Age-related changes in linoleic acid bioconversion by isolated hepatocytes from spontaneously hypertensive and normotensive rats

Narce, Michel; Asdrubal, Philippe; Delachambre, Marie-Claire; Véricel, Evelyne; Lagarde, Michel; Poisson, Jean‐Pierre

doi:10.1007/bf00935585

Cited by 18 publications

(9 citation statements)

References 24 publications

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“…Nonetheless, the use of a product to precursor ratio (like AA/LA ratio or EPA/ALA ratio) as a surrogate measure to estimate desaturase activity is well established [44] . Thus, indirect information can be gathered from the analysis of membrane lipid composition in red blood cells that provide a simple, suitable model for studying the fatty acid metabolism.…”

Section: How To Estimate the Desaturase Activity In Vivo? A Product Tmentioning

confidence: 99%

“…Desaturase activity is assayed in vitro or in animals by measuring the rate of the conversion of radiolabeled precursor fatty acids to their respective products [44] , but ethical and practical reasons prevent this possibility in humans. Nonetheless, the use of a product to precursor ratio (like AA/LA ratio or EPA/ALA ratio) as a surrogate measure to estimate desaturase activity is well established [44] .…”

Section: How To Estimate the Desaturase Activity In Vivo? A Product Tmentioning

confidence: 99%

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A ‘Desaturase Hypothesis’ for Atherosclerosis: Janus-Faced Enzymes in ω–6 and ω–3 Polyunsaturated Fatty Acid Metabolism

Martinelli

Consoli

Olivieri³

2009

Lifestyle Genomics

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The delta-5 and delta-6 desaturases are key enzymes in the metabolism of omega-3 (ω–3) and omega-6 (ω–6) polyunsaturated fatty acids (PUFA), which in turn influence cellular functions by regulating several metabolic pathways with well-known effects on the cardiovascular system. At present, data about desaturase activity and cardiovascular risk remain inconclusive. In this short review we propose a ‘desaturase hypothesis’ of atherosclerosis, providing suggestions for the Janus-faced role of desaturases, with both more favorable (mainly related to ω–3 long-chain fatty acids) and more harmful (mainly related to ω–6 long-chain fatty acids) cardiovascular effects than those obtained in subjects with lower desaturase activity. In particular in populations eating a Western diet rich in ω–6 PUFA, a high desaturase activity may promote an increased bioavailability of arachidonic acid with prevailing synthesis of arachidonic acid-derived proinflammatory eicosanoids, finally favoring atherosclerotic vascular damage. In contrast, high desaturase activity in subjects consuming a diet rich in ω–3 PUFA or receiving ω–3 PUFA supplementation could result in the opposite situation with a preferential synthesis of anti-inflammatory eicosanoids. For these reasons, carriers of specific FADS haplotypes may be predisposed to more pronounced vascular inflammatory damage, but also to an increased beneficial effect with ω–3 PUFA supplementation.

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Section: How To Estimate the Desaturase Activity In Vivo? A Product Tmentioning

confidence: 99%

Section: How To Estimate the Desaturase Activity In Vivo? A Product Tmentioning

confidence: 99%

A ‘Desaturase Hypothesis’ for Atherosclerosis: Janus-Faced Enzymes in ω–6 and ω–3 Polyunsaturated Fatty Acid Metabolism

Martinelli

Consoli

Olivieri³

2009

Lifestyle Genomics

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“…Both humans and animals suffering from genetic hypertension have abnormal fatty acid metabolism (1)(2)(3)(4)(5)(6)(7). The synthesis of polyunsaturated fatty acids (PUFA) in the liver of spontaneously hypertensive rats (SHR) differs significantly from that of normotensive Wistar Kyoto (WKY) rats, depending on the age of the animals and the pathogenesis of hypertension (7)(8)(9). The activities of liver microsomal desaturases, which are key enzymes in PUFA synthesis, are greatly reduced, and this becomes more severe once the rats are hypertensive (after 3 mon of age) than during the prehypertensive period.…”

mentioning

confidence: 99%

Changes in tissue polyunsaturated fatty acids with age, in spontaneously hypertensive rats

Delachambre

Narce

Asdrubal

et al. 1998

Lipids

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The relationship between the biosynthesis of long-chain fatty acids and their distribution in the key organs of hypertension is of considerable interest because of their role in the production of vasoactive eicosanoids and their effects on membrane properties. The present study analyzed the fatty acid compositions of the total lipids in the kidney, aorta, heart, and hepatocytes of 1-, 3-, and 6-mon-old spontaneously hypertensive rats (SHR) and their normotensive controls, Wistar Kyoto rats (WKY) by capillary gas chromatography . The major changes concerned the polyunsaturated fatty acids (PUFA). The percentage of arachidonic acid (AA) was significantly greater in the 1-mon-old SHR kidney than in the WKY kidney, but it was lower at 3 and 6 mon. The percentage of eicosapentaenoic acid was very low in the SHR kidney. The results for the aorta were similar, with marked decreases in 18:2n-6 and 18:3n-3 in SHR aged 1 and 6 mon. Despite a higher proportion of 18:2n-6 and AA at 6 mon, there was no major change in the SHR heart lipids. The fatty acid spectrum in the liver provides additional evidence for the previously reported inhibition of desaturase activities in SHR. Thus, this study shows that the PUFA composition is modified differently in different tissues in SHR, and this may be related to the pathogenesis of hypertension in these animals.

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“…Enzyme activities have been expressed as pmol/10 6 cells. The hepatocyte fatty acid composition was analyzed as described previously (Narce et al, 1994).…”

Section: Desaturase Activity Measurementsmentioning

confidence: 99%

“…On the other hand, ethanol has been shown to induce hypertension in normotensive Wistar Kyoto (WKY) rats (Vasdev et al, 1993a,b). Previously, we studied the hepatocyte conversion of essential fatty acids (EFA) during hypertension (Narce et al, 1994) and showed that liver fatty acid composition was related to an impairment of n-6 PUFA metabolism in SHR. This impairment of desaturase activities was greater when blood pressure increased and was related to the age of the animals.…”

mentioning

confidence: 99%

Effect of Ethanol on Polyunsaturated Fatty Acid Biosynthesis in Hepatocytes From Spontaneously Hypertensive Rats

Narce

Poisson

Bellenger

et al. 2001

Alcoholism Clin & Exp Res

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Our study showed that hepatocyte PUFA biogenesis is dependent on ethanol concentration. Ethanol strongly inhibits the synthesis of PUFA in hepatocytes from SHR, which can explain the deficit of prostaglandin precursors observed in cardiovascular diseases linked to ethanol intoxication. n-3 PUFA supplemented diet reinforces the inhibition of arachidonic acid synthesis, likely by a substrate competition toward Delta5 desaturation. This in vitro approach provides a better understanding of the effects of ethanol on fatty acid metabolism in relation to hypertension.

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Age-related changes in linoleic acid bioconversion by isolated hepatocytes from spontaneously hypertensive and normotensive rats

Cited by 18 publications

References 24 publications

A ‘Desaturase Hypothesis’ for Atherosclerosis: Janus-Faced Enzymes in ω–6 and ω–3 Polyunsaturated Fatty Acid Metabolism

A ‘Desaturase Hypothesis’ for Atherosclerosis: Janus-Faced Enzymes in ω–6 and ω–3 Polyunsaturated Fatty Acid Metabolism

Changes in tissue polyunsaturated fatty acids with age, in spontaneously hypertensive rats

Effect of Ethanol on Polyunsaturated Fatty Acid Biosynthesis in Hepatocytes From Spontaneously Hypertensive Rats

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