Search results for: Arachidonic Acid100 mg
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Conjugated linoleic acid inhibits proliferation but stimulates lipid filling of murine 3T3-L1 preadipocytes.
This study documented the effects of conjugated linoleic acid (CLA) on the proliferation and differentiation of 3T3-L1 preadipocytes. During proliferation, preadipocytes were cultured in Dulbecco's modified Eagle's medium (DMEM), 100 g/L fetal bovine serum (FBS), 0. 584 g/L L-glutamine and 0 (control), 0.5, 1.0, 5.0 or 10.0 mg/L CLA. Proliferation of 3T3-L1 preadipocytes was measured directly by cell counting and indirectly by radiolabeled thymidine incorporation into DNA at 96 h postinoculation. Conjugated linoleic acid was not cytotoxic during proliferation or differentiation. The 0.5, 1.0, 5.0 or 10.0 mg/L CLA treatments inhibited proliferation by 8, 12, 31 and 36%, respectively (all P < 0.05). Treatment with 10 mg/L CLA or 10 mg/L linoleic acid (cis-9,12) reduced the incorporation of 3H-thymidine into DNA by 56 and 35%, respectively, suggesting that some portion of the effect of CLA on preadipocyte proliferation was nonspecific. After the initiation of differentiation, preadipocytes were cultured in DMEM, 100 g/L FBS, 0.584 g/L L-glutamine, 1.7 micromol/L insulin and 0 (control), 0.5, 1.0, 5.0 or 10.0 mg/L CLA. Radiolabeled glucose incorporation into cellular lipids was increased from 7.4 to 11.1, 11.1, 17.4 and 22.5 nmol/(h.10(6 )cells) (all P < 0.05) by 0.5, 1.0, 5.0 and 10.0 mg/L CLA, respectively. A media concentration of 10 mg/L CLA increased total cellular CLA (from 0 to 0.16 +/- 0.01 micromol/10(6 )cells), palmitic acid (from 0.47 to 1.10 +/- 0.03 micromol/10(6 )cells) and palmitoleic acid (from 0.24 to 0.81 +/- 0.03 micromol/10(6 )cells) (means +/- pooled SEM; all P < 0.05). Conjugated linoleic acid had no effect on arachidonic acid content, but decreased its proportion (g arachidonic acid/100 g total fatty acids) by >50% (P < 0.05). These data indicate that CLA inhibited proliferation and promoted de novo lipogenesis and lipid filling in 3T3-L1 preadipocytes, suggesting that CLA may reduce overall fat accumulation in growing animals by inhibiting stromal vascular preadipocyte hyperplasia.D L Satory, S B Smith
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Does an increase in dietary linoleic acid modify tissue concentrations of cervonic acid and consequently alter alpha-linolenic requirements? Minimal requirement of linoleic acid in adult rats.
Rats were fed a control diet containing both linoleic and alpha-linolenic acid. When 60-days-old they were divided into 8 groups, each receiving the same amount of alpha-linolenic acid, but varying amounts of linoleic acid. When the (n-6)/(n-3) ratio in the diet varied from 2 to 32 (with a constant amount of 150 mg alpha-linolenic acid per 100 g diet), tissue levels of the (n-3) series fatty acids were not significantly modified, except in the liver, heart and testes. In all organs studied, the saturated and monounsaturated fatty acids were practically unchanged. For the (n-6) series fatty acids, arachidonic acid was not significantly affected, in muscle, kidney, brain, myelin, nerve-endings or sciatic nerve, whatever the quantity of linoleic acid in the diet. In liver, arachidonic acid plateaued at 2400 mg linoleic acid/100 g diet and at 400 mg/100 g diet in heart. Results for 22:5(n-6) showed a marked increase in heart, a moderate increase in liver and kidney, and no effect in muscle, testes, brain, myelin, nerve-endings or sciatic nerve. This experiment defined the minimum amount of linoleic acid required in the diet to maintain fatty acids of the linoleic family in the young adult rat. For the first time it was demonstrated that 1200 mg/100 g diet are sufficient for the liver, as evidenced by maintenance of the arachidonic acid concentration. For the other organs, there is either a very marked preservation of this acid, or the dietary level is less than 300 mg/100 g diet. For the essential fatty acid precursors (i.e. linoleic and alpha-linolenic acids), the optimal (n-6)/(n-3) ratio required in the diet is about 8.J M Bourre, O Dumont, G Durand