scholarly journals The selective mobilization of fatty acids is not based on their positional distribution in white-fat-cell triacylglycerols

1995 ◽  
Vol 311 (3) ◽  
pp. 911-916 ◽  
Author(s):  
T Raclot ◽  
C Leray ◽  
A C Bach ◽  
R Groscolas

Fatty acids have been shown to be selectively mobilized from rat white fat-cells, whatever the dietary manipulations. For convenience, fatty acids have been classified as being highly, weakly and moderately mobilizable. The aim of this study was to examine whether the selective mobilization of fatty acids can be explained, even partly, by their positional distribution in adipose-tissue triacylglycerols (TAG) via the known specificity of hormone-sensitive lipase for the sn-1 and sn-3 positions. Adipose tissue was dietarily manipulated in order to obtain a wide spectrum of fatty acids, including large amounts of either very-long-chain polyunsaturated fatty acids (VLC-PUFA) or very-long-chain monounsaturated fatty acids (VLC-MUFA). The determination of fatty acid distribution in adipose tissue TAG was based on random formation of 1,2-diacyl-rac-glycerols by Grignard degradation, followed by synthesis of phosphatidic acids and hydrolysis in the sn-2 position by phospholipase A2. Regardless of the fatty acid composition and location of fat depots, highly (e.g. 18:4n-3 and some of the VLC-PUFA) and weakly (e.g. VLC-MUFA) mobilizable fatty acids were located mainly in the outer (sn-1 and sn-3) positions of the glycerol moiety (79.5% and 92.5% on average, respectively). Other fatty acids, which are rather moderately mobilizable, were more randomly distributed. We conclude that the selective mobilization of white-fat-cell fatty acids is not based on their positional distribution in TAG.

1997 ◽  
Vol 322 (2) ◽  
pp. 483-489 ◽  
Author(s):  
Thierry RACLOT

Fatty acids are selectively released from white fat cells in accordance with well-defined rules relating their molecular structure and their mobilization rate, emphasizing the possible role of their physicochemical properties. Lipolysis is widely reported to work for conditions where only small amounts of substrate are available. We hypothesize that the preferential hydrolysis of a substrate fraction enriched in the most polar triacylglycerols (TAGs) reflects the pattern of selective fatty acid mobilization. Rat adipose tissue was first manipulated by dietary means to obtain a wide spectrum of fatty acids. Fat cell TAGs were separated into eight fractions according to polarity by liquid–liquid partition chromatography and their fatty acid proportions and compositions were determined by GLC. In the most polar TAG fractions, the relative enrichment of fatty acids (percentage in a TAG fraction divided by percentage in total TAGs) increased with the number of double bonds for a given chain length, whereas it decreased with increasing chain length for a given degree of unsaturation. The relative enrichment of highly mobilized fatty acids (16–20 carbon atoms and four or five double bonds) was very high (more than 2.5) in the most polar TAG fractions, whereas that of weakly mobilized fatty acids (20–24 carbon atoms and no or one double bond) was very low (less than 0.5). The relative enrichment of moderately mobilized fatty acids (comprising all the others) was close to unity. Our study shows that the relative enrichment of fatty acids in the most polar adipose tissue TAGs is consistent with their relative mobilization rates. This supports our hypothesis and raises the possibility that the molecular species of TAGs might be one of the regulating factors.


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.


1999 ◽  
Vol 1999 ◽  
pp. 115-115 ◽  
Author(s):  
A.M. Wachira ◽  
L.A. Sinclair ◽  
R.G. Wilkinson ◽  
G. Demirel ◽  
M. Enser ◽  
...  

The benefits of long chain polyunsaturated fatty acids (PUFA) to human health, especially those of the n-3 series are now widely recognised. In a previous experiment (Wachira et al. 1998) supplementing diets with whole linseed or fish oil increased n-3 fatty acid levels in lamb muscle. To raise these further the whole linseed can be treated with formaldehyde to increase protection in the rumen. Dietary antioxidants such as vitamin E can control lipid oxidation but information on their effects on lamb performance and fatty acid composition is limited. The current experiments investigated the effects of different dietary PUFA sources and vitamin E levels on growth and fatty acid composition in two sheep breeds. Detailed results of the effects of vitamin E are presented in the accompanying abstract by Enser et al.


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.


1981 ◽  
Vol 59 (1) ◽  
pp. 9-15 ◽  
Author(s):  
F. Moller ◽  
K. H. Wong ◽  
P. Green

The Mg2+-dependent phosphatidate phosphohydrolase activity increased in the microsomal and decreased in the soluble fraction of isolated rat fat cells incubated for short periods with the lipolytic hormones or agents, epinephrine, cyclic AMP, theophylline, and dibutyryl cyclic AMP. Adrenocorticotropin, on the other hand, increased not only the microsomal but also the soluble activity. The increases in microsomal activity ranged from 30 to 134% with epinephrine to almost 200% with dibutyryl cyclic AMP. The decreases in soluble activity were more modest. The effect of epinephrine was inhibited by the β-adrenergic antagonist propranolol while the α-antagonist phentolamine enhanced it. These results strongly suggest that the fat cell phosphatidate phosphohydrolase is controlled through the β-adrenergic receptor and the activity of adenylate cyclase. Lipolysis, as measured by fatty acid release, was stimulated in a similar pattern as the microsomal activity suggesting parallel activation of the hormone sensitive lipase and phosphatidate phosphohydrolase. It is speculated that the activation of this lipogenic enzyme by lipolytic stimuli may represent a mechanism whereby fatty acid release from adipose tissue may be modulated and intracellular fatty acid accumulation maybe counteracted during accelerated lipolysis in adipose tissue.


2004 ◽  
Vol 287 (2) ◽  
pp. E282-E288 ◽  
Author(s):  
Mélanie Fortier ◽  
Shu Pei Wang ◽  
Pascale Mauriège ◽  
Meriem Semache ◽  
Léandra Mfuma ◽  
...  

In white adipose tissue, lipolysis can occur by hormone-sensitive lipase (HSL)-dependent or HSL-independent pathways. To study HSL-independent lipolysis, we placed HSL-deficient mice in conditions of increased fatty acid flux: β-adrenergic stimulation, fasting, and dietary fat loading. Intraperitoneal administration of the β3-adrenergic agonist CL-316243 caused a greater increase in nonesterified fatty acid level in controls (0.33 ± 0.05 mmol/l) than in HSL−/− mice (0.12 ± 0.01 mmol/l, P < 0.01). Similarly, in isolated adipocytes, lipolytic response to CL-316243 was greatly reduced in HSL−/− mice compared with controls. Fasting for ≤48 h produced normal mobilization and oxidation of fatty acids in HSL−/− mice, as judged by similar values of respiratory quotient and oxygen consumption as in HSL+/+ controls. In isolated adipocytes, lipolysis in the absence of β-adrenergic stimulation was 1.9-fold greater in HSL−/− than in HSL+/+ cells ( P < 0.05), increasing to 6.5-fold after fasting ( P < 0.01). After 6 wk of a fat-rich diet containing 31.5% of energy as lipid, weight gain of HSL−/− mice was 4.4-fold less than in HSL+/+ mice ( P < 0.01), and total abdominal fat mass was 5.2-fold lower in HSL−/− than in HSL+/+ mice ( P < 0.01). In white adipose tissue, HSL is essential for normal acute β-adrenergic-stimulated lipolysis and permits normal triglyceride storage capacity in response to dietary fat loading. However, HSL-independent lipolysis can markedly increase during fasting, both in isolated adipocytes and in intact mice, and can mediate a normal flux of fatty acids during fasting.


1973 ◽  
Vol 40 (3) ◽  
pp. 353-360 ◽  
Author(s):  
R. W. Smith

SummaryThe incorporation of 14C from [1-14C] and [6-14C]glucose into CO2, fatty acids and glycerol by rat parametrial adipose tissue was measured at intervals during pregnancy, lactation and involution. There were small increases in the incorporation of both the C-1 and C-6 atoms into CO2 and glycerol on the seventh and sixteenth days of pregnancy. Fatty acid synthesis from glucose was negligible on the twentieth day of pregnancy and during lactation. Three days after weaning the rate of oxidation of the C-1 atom was doubled and the incorporation of both carbon atoms into fatty acids was increased at least 20-fold. There were no changes in the activities of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase during pregnancy and lactation, but 3 days after weaning the activities of both enzymes were doubled. These results are discussed in relation to other evidence that the total body fat is increased during pregnancy, and to the idea that the fat depots are mobilized during lactation.


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