scholarly journals Studies on the conversion of pyruvate into fatty acids in white adipose tissue. Effects of insulin, alloxan-diabetes and starvation

1971 ◽  
Vol 124 (3) ◽  
pp. 615-621 ◽  
Author(s):  
Mitchell L. Halperin
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Insulin Treatment ◽  
Acid Synthesis ◽  
Diabetic Rats ◽  
Epididymal Adipose Tissue ◽  
Lag Phase ◽  
Metabolic States ◽  
Normal Rat

The effect of insulin on the conversion of pyruvate into fatty acids in the presence and in the absence of glucose was studied in epididymal adipose tissue of the rat. 1. In adipose tissue from the normal rat, conversion of pyruvate into fatty acids is directly related to its concentration, the maximal rates occurring with 40mm- and the half-maximal rates with approx. 4mm-pyruvate. Insulin treatment did not greatly influence the maximal rates, but the half-maximal rates were at much lower pyruvate concentrations. This effect of insulin could be seen with physiological concentrations of this hormone (50–100μunits/ml). 2. In adipose tissue from acute-alloxan-diabetic and 36h-starved rats the conversion of pyruvate into fatty acids was almost zero until its concentration exceeded 3mm and then increased markedly as the concentration of pyruvate was increased. The lag phase of this S-shaped curve was decreased but not eliminated when insulin was present. This could account for the very low rates of glucose conversion into fatty acids in these metabolic states. Maximum rates of fatty acid synthesis were similar in the presence and in the absence of insulin, but only when 30–40mm-pyruvate was employed. Re-feeding of the starved rats or insulin treatment of the diabetic rats in vivo for several days restored these patterns to normal.

FREE FATTY ACID METABOLISM IN CHINESE HAMSTERS

1966 ◽  
Vol 44 (1) ◽  
pp. 47-57 ◽  
Author(s):  
James Campbell ◽  
G. R. Green
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Spontaneous Diabetes ◽  
Chinese Hamster ◽  
Diabetic Rats ◽  
Epididymal Adipose Tissue ◽  
Time Interval ◽  
Adipose Tissues ◽  
Chinese Hamsters

In normal Chinese hamsters (Cricetulus griseus) the mean concentration of free fatty acids (FFA) in serum varied from group to group, but was (i) consistently 4 to 9 times greater than in rats, dogs, or man; (ii) slightly higher than in Syrian hamsters; (iii) two- to four-fold higher than in fasting or alloxan-diabetic rats. The epididymal adipose tissue of the Chinese hamster (i) had initial concentrations of FFA comparable to those in the rat and Syrian hamster; (ii) released, in the same time interval, 8- to 10-fold more FFA in vitro than this tissue of the rat; (iii) had higher concentrations of FFA after incubation than the incubated tissue of the rat. The retroperitoneal (perirenal) adipose tissue of the Chinese hamster was less active in release of fatty acids in vitro than the epididymal, but was, however, more active than the epididymal adipose tissue of the rat. These characteristics of FFA metabolism in the Chinese hamster were apparently attributable to species, not to age, diet, or sex. In the Chinese hamster, the weight of the epididymal adipose tissue per gram of body was relatively high. It appears that in this species the rate of release of fatty acids from adipose tissue is great, leading to high FFA concentrations in serum.In Chinese hamster and rat adipose tissues in vitro, glucose and insulin (separately) reduced the rate of release of FFA and the amount of FFA in the tissues, but glucose and insulin together produced the greatest reductions. The net reduction in FFA release by glucose and insulin in vitro was greater in tissue from the Chinese hamster. Insulin markedly increased glucose uptake by the adipose tissues of both species. The possible relation of the results to spontaneous diabetes in the Chinese hamster is discussed.

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.

Effect of the β-adrenoceptor agonist BRL 26830 on fatty acid synthesis and on the activities of pyruvate dehydrogenase and acetyl-CoA carboxylase in adipose tissues of the rat

1989 ◽  
Vol 9 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Shelagh Wilson
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Diabetic Rats ◽  
Adipose Tissues ◽  
Adrenoceptor Agonist ◽  
Brown Adipose

BRL 26830 is a thermogenic β-adrenoceptor agonist which stimulates lipolysis and fatty acid oxidation in vivo. It also stimulates insulin secretion, and hence promotes glucose utilisation in vivo. The effect of this agent on white and brown adipose tissue of the rat was investigated. BRL 26830 increased the rate of fatty acid synthesis in vivo in white adipose tissue by 135% but reduced the rate of fatty acid synthesis in vivo in brown adipose tissue by 78%. The increase was abolished in white adipose tissue of streptozotocin-diabetic rats, indicating that the effect involved a rise in circulating insulin levels. The reduction in fatty acid synthesis in brown adipose tissues was associated with a reduction in the activity of acetyl-CoA carboxylase in the tissue consistent with a direct β-adrenoceptor-mediated effect. BRL 26830 also increased the proportion of pyruvate dehydrogenase in its active form in vivo in brown adipose tissue and this increase was abolished in streptozotocin-diabetic rats. These findings illustrate different sensitivities of white and brown adipose tissues to combined β-adrenergic and insulin stimulation.

scholarly journals Effects of insulin treatment of diabetic rats on hepatic partitioning of fatty acids between oxidation and esterification, phospholipid and acylglycerol synthesis, and on the fractional rate of secretion of triacylglycerol in vivo

1994 ◽  
Vol 304 (1) ◽  
pp. 177-182 ◽  
Author(s):  
A M B Moir ◽  
V A Zammit
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Insulin Treatment ◽  
Acid Metabolism ◽  
Diabetic Rats ◽  
Acid Oxidation ◽  
Phospholipid Synthesis ◽  
Fractional Rate

1. The hypothesis that insulin treatment of streptozotocin-diabetic rats does not alter acutely the ability of acylcarnitine synthesis to compete successfully for cytosolic long-chain acyl-CoA [Grantham and Zammit (1988) Biochem. J. 249, 409-414], was tested in vivo by using the technique of selective labelling of hepatic fatty acids in awake unrestrained rats. In the same animals, the partitioning of hepatic fatty acids between acylglycerol and phospholipid synthesis, and of newly labelled triacylglycerol between secretion into the plasma and retention in the liver, was also studied. 2. In untreated diabetic animals, the ratio of fatty acid oxidation to esterification was double that found in normal fed animals, whereas there were no differences in the values of the above-mentioned parameters of glycerolipid metabolism. Thus the insulin status of the rats only has chronic effects on specific aspects of fatty acid metabolism in the liver. 3. Treatment of diabetic rats with insulin resulted in no change in the oxidation/esterification ratio for the first 5 h after the start of insulin administration. Thereafter, there were reciprocal changes in the 14CO2 expired (an index of oxidation) and 14C label recovered in hepatic and plasma glycerolipids. However, the pattern of partitioning observed in normal fed rats was still not re-established after 8 h of insulin treatment. 4. There was a small and transient decrease in the fractional rate of triacylglycerol secretion by the liver at the start of insulin treatment and an increase in the proportion of labelled fatty acid that was utilized for phospholipid synthesis such that phospholipid labelling as a proportion of that of total glycerolipids was doubled after 8 h of insulin treatment. 5. The data are discussed in relation to the roles of insulin in mediating acute changes in hepatic fatty acid metabolism and very-low-density-lipoprotein triacylglycerol secretion by the liver.

scholarly journals Acute effects in vivo of anti-insulin serum on rates of fatty acid synthesis and activities of acetyl-coenzyme A carboxylase and pyruvate dehydrogenase in liver and epididymal adipose tissue of fed rats

1976 ◽  
Vol 160 (2) ◽  
pp. 413-416 ◽  
Author(s):  
D Stansbie ◽  
R W Brownsey ◽  
M Crettaz ◽  
R M Denton
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Pyruvate Dehydrogenase ◽  
Acid Synthesis ◽  
Epididymal Adipose Tissue ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Carboxylase Activity

Plasma insulin concentrations in fed rats were altered acutely by administration of glucose or anti-insulin serum. Rates of fatty acid synthesis in adipose tissue and liver were estimated from the incorporation of 3H from 3H2O. In the adipose tissue dehydrogenase and acetyl-CoA carboxylase were evident. In liver, although changes in rates of fatty acid synthesis were found, the initial activity of pyruvate dehydrogenase did not alter, but small parallel changes in acetyl-CoA carboxylase activity were observed.

Fatty Acid Synthesis from Pyruvate in White Adipose Tissue: the Effect of Norepinephrine

1971 ◽  
Vol 49 (6) ◽  
pp. 736-741 ◽  
Author(s):  
M. L. Halperin
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Pentose Phosphate ◽  
Epididymal Adipose Tissue ◽  
Phenazine Methosulfate ◽  
Fasted Rats ◽  
Lines Of Evidence

Pyruvate incorporation into fatty acids has been studied in epididymal adipose tissue taken from normal and 24-h-fasted rats. This rate was limited by the rate of cytoplasmic NADPH2 generation as suggested by three lines of evidence.(1) D-Glucose-12C increased pyruvate-U-14C incorporation into fatty acids threefold. This augmentation was independent of L-glycerol 3-phosphate concentrations as the level of this metabolite was not increased. Addition of lactate-U-14C to the pyruvate medium increased the tissue L-glycerol 3-phosphate levels but did not increase the rate of fatty acid synthesis.(2) Phenazine methosulfate (2 μM) inhibited pyruvate or pyruvate plus lactate (L/P = 3/1) conversion to fatty acids whilst stimulating fatty acid synthesis from glucose or lactate alone.(3) Norepinephrine stimulated pyruvate but not glucose or glucose plus pyruvate incorporation into fatty acids. This correlated with norepinephrine-induced glycogenosis and NADPH2 production in the pentose phosphate pathway. This was shown by increased 1-14CO2/6-14CO2 production from endogenously labelled glycogen and the absence of this effect in glycogen-depleted adipocytes (24-h-fasted rats).

scholarly journals Regulation of phosphoenolpyruvate carboxykinase (GTP) in adipose tissue in vivo by glucocorticoids and insulin

1976 ◽  
Vol 158 (1) ◽  
pp. 1-7 ◽  
Author(s):  
O Meyuhas ◽  
L Reshef ◽  
J M Gunn ◽  
R W Hanson ◽  
F J Ballard
Keyword(s):  
Adipose Tissue ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Enzyme Synthesis ◽  
Diabetic Rats ◽  
Epididymal Adipose Tissue ◽  
Synthesis Rate ◽  
Regulatory Systems ◽  
Liver And Kidney ◽  
Selective Increase

1. The regulation of the synthesis of phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) in epididymal adipose tissue, liver and kidney in vivo was studied immunochemically. 2. Phosphoenolpyruvate carboxykinase (GTP) synthesis in adipose tissue is increased by starvation, diabetes and noradrenaline, and decreased by re-feeding and insulin. These changes were also seen in adrenalectomized rats and are qualitatively similar to those observed for the liver enzyme. This indicates the involvement of cyclic AMP as an inducer and insulin as a de-inducer in the regulation of phosphoenolpyruvate carboxykinase (GTP) in both tissues. (Induction and de-induction are defined as selective increase and decrease respectively in the rate of enzyme synthesis, regardless of the mechanism involved.)3. Adrenalectomy had little effect on phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney, but increased the synthesis rate of the adipose-tissue enzyme. Starvation and adrenalectomy had additive effects in increasing the synthesis rate of adipose-tissue phosphoenolpyruvate carboxykinase (GTP). In adrenalectomized diabetic rats glucocorticoids increased phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney while decreasing enzyme synthesis in adipose tissue. De-induction of adipose tissue phosphoenolpyruvate carboxykinase (GTP) is therefore regulated independently by glucocorticoids and insulin. 4. Although liver, kidney and adipose-tissue phosphoenolpyruvate carboxykinases (GTP) are seemingly identical, there is an apparent tissue-specific differentiation in regulatory systems for the enzyme.

PRESS echo time behavior of triglyceride resonances at 1.5T: Detecting ω-3 fatty acids in adipose tissue in vivo

2009 ◽  
Vol 201 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Jesper Lundbom ◽  
Sami Heikkinen ◽  
Barbara Fielding ◽  
Antti Hakkarainen ◽  
Marja-Riitta Taskinen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Time Behavior ◽  
Echo Time
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