Ratio of in vivo incorporation of3H arachidonic acid and14C linoleic acid into liver lipids from normal and diabetic rats

Lipids ◽  
1971 ◽  
Vol 6 (3) ◽  
pp. 203-207 ◽  
Author(s):  
Osvaldo Mercuri ◽  
Maria Elena De Tomas
1969 ◽  
Vol 47 (1) ◽  
pp. 11-17 ◽  
Author(s):  
R. L. Lyman ◽  
C. Giotas ◽  
M. A. Fosmire ◽  
P. Miljanich

Male rats fed a 9% casein-purified diet for 14 days were compared with a similar group of rats whose diet contained 0.25% DL-ethionine. At the end of the feeding period, the animals were tube fed their respective diets plus 1-14C-linoleic acid, and control and experimental rats randomly chosen were then killed 18 h and 30 h thereafter. Composition and radioactivity were determined in carcass and liver lipids. Total amounts of carcass and liver lipids did not differ among the groups, nor were there any differences in the distribution or specific activity of the carcass linoleate. Liver triglyceride of rats fed ethionine, while being no higher in concentration than that of control animals, did, however, have a higher proportion of radioactivity and more linoleic acid with a higher specific activity than did the controls. The differences were greatest at the 18-h post-feeding period. Ethionine also increased the proportion of linoleic acid and decreased that of arachidonic acid in the liver phospholipids as compared with controls. Analysis of the phosphatidylethanolamines and phosphatidylcholines showed that by the 18-h post-feeding period, the proportions of radioactivity and specific activity of arachidonic acid in both phospholipid fractions were reduced far below control values, whereas the specific activity of linoleic acid was high and similar for all groups. However, by 30 h after administration of the labeled linoleic acid, specific activities, but not the distribution of the label, had returned to normal ranges. From the results it was concluded that the liver phospholipid fatty acid patterns seen in rats fed ethionine were a consequence of an impairment by the analogue in the normal utilization and conversion of linoleic acid to arachidonic acid.


1987 ◽  
Author(s):  
E Bastida ◽  
L Almirall

We and others reported that endothelial cells (ECs) convert linoleic acid into 13-hydroxyoctadecadienoic acid (13-H0DE) under basal conditions, and arachidonic acid into 15-hydroxyeicosatet-raenoic acid (15-HETE) following stimulation (1,2). We also reported that lipoxygenase metabolism influenced platelet (PLT) interactions with ECs, tumor cells (TCs) and extracellular matrix (BM) (1,3,4). Thus, we performed studies to determine i) if TCs also produce 13-H0DE and HETEs, and ii) the effect of TC and EC 13-H0DE and HETEs synthesis on TC/EC adhesion. We measured i) the ratios of 13-H0DE:HETE in 5TC lines, under basal and stimulated conditions, in metastatic and non-metastatic TCs of the same cell line, and TCs treated with salicylate (SAL) or dipyridamole (DIP), and ii) their relationships with TC adhesion to ECs and BM. 13-H0DE and HETEs were assayed by HPLC. TC adhesion was assayed as the # radiolabelled TCs adherent to ECs or BM. cAMP was assayed by RIA. Under basal conditions, TCs produced 13-H0DE and HETEs, the intracellular ratio of which markedly affected their adhesivity; e.g. the least adhesive TC (U87MG glioblastoma) produced 21Xs more 13-H0DE than HETE’s, while a more adhesive TC (A549, adenocarcinoma) produced 4Xs more HETEs than 13-H0DE. Non-metastatic TCs preferentially produced 13-H0DE while metastatic TCs of the same cell line, produced HETEs. Stimulation of TCs or ECs decreased 13-H0DE, and increased HETE synthesis and TC/EC adhesion. Inhibiting intracellular 13-H0DE synthesis in either TCs or EC (SAL RX) enhanced TC/EC and TC/BM adhesion. Enhancing 13-H0DE synthesis by elevating cAMP (DIP RX) inhibited TC/EC and TC/BM adhesion. We conclude that 1) in vitro TCs produce 13-H0DE and HETEs, 2) the ratio of 13-H0DE:HETEs in TCs and ECs affects their adhesivity; and 3) the ratio of intracellular 13-H0DE:HETEs depends upon cAMP. This suggests that 13-H0DE:HETE ratios in TCs and ECs influence the adhesion process in the pathogenesis of thrombosis and metastasis in vivo. (1) Buchanan et al, JBC 30:1985. (2) Hopkins et al, JBC 29:1984. (3) Bastida et al, Int. J. Cane. 1987. (4) Buchanan et al, Prost. Leuk. Med., 1986.


2017 ◽  
Vol 5 (1) ◽  
pp. 22-28
Author(s):  
Nazi Aghaalikhani ◽  
Mohammad Taghi Goodarzi ◽  
Zeinab Latifi ◽  
Azam Rezaei Farimani ◽  
Amir Fattahi

Background: Several studies have shown association of fatty acids with type 2 diabetes (T2D), as well as metformin effects on blood glucose concentrations through affecting lipid metabolism. Objectives: Since the exact therapeutic mechanism of metformin is not clear, in this study we investigated effects of different doses of metformin on serum fatty acids in rats with T2D. Materials and Methods: Twenty-five adult albino male Wistar rats were divided into the following groups: Healthy, untreated T2D, and T2D rats receiving metformin for 4 weeks with doses of 100, 150, and 200 mg/kg/d. Serum insulin and triglyceride (TG) were measured using commercial kits. Serum total lipids were extracted by the Bligh-Dyer method and then compositions of fatty acids were evaluated using gas chromatograph. Results: Monounsaturated fatty acid (MUFA) levels in T2D rats were lower than those in healthy rats (P < 0.05). We also observed that diabetic rats treated with 100 or 150 mg/kg/d of metformin had higher levels of arachidonic acid and polyunsaturated fatty acids (PUFA) in comparison with the healthy group (P < 0.05). Moreover, the T2D+Met (150 mg/kg) group showed increased levels of MUFA compared with the T2D group. Such a difference was seen in levels of arachidonic acid between the T2D+Met 100 mg/ kg group and untreated T2D group. In the group treated with high doses of metformin (200 mg/kg/d), levels of palmitic acid, palmitoleic acid, and saturated fatty acid (SFA) were higher and levels of oleic acid, linoleic acid, arachidonic acid, MUFA, PUFA, and also SFA/UFA ratio were lower compared with other metformin treated and untreated groups (P < .05). In untreated T2D group, there were positive correlations between glucose levels and linoleic acid and PUFA levels (r = 0.707, P = .049 and r = 0.726, P = .041 respectively). Arachidonic acid levels were positively correlated with glucose levels in T2D rats treated with 100 mg/kg/d of metformin (r = 0.969, P = .031). Conclusions: Our study showed that different doses of metformin could have different effects on serum levels of saturated and unsaturated fatty acids, as 200 mg/kg/d of metformin could increase and decrease saturated and unsaturated fatty acids respectively, while lower doses increased unsaturated fatty acids, particularly arachidonic acid.


1999 ◽  
Vol 60 (5-6) ◽  
pp. 407-410 ◽  
Author(s):  
N. Salem ◽  
R. Pawlosky ◽  
B. Wegher ◽  
J. Hibbeln

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