ESTERIFICATION OF INTRA- AND EXTRA-CELLULAR FREE FATTY ACIDS BY RAT ADIPOSE TISSUE

1965 ◽  
Vol 43 (6) ◽  
pp. 635-645 ◽  
Author(s):  
David Rubinstein ◽  
Anna M. Daniel ◽  
Lydia Lechter ◽  
John C. Beck

The esterification of intracellular and extracellular FFA by rat adipose tissue in vitro was investigated. The rate of incorporation of FFA into neutral lipids was proportional to the FFA concentration in the incubation medium. Both in the presence and absence of a lipolytic agent (epinephrine), heptadecanoate-1-C14, which is not specifically diluted by tissue fatty acids, was esterified in the same manner as palmitate-9,10-H3. Stearate, palmitate, and oleate were esterified at similar rates by adipose tissue taken from fed animals and incubated with glucose. The rate of esterification of one fatty acid was not significantly affected by the presence of another. Similar results were obtained when tissues were taken from fasted animals and incubated in the absence of glucose, except that the overall rate of esterification was diminished and FFA accumulated in the tissue. It is concluded that long-chain fatty acids do not compete for esterification or entry into the adipose tissue cell.In some experiments tissue FFA esterification was studied by measuring the incorporation of glucose-U-C14 carbons into glyceride–glycerol. Esterification, assayed in this manner, increased when albumin was present in the incubation medium and allowed FFA to diffuse from the tissue. However, pre-incubation of adipose tissue in medium containing labelled FFA indicates that much of the intracellular FFA may be esterified without its mixing with the extracellular FFA pool.

1968 ◽  
Vol 106 (1) ◽  
pp. 179-183 ◽  
Author(s):  
W. G. Duncombe

1. The use of labelled acetate for studying the synthesis of long-chain fatty acids in rat adipose tissue in vitro has been examined, with special reference to the effect of acetate concentration. 2. The incorporation of acetate into fatty acids is proportional to the concentration of acetate in the medium when the latter does not exceed about 10μm. Above this concentration, the relative incorporation becomes progressively less, and reasons for this are discussed. 3. In particular it is shown that this is not necessarily due to disturbance of the endogenous rate of fatty acid synthesis by a relatively large amount of acetyl-CoA derived from added acetate. 4. However, to ensure that the added acetate does not cause such a disturbance its concentration must be kept sufficiently low. For labelled acetate used under present conditions, this concentration should not be more than about 10μm.


1961 ◽  
Vol 200 (4) ◽  
pp. 847-850 ◽  
Author(s):  
Judith K. Patkin ◽  
E. J. Masoro

Cold acclimation is known to alter hepatic lipid metabolism. Liver slices from cold-acclimated rats have a greatly depressed capacity to synthesize long-chain fatty acids from acctate-1-C14. Since adipose tissue is the major site of lipogenic activity in the intact animal, its fatty acid synthetic capacity was studied. In contrast to the liver, it was found that adipose tissue from the cold-acclimated rat synthesized three to six times as much long-chain fatty acids per milligram of tissue protein as the adipose tissue from the control rat living at 25°C. Evidence is presented indicating that adipose tissue from cold-acclimated and control rats esterify long-chain fatty acids at the same rate. The ability of adipose tissue to oxidize palmitic acid to CO2 was found to be unaltered by cold acclimation. The fate of the large amount of fatty acid synthesized in the adipose tissue of cold-acclimated rats is discussed.


FEBS Letters ◽  
1974 ◽  
Vol 49 (1) ◽  
pp. 65-69 ◽  
Author(s):  
P. Zumstein ◽  
J. Zapf ◽  
E.R. Froesch

2007 ◽  
Vol 48 (10) ◽  
pp. 2236-2246 ◽  
Author(s):  
Jan Polak ◽  
Cédric Moro ◽  
David Bessière ◽  
Jindra Hejnova ◽  
Marie A. Marquès ◽  
...  

1985 ◽  
Vol 71 (2-3) ◽  
pp. 301-306 ◽  
Author(s):  
Tetsuo Sakai ◽  
Yasunobu Antoku ◽  
Ikuo Goto ◽  
Jun Ochiai ◽  
Hiroshi Iwashita ◽  
...  

2000 ◽  
Vol 350 (1) ◽  
pp. 93-98 ◽  
Author(s):  
Chantal JEHL-PIETRI ◽  
Claire BASTIE ◽  
Isabelle GILLOT ◽  
Serge LUQUET ◽  
Paul A. GRIMALDI

Nutritional long-chain fatty acids control adipose tissue mass by regulating the number and the size of adipocytes. It is now established that peroxisome-proliferator-activated receptors (PPARs) play crucial functions in the control of gene expression and the level of cell differentiation. PPARγ, which is activated by specific prostanoids, is a key factor in activating terminal differentiation and adipogenesis. We have recently demonstrated that PPARδ, once activated by fatty acids, drives the expression of a limited set of genes, including that encoding PPARγ, thereby inducing adipose differentiation. Thus far, the mechanism of action of fatty acids in the control of preadipocyte proliferation has remained unknown. We show here that PPARδ is directly implicated in fatty acid-induced cell proliferation. Ectopic expression of PPARδ renders 3T3C2 cells capable of responding to treatment with long-chain fatty acids by a resumption of mitosis, and this effect is limited to a few days after confluence. This response is restricted to PPARδ activators and, for fatty acids, takes place within the range of concentrations found to trigger differentiation of preadipocytes both in vitro and in vivo. Furthermore, the use of a mutated inactive PPARδ demonstrated that transcriptional activity of the nuclear receptor is required to mediate fatty acid-induced proliferation. These data demonstrate that PPARδ, as a transcription factor, is directly implicated in fatty acid-induced proliferation, and this could explain the hyperplastic development of adipose tissue that occurs in high-fat-fed animals.


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