scholarly journals Thiazolidinediones Block Fatty Acid Release by Inducing Glyceroneogenesis in Fat Cells

2003 ◽  
Vol 278 (21) ◽  
pp. 18785-18790 ◽  
Author(s):  
Joan Tordjman ◽  
Geneviève Chauvet ◽  
Joëlle Quette ◽  
Elmus G. Beale ◽  
Claude Forest ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fat Cells ◽  
Fatty Acid Release ◽  
Acid Release

scholarly journals Mechanisms Involved in the Regulation of Free Fatty Acid Release from Isolated Human Fat Cells by Acylation-stimulating Protein and Insulin

1999 ◽  
Vol 274 (26) ◽  
pp. 18243-18251 ◽  
Author(s):  
Vanessa Van Harmelen ◽  
Signy Reynisdottir ◽  
Katherine Cianflone ◽  
Eva Degerman ◽  
Johan Hoffstedt ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fat Cells ◽  
Acylation Stimulating Protein ◽  
Fatty Acid Release ◽  
Acid Release

Catecholamine sensitivity in brown fat cells from cold-acclimated hamsters and rats

1982 ◽  
Vol 242 (3) ◽  
pp. C250-C257 ◽  
Author(s):  
J. Nedergaard
Keyword(s):  
Oxygen Consumption ◽  
Fatty Acid ◽  
Brown Fat ◽  
Fat Cells ◽  
Fatty Acid Level ◽  
Serum Fatty Acid ◽  
Bicarbonate Buffer ◽  
Rate Of Oxygen Consumption ◽  
Fatty Acid Release ◽  
Acid Release

Brown fat cells, freshly isolated from cold-acclimated hamsters and rats, did not respond to norepinephrine addition with the characteristic increase in oxygen consumption (heat production) seen in cells from control animals. However, incubation of these cells for 1 h in a Krebs-Ringer bicarbonate buffer, in the presence of 10 mM pyruvate, fully restored norepinephrine responsiveness. Cells treated in this way from cold-acclimated hamsters (a hibernator) increased the rate of oxygen consumption after maximal norepinephrine stimulation as much as cells from control hamsters; also norepinephrine-stimulated fatty acid release was unaltered, indicating that brown fat cells may partly be responsible for the increase in serum fatty acid level seen during arousal from hibernation. Similarly, preincubated cells from cold-acclimated rats (a nonhibernator) increased oxygen consumption and fatty acid release as much as cells from control rats; this suggests that also in cold-acclimated rats brown fat may supply the circulation with fatty acids during cold stress. Cells from cold-acclimated animals were, however, about 10 times less sensitive to norepinephrine than cells from control animals; this desensitization may be the result of a stimulated phosphodiesterase.

Ouabain-sensitive fatty acid release from isolated fat cells

1966 ◽  
Vol 22 (2) ◽  
pp. 86-87 ◽  
Author(s):  
R. -J. Ho ◽  
B. Jeanrenaud ◽  
A. E. Renold
Keyword(s):  
Fatty Acid ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Fatty Acid Release ◽  
Acid Release

scholarly journals Biochemical actions of vasoactive peptide hormones. Time-synchronized activation of lipolysis and decreased fatty-acid release by bradykinin and angiotensin in the perfused rabbit kidney

1980 ◽  
Vol 192 (1) ◽  
pp. 127-131 ◽  
Author(s):  
M Schwartzman ◽  
A Raz
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Time Lag ◽  
Rabbit Kidney ◽  
Subsequent Decrease ◽  
Fatty Acid Release ◽  
Initial Activation ◽  
Acid Release ◽  
Sequential Processes ◽  
Vasoactive Peptide

Bradykinin and angiotensin administered to the isolated perfused rabbit kidney activate two sequential processes: (1) a selective release of the prostaglandin precursor arachidonate with concomitant partial conversion of the arachidonate into prostaglandin E2; (2) activation of a process that leads to decreased release of all fatty acids in the perfusate. There is a time lag of approx. 1 min between the initial activation of the arachidonate-specific deacylation reaction that is coupled to prostaglandin generation, and the subsequent decrease in the release of all fatty acids. This synchronized cycle provides for instant generation of required amounts of prostaglandins and at the same time serves to conserve cellular arachidonate.

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