HSL and intact lipid droplets or a lipid emulsion containing phosphatidylcholine increased lipolysis. These results suggest that phosphatidylcholine on the surface of the lipid droplets may be a regulatory factor for lipolysis in fat cells.
Highlights
Sonication of rat fat cells caused an increase in lipolysis in the absence of lipolytic stimulants and loss of epinephrine responsiveness
Fat cells are known to contain two major lipase systems, hormone-sensitive lipase (HSL) and lipoprotein lipase, which catalyze the hydrolysis of triglyceride to free fatty acids (FFA) and glycerol in about neutral and alkaline pH ranges [1, 15, 16]
It seemed probable that the increase in the basal lipolysis in sonicated fat cells might be due to the lipolytic activity of lipoprotein lipase
Summary
Sonication of rat fat cells caused an increase in lipolysis in the absence of lipolytic stimulants (basal lipolysis) and loss of epinephrine responsiveness. Sonication of endogenous lipid droplets from fat cells induced an increase in lipolysis in the presence of hormone-sensitive lipase (HSL) and loss of epinephrine responsiveness in a cell-free system consisting of lipid droplets and HSL. Muderkwa, and Brockman [9] examined the hydrolysis of 1,3-dioleoylglycerol in mixed lipid films of the substrate and l-palmitoyl-2-oleoyl-sn-glycero-3phosphocholine by human pancreatic carboxylester lipase, porcine pancreatic carboxylester lipase, and human milk bile salt-stimulated lipase They found that the percentage of 1,3-dioleoyl-glycero hydrolyzed increased abruptly from almost zero to nearly 100% with an increase in the proportion of substrate in the films. It seems likely that the physicochemical nature of the surface of endogenous lipid droplets is quite different from that in artificial lipid emulsions
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Published Version
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