Adipose tissue in experimental nephrotic syndrome

1963 ◽  
Vol 205 (4) ◽  
pp. 702-706 ◽  
Author(s):  
Alisa Gutman ◽  
Eleazar Shafrir
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Nephrotic Syndrome ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Lipoprotein Lipase ◽  
Epididymal Adipose Tissue ◽  
Adequate Nutrition ◽  
Defective Metabolism ◽  
Inadequate Food Intake

Epididymal adipose tissue of aminonucleoside-treated rats, investigated 3 to 6 days after induction of the nephrotic syndrome, had low glycogen levels and showed impaired esterification of free fatty acids and assimilation of lipoprotein triglyceride and markedly reduced liberation of lipoprotein lipase. These results were found to be influenced by the inadequate food intake of the acutely nephrotic animals and comparable to the values of control rats fasted for 2 days. On return to adequate nutrition, which occurred 12–20 days after aminonucleoside treatment, adipose tissue glycogen and free fatty acid assimilation returned toward normal levels but lipoprotein-lipase liberation remained below normal. In rats rendered nephrotic by antikidney serum, the assimilation of free fatty acids and lipoprotein-triglyceride by adipose tissue was impaired in spite of only minor reduction in food consumption. The results indicate that the defective metabolism of adipose tissue in nephrotic animals may be contributory to the nephrotic hypertriglyceridemia.

CONVERSION OF METHIONINE AND THREONINE TO FATTY ACIDS BY ADIPOSE TISSUE

1963 ◽  
Vol 41 (1) ◽  
pp. 269-273 ◽  
Author(s):  
D. D. Feller ◽  
E. Feist
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Epididymal Adipose Tissue

Epididymal adipose tissue was incubated with uniformly labelled (14C)-methionine, (2-14C)-methionine, and uniformly labelled (14C)-threonine. Each of these compounds is actively metabolized by adipose tissue, as evidenced by the generation of 14CO2 and (14C)-fatty acid. Evidence was gathered in regard to the intermediary pathways by which these amino acids are utilized by adipose tissue and the general conclusion is drawn that these pathways are similar to those postulated for other tissues. These experiments further emphasize the central role that propionate plays in adipose tissue lipogenesis.

Hydrolysis of long-chain, n-3 fatty acid enriched chylomicrons by cardiac lipoprotein lipase

1999 ◽  
Vol 77 (10) ◽  
pp. 813-818 ◽  
Author(s):  
Ryna Levy ◽  
Gene R Herzberg
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Docosahexaenoic Acid ◽  
Stearic Acid ◽  
Eicosapentaenoic Acid ◽  
Free Fatty Acids ◽  
Lipoprotein Lipase ◽  
Alpha Linolenic Acid ◽  
Hydrolysis Of ◽  
Long Chain

The hydrolysis of chylomicrons enriched in long-chain n-3 fatty acids by cardiac lipoprotein lipase was studied. In 60 min, 24.8% of the triacylglycerol fatty acids were released as free fatty acids. The fatty acids were hydrolyzed at different rates. DHA (docosahexaenoic acid, 22:6n-3) and EPA (eicosapentaenoic acid, 20:5n-3) were released at rates significantly less than average. Stearic acid (18:0), 20:1n-9, and alpha-linolenic acid (18:3n-3) were released significantly faster than average. There was no relationship between the rate of release of a fatty acid and the number of carbons or the number of double bonds. Lipoprotein lipase selectively hydrolyzes the fatty acids of chylomicron triacylglycerols. This selectively will result in remnants that are relatively depleted in 18:0, 20:1, and 18:3 and relatively enriched in 20:5 and 22:6.Key words: lipoprotein lipase, chylomicrons, fish oil, eicosapentaenoic acid, docosahexaenoic acid.

The 1990 Borden Award Lecture Dietary regulation of fatty acid and triglyceride metabolism

1991 ◽  
Vol 69 (11) ◽  
pp. 1637-1647 ◽  
Author(s):  
Gene R. Herzberg
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipoprotein Lipase ◽  
Fatty Acid Synthesis ◽  
Dietary Fat ◽  
Acid Synthesis ◽  
Fish Oils ◽  
Dietary Fish

The level of circulating triacylglycerols is determined by the balance between their delivery into the plasma and their removal from it. Plasma triacylglycerols are derived either from dietary fat as chylomicrons or from endogenous hepatic synthesis as very low density lipoproteins. Their removal occurs through the action of lipoprotein lipase after which the fatty acids are either stored in adipose tissue or oxidized, primarily in skeletal muscle and heart. The composition of the diet has been shown to influence many of these processes. Hepatic fatty acid synthesis and triacylglycerol secretion are affected by the quantity and composition of dietary fat, carbohydrate, and protein. Polyunsaturated but not saturated fats reduce hepatic fatty acid synthesis by decreasing the amount of the lipogenic enzymes needed for de novo fatty acid synthesis. Dietary fish oils are particularly effective at reducing both fatty acid synthesis and triacylglycerol secretion and as a result are hypotriacylglycerolemic, particularly in hypertriacylglycerolemic individuals. In addition, dietary fish oils can increase the oxidation of fatty acids and lead to increased activity of lipoprotein lipase in skeletal muscle and heart. It appears that the hypotriacylglycerolemic effect of dietary fish oils is mediated by effects on both synthesis and removal of circulating triacylglycerols.Key words: lipid, fish oil, fructose, liver, adipose tissue, oxidation.

Correlation Between Release of Individual Free Fatty Acids and Fatty Acid Composition of Adipose Tissue.

1966 ◽  
Vol 122 (4) ◽  
pp. 1276-1279 ◽  
Author(s):  
J. J. Spitzer ◽  
H. Nakamura ◽  
M. Gold ◽  
H. Altschuler ◽  
M. Lieberson
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Acid Composition

LIPOGENESIS IN ADIPOSE TISSUE OF MEAL-FED RATS: A POSSIBLE REGULATORY ROLE OF α-GLYCEROPHOSPHATE FORMATION

1967 ◽  
Vol 45 (2) ◽  
pp. 201-214 ◽  
Author(s):  
Gilbert A. Leveille
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Incubation Medium ◽  
Control Mechanism ◽  
Acid Synthesis ◽  
Fatty Acyl ◽  
Epididymal Adipose Tissue ◽  
Malic Dehydrogenase

The incorporation of acetate-1-14C into fatty acids by isolated epididymal adipose tissue of fed and fasted rats adapted to a single daily 2-hour meal (meal eaters) or fed ad libitum (nibblers) was investigated. Fasting (22 hours) markedly depressed lipogenesis whereas fatty acid synthesis increased linearly with time of refeeding in meal-fed but not in nibbling rats. The activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and NADP-malic dehydrogenase in adipose tissue of meal-fed or nibbling rats were not altered as a consequence of a 22-hour fast or of subsequent feeding for 2 hours. The incorporation of acetate-1-l4C into fatty acids by adipose tissue of fasted meal-eating or nibbling animals was markedly enhanced by the addition of unlabeled pyruvate or oxaloacetate to the incubation medium. This stimulatory effect was not observed with adipose tissue front fed meal-eating rats. The addition of unlabeled glucose and insulin to the incubation medium markedly enhanced acetate-1-14C incorporation into fatty acids by isolated adipose tissue and completely overcame any effect of fasting. Adipose tissue converted pyruvate-1-14C, -2-14C, or -3-14C to fatty acids and glyceride-glycerol. The results obtained are consistent with the functioning of a pathway in adipose tissue involving mitochondrial carboxylation of pyruvate to oxaloacetate, and equilibration of the newly formed oxaloacetate with malate and fumarate, followed by cytoplasmic conversion of oxaloacetate to phosphoenol pyruvate. The data are interpreted to support a control mechanism in which fatty acid synthesis is inhibited by tissue fatty acids and fatty acyl-CoA derivatives. The inhibition could in turn be reduced by the availability of α-glycerophosphate, for the esterification of fatty acids. This control mechanism is proposed as the explanation for the refeeding response observed in adipose tissue of meal-fed rats.

THE STIMULATING EFFECTS OF ADRENALINE AND ANTERIOR PITUITARY HORMONES ON THE RELEASE OF FREE FATTY ACIDS FROM ADIPOSE TISSUE

1962 ◽  
Vol 25 (2) ◽  
pp. 189-198 ◽  
Author(s):  
R. M. BUCKLE
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Pituitary Hormones ◽  
Thyroid Stimulating Hormone ◽  
Adrenocorticotrophic Hormone ◽  
Fat Pads

SUMMARY The quantity of free fatty acids (FFA) released from rat epididymal fat pads in vitro and their concentration within the tissue were determined. The addition of adrenaline, adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH) and growth hormone (GH) each increased the release of FFA, and their respective minimum effective concentrations were 0·125, 0·004, 0·5 and 1·25 μg./ml. of medium. In every case, the increased release of FFA was associated with a rise in the quantity present within the pads, and the amount released closely paralleled their concentration within the tissue. It is suggested that the stimulatory effect of all four hormones on the release of FFA from adipose tissue is largely a manifestation of their activity of increasing the concentration of FFA within the cells, and this they do by facilitating the net conversion of storage triglyceride to fatty acid. The significance of the relative activities of the hormones in vitro is discussed and compared with their fatty acid mobilizing effects in vivo.

Lipogenesis in the sand rat (Psammomys obesus)

1983 ◽  
Vol 244 (5) ◽  
pp. E480-E486 ◽  
Author(s):  
B. Kalderon ◽  
J. H. Adler ◽  
E. Levy ◽  
A. Gutman
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthetase ◽  
Epididymal Adipose Tissue ◽  
Albino Rats ◽  
Hepatic Lipogenesis ◽  
Very Low Density Lipoproteins ◽  
Sand Rat

Synthesis of fatty acids was measured in the liver and in epididymal adipose tissue of sand rats and albino rats. In chow-fed sand rats the rate of hepatic lipogenesis, as measured by the incorporation of 3H2O into fatty acids, was four- to sevenfold higher than in albino rats and in sand rats on a low-calorie saltbush diet. The contribution of [14C]glucose to lipogenesis in sand rat liver was lower than in albino rats. In fed sand rats lipogenesis incorporating 3H2O was stimulated by casein but not by glucose. In adipose tissue, lipogenesis measured 1 h after administration of 3H2O was much lower in sand rats than in albino rats. In vitro incorporation of [14C]glucose or acetate into adipose tissue fatty acids was negligible. In adipose tissue, uptake of very-low-density lipoproteins (VLDL) and lipoprotein lipase activity were sevenfold higher than in albino rats. Activities of NADP-malate dehydrogenase, acetyl CoA carboxylase, and fatty acid synthetase were considerably higher in the liver of chow-fed sand rats than in albino rats. It was concluded that obesity in sand rats originates from hepatic lipogenesis without a significant contribution of local fatty acid synthesis in adipose tissue.

Removal and mobilization of individual free fatty acids in dogs

1962 ◽  
Vol 202 (2) ◽  
pp. 370-374 ◽  
Author(s):  
Harvey I. Miller ◽  
Martin Gold ◽  
John J. Spitzer
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Thoracic Duct Lymph ◽  
Similar Distribution ◽  
Arterial Blood ◽  
Oleic And Linoleic Acids

Plasma free fatty acids were determined chemically and by gas chromatography in different anatomical sites. The myocardium removed palmitic and oleic acids and lesser amounts of stearic and linoleic acids. Electrically stimulated skeletal muscle took up oleic acid in greatest quantities. Liver showed consistent removal of stearic, oleic, and linoleic acids and an occasional uptake of other acids. The splanchnic area did not remove or mobilize free fatty acids. The composition of free fatty acids in thoracic duct lymph was similar to that in arterial blood, with the exception of a higher percentage of linoleic and possibly oleic acid. The total and free fatty acid fractions of the inguinal subcutaneous adipose tissue showed a similar distribution of fatty acids. Both were relatively high in oleic and linoleic acids. Free fatty acid released by adipose tissue had a lower oleic and linoleic acid content than that present in the cell.

scholarly journals Lipoprotein lipase and the disposition of dietary fatty acids

1998 ◽  
Vol 80 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Barbara A. Fielding ◽  
Keith N. Frayn
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Dietary Fatty Acids ◽  
The Body ◽  
Acid Uptake ◽  
Peripheral Tissues

Lipoprotein lipase (EC 3.1.1.34; LPL) is a key enzyme regulating the disposal of lipid fuels in the body. It is expressed in a number of peripheral tissues including adipose tissue, skeletal and cardiac muscle and mammary gland. Its role is to hydrolyse triacylglycerol (TG) circulating in the TG-rich lipoprotein particles in order to deliver fatty acids to the tissue. It appears to act preferentially on chylomicron-TG, and therefore may play a particularly important role in regulating the disposition of dietary fatty acids. LPL activity is regulated according to nutritional state in a tissue-specific manner according to the needs of the tissue for fatty acids. For instance, it is highly active in lactating mammary gland; in white adipose tissue it is activated in the fed state and suppressed during fasting, whereas the reverse is true in muscle. Such observations have led to the view of LPL as a metabolic gatekeeper, especially for dietary fatty acids. However, closer inspection of its action in white adipose tissue reveals that this picture is only partially true. Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow. LPL appears to act as one member of a series of metabolic steps which are regulated in a highly coordinated manner. In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL. This involves regulation of the pathway of fatty acid uptake and esterification, and appears to be regulated by a number of factors including insulin, acylation-stimulating protein and possibly leptin.

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