Essential fatty acids in the liver and adipose tissue of genetically obese mice: effect of supplemental linoleic and γ-linolenic acids

Cunnane, Stephen C.; Manku, M.S.; Horrobin, David F.

doi:10.1079/bjn19850053

Cited by 17 publications

(11 citation statements)

References 22 publications

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“…Contributions of AA to plasma and tissue phospholipid fatty acids were lower in obese Zucker rats (fa/fa) than in lean (fa/-) animals (Guesnet et al, 1990). In contrast, increased conversion of LA to AA was reported in obese mice (Cunnane et al, 1985a). Hence, so far neither animal data nor human observations elucidated the dietary role of EFAs and/or LC-PUFAs in weight reduction diets.…”

Section: Metabolism Of Essential Fatty Acids In Obese Childrenmentioning

confidence: 82%

The effect of under- and overnutrition on essential fatty acid metabolism in childhood

1998

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Both protein-energy malnutrition (PEM) and obesity represent major challenges for paediatric nutrition. The aim of this review is to summarise available data regarding the effect of PEM and obesity on the availability of essential-and long-chain polyunsaturated fatty acids (LC-PUFAs) in childhood.Signi®cantly lower arachidonate (C20: 4n-6, AA) values in malnourished children than in controls is a consistent ®nding in all studies, whereas it is controversial whether the availability of docosahexaenoate (C22: 6n-3, DHA) is also affected. We found signi®cantly lower percentages (% wt/wt) of both AA and DHA in plasma phospholipids [AA: 7.0 (0.7) vs 8.7 (0.8); DHA: 0.90 (0.2) vs 2.6 (0.7), median (interquartile range), P`0.001] in severely malnourished children aged 29 (7) months than in control subjects. Product/substrate ratios indicated reduced delta-5-desaturation in children with PEM. We speculate that severely malnourished children may bene®t from enhanced dietary supply of both n-6 and n-3 LC-PUFAs.In obese adults AA has been reported to constitute a lower percentage of plasma phospholipid fatty acids, and AA supplementation of weight reduction diets has been suggested. In contrast, we found signi®cantly higher plasma phospholipid AA values [12.6 (2.4) vs 8.3 (1.4), P`0.001] in markedly obese children aged 13.8 (1.1) years than in non-obese controls. Product/substrate ratios of the delta-6-desaturase enzyme indicated enhanced conversion activity. These data suggest that obese children do not require LC-PUFA supplementation to low fat diets.The available data indicates that both PEM and obesity alter fatty acid composition of plasma and erythrocyte membrane lipids. The underlying mechanism appears to be altered activity of the bioconversion of essential fatty acids to their LC-PUFA metabolites. Sponsorship:

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Section: Metabolism Of Essential Fatty Acids In Obese Childrenmentioning

confidence: 82%

The effect of under- and overnutrition on essential fatty acid metabolism in childhood

1998

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“…In the ob/ob mouse model of obesity, significantly reduced LA but significantly enhanced DHGLA and AA values were reported (25). In another study in ob/ob mice, significant enhancement of the ∆6-desaturase index (DHGLA/LA) and significant reduction of the ∆5-desaturase index (AA/DHGLA) were reported (29).…”

Section: Phospholipidsmentioning

confidence: 94%

“…Metabolism of n-6 PUFA has been investigated in various experimental models of obesity (25)(26)(27)(28)(29). In the Zucker rat model of monogenic obesity, significantly reduced LA, significantly enhanced DHGLA, and significantly reduced AA values were found in total liver lipids, liver PL, and total microsomal liver lipids in the genetically obese (fa/fa) as compared to the genetically lean (Fa/−) animals investigated at the ages of 6, 9, and 12 wk (26).…”

Section: Phospholipidsmentioning

confidence: 99%

Polyunsaturated fatty acids in plasma lipids of obese children with and without metabolic cardiovascular syndrome

Décsi

Csábí

Török

et al. 2000

Lipids

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Previously we reported significantly higher values of γ-linolenic acid (GLA, 18:3n-6), dihomo-γ-linolenic acid (DHGLA,, and arachidonic acid (20:4n-6) in plasma lipid classes in obese children than in nonobese controls. In the present study, fatty acid composition of plasma phospholipids (PL) and sterol esters (STE) was determined by high-resolution capillary gas-liquid chromatography in obese children with and without metabolic cardiovascular syndrome [MCS: defined as simultaneous presence of (i) dyslipidemia, (ii) hyperinsulinemia, (iii) hypertension, and (iv) impaired glucose tolerance] and in nonobese controls. Fatty acid composition of PL and STE lipids did not differ between obese children without MCS and controls. Obese children with MCS exhibited significantly lower linoleic acid (LA, values in PL (17.43 [2.36], % wt/wt, median [range from the first to the third quartile]) than obese children without MCS (19.14 [3.49]) and controls (20.28 [3.80]). In contrast, PL GLA values were significantly higher in obese children with (0.13 [0.08]) than in those without MCS (0.08 [0.04]), whereas STE GLA values were higher in obese children with MCS (1.04 [0.72]) than in controls (0.62 [0.48]). DHGLA values in PL were significantly higher in obese children with MCS (4.06 [0.74]) than in controls (2.69 [1.60]). The GLA/LA ratio was significantly higher, whereas the AA/DHGLA ratio was significantly lower in obese children with MCS than in obese children without MCS and in controls. In this study, LA metabolism was affected only in obese children with but not in those without MCS. In obese children with MCS, ∆6-desaturase activity appeared to be stimulated, whereas ∆5-desaturase activity appeared to be inhibited. Disturbances in LA metabolism may represent an additional health hazard within the multifaceted clinical picture of MCS.Prevalence of childhood obesity is high and still increasing in many affluent countries. In children and adolescents investigated from 1988 to 1991 in the United States, the prevalence of overweight based on body mass index was 11% according to the 95th and 22% according to the 85th percentile cutoff points (1). In Hungary, the prevalence of childhood obesity defined as body mass index exceeding the 90th percentile is around 13% (2). The long-term morbidity and mortality associated with childhood obesity are closely connected to the cardiovascular and metabolic status detectable in the pediatric age group (3). Therefore, identification of cardiovascular risk factors in obese children is of practical importance.Previously we found significantly higher percentage contributions of the n-6 long-chain polyunsaturated fatty acids (LCPUFA), γ-linolenic acid (GLA, 18:3n-6), dihomo-γ-linolenic acid (DHGLA, 20:3n-6), and arachidonic acid (AA, 20:4n-6) to the fatty acid composition of plasma lipid classes in obese children than in nonobese controls (4). Since LCPUFA are prone to lipid peroxidation, their enhanced availability in circulating lipids may represent a further risk factor of atherogenesis in ob...

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“…In these animals, the proportion of 20:4n-6 in phospholipids (PL) of serum, platelets, liver and heart is significantly decreased as compared to the values seen in lean controls (Fa/-) (18)(19)(20)(21). Surprisingly, the reverse process, i.e., an increase in the conversion of 18:2n-6 to 20:4n-6, has been observed in genetically obese mice (ob/ob) (22,23).…”

Section: Lipids 25 517-522 (1990)mentioning

confidence: 95%

Tissue phospholipid fatty acid composition in genetically lean (Fa/−) or obese (fa/fa) zucker female rats on the same diet

Guesnet

Bourre²,

Guerre-Millo

et al. 1990

Lipids

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The fatty acid composition of serum total lipids, of phospholipids of various organs (liver, heart, kidney), and of nervous structures (brain, retina, sciatic nerve, myelin, synaptosomes) have been compared in lean (Fa/-) and genetically obese (fa/fa) Zucker female rats. Both received a standard commercial diet including 37% of 18:2n-6 and 5% of n-3 polyunsaturated fatty acids (PUFA), 1.7% of which were in the form of 20:5n-3 and 22:6n-3. In comparison with lean rats, the results for the obese rats pointed out (i) no difference in the fatty acid composition of nervous structures; (ii) a decrease of 18:2n-6 (from -8% to -35%) and of 20:4n-6 (from -9% to -49%) in serum, liver and in kidney; this was compensated for by an increase in 20:3n-6 (from +30% to +320%) and in total n-3 PUFA (from +68% to +76%); (iii) a decrease of 20:4n-6 (-18%) and of 22:6n-3 (-24%) in heart compensated for by an increase in 18:2n-6 (+39%) and in 20:3n-6 (+233%); and (iv) constant levels of total PUFA (n-6 and n-3) in the various fractions studied, except in serum where this level decreased (-23%). Finally, except for the nervous structures, tissue phospholipids of obese rats included a lower proportion of 20:4n-6 and a higher proportion of 20:3n-6. This resulted in a significant reduction in the 20:4n-6/20:3n-6 ratio; by contrast, the 20:3n-6/18:2n-6 ratio increased. The results suggest that in Zucker rats, the obese character (fa/fa) affects the desaturation-elongation process of 18:2n-6 to 20:4n-6 by specifically decreasing delta 5-desaturase activity.

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Essential fatty acids in the liver and adipose tissue of genetically obese mice: effect of supplemental linoleic and γ-linolenic acids

Cited by 17 publications

References 22 publications

The effect of under- and overnutrition on essential fatty acid metabolism in childhood

The effect of under- and overnutrition on essential fatty acid metabolism in childhood

Polyunsaturated fatty acids in plasma lipids of obese children with and without metabolic cardiovascular syndrome

Tissue phospholipid fatty acid composition in genetically lean (Fa/−) or obese (fa/fa) zucker female rats on the same diet

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