Increased 4‐enoyl‐CoA reductase activity in liver mitochondria of rats fed high‐fat diets and its effect on fatty acid oxidation and the inhibitory action of pent‐4‐enoate

Borrebæk, Borgar; Osmundsen, Harald; Christiansen, Erling N.; Bremer, Jon

doi:10.1016/0014-5793(80)81257-9

Cited by 21 publications

(6 citation statements)

References 15 publications

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“…2,4-Dienoyl-CoA reductase and A 3 ,A 2 -enoyl-CoA isomerase are enzymes located in both mitochondria and peroxisomes (Dommes et al 1981;Kaki et al 1987;Palosaari et al 1990;Hakkola et al 1994) and are required for the degradation by the jS-oxidation pathway of unsaturated fatty acids having double bonds at even-numbered and odd-numbered positions respectively (Dommes et al 1981;Kaki et al 1987;Osmundsen & Hovik, 1988;1991, Hakkola et al 1994. It has been reported that experimental conditions which induce the jS-oxidation pathway, such as diabetes (Osmundsen & Bjornstad, 1985) and the administration of clofibrate (Dommes et al 1981;Hakkola et al 1994), and partially hydrogenated marine oil (Borrebaek et al 1980) increased the activity of 2,4-dienoyl-CoA reductase in the rat liver. Also, there is evidence to indicate that clofibrate feeding increases A 3 ,A 2 -enoyl-CoA isomerase activity in both mitochondria and peroxisomes (Palosaari et al 1990;Hakkola et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Reciprocal responses to dietary diacylglycerol of hepatic enzymes of fatty acid synthesis and oxidation in the rat

1997

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The activities of hepatic enzymes of fatty acid synthesis and oxidation were compared in rats fed on diacylglycerol and triacylglycerol. In the first trial, rats were fed on diacylglycerol or triacylglycerol (rapeseed oil) for 14 d. The diacylglycerol preparation contained 65-2 g and 32*6 g fatty acids/100 g total fatty acids as 1,3-species and 1,2-species respectively. Fatty acid compositions of these dietary lipids were similar. Dietary acylglycerols were added to experimental diets to provide the same amounts of fatty acids (93*9 g/kg diet). Dietary diacylglycerol compared with triacylglycerol significantly reduced the concentrations of serum and liver triacylglycerol. The activities of enzymes of fatty acid synthesis (fatty acid synthetase, glucose 6-phosphate dehydrogenase (EC 1.1.1.49) and malic enzyme (EC 1.1.1.40)) were significantly lower in rats fed on diacylglycerol than in those fed on triacylglycerol. In contrast, the rates of mitochondrial and peroxisomal oxidation of palmitoylCoA in liver homogenates were higher in rats fed on diacylglycerol than in those fed on triacylglycerol. In the second trial, varying amounts of dietary triacylglycerol were replaced by diacylglycerol while the dietary fatty acid content was maintained (93*9 g/kg diet). After 21 d of the feeding period the significant reductions in serum and liver triacylglycerol levels were confirmed in groups of rats fed on the diets in which diacylglycerol supplied more than 65-8 g fatty acids/kg diet (65-8 and 93-9 g/kg). Reductions in the activities of enzymes of fatty acid synthesis and increases in palmitoyl-CoA oxidation rates by both mitochondrial and peroxisomal pathways were also apparent when diacylglycerol replaced triacylglycerol in diets to supply more than 65-8 g fatty acid/kg. Increasing dietary levels of diacylglycerol also progressively increased the activities of enzymes involved in the ^-oxidation pathway (carnitine palmitoyltransferase (EC 2.3.1.21), acyl-CoA dehydrogenase (EC 1.3.99.3), acyl-CoA oxidase (EC 1.3.3.6), enoyl-CoA hydratase (EC 4.2.1.17), 3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.35), 2,4-dienoyl-CoA reductase (EC 1.3.1.34) and A 3 ,A 2 -enoyl-CoA isomerase (EC 5.3.3.8)) in the liver. These results suggest that alteration of fatty acid metabolism in the liver is a factor responsible for the serum triacylglycerol-lowering effect of dietary diacylglycerol.

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Section: Discussionmentioning

confidence: 99%

Reciprocal responses to dietary diacylglycerol of hepatic enzymes of fatty acid synthesis and oxidation in the rat

1997

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“…1.3.1}, which is an auxiliary enzyme in the metabolism of polyunsaturated fatty acids (8)(9)(10)(11). Liver mitochondria from rats fed these diets show an increased capacity to oxidize polyunsaturated fatty acids, and this increased capacity is at least partially explained by the increased activity of the 2,4-dienoyl-CoA reductase (6,7,9,11 In the present study, we have fed rats different fat diets and clofibrate and studied the capacity of isolated hepatocytes from these animals to oxidize fatty acids of different chain lengths and unsaturation.…”

mentioning

confidence: 91%

“…Another interesting observation was that both a high fat diet (6) and clofibrate (7) lead to an increased activity of the enzyme 2,4-dienoyl-CoA reductase (ETC. 1.3.1}, which is an auxiliary enzyme in the metabolism of polyunsaturated fatty acids (8)(9)(10)(11).…”

mentioning

confidence: 99%

The effect of feeding fish oils, vegetable oils and clofibrate on the ketogenesis from long chain fatty acids in hepatocytes

Bergseth

Christiansen

Bremer

1986

Lipids

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Groups of rats were fed diets containing 25% fish oil (FO), 25% soybean oil, 25% partially hydrogenated fish oil (PHFO), 25% partially hydrogenated soybean oil (PHSO), 25% partially hydrogenated coconut oil or 0.3% clofibrate for 3 wk. After the animals were fasted for 24 hr, hepatocytes were isolated and ketogenesis from added palmitate, linoleate cis and trans, arachidonate and docosahexaenoate was measured. Ketogenesis after oil feeding was significantly stimulated (two- to threefold) only in cells from the PHFO- and PHSO-fed rats. The stimulation was most apparent with the long chain unsaturated fatty acids as substrates. These fatty acids were relatively poor ketone body precursors in control hepatocytes. Essential fatty acid deficiency did not seem to be the reason for this stimulation. Clofibrate also stimulated ketogenesis significantly (1.5- to 3-fold). The degree of stimulation increased with chain length and degree of unsaturation of the substrate. The activity of the enzyme 2,4-dienoyl-CoA reductase was also studied in the same groups. Its activity was stimulated about fourfold in the clofibrate-treated rats and to a lesser extent by the PHFO, PHSO and FO diets. The activity showed no correlation with the content of unsaturated fatty acids in the diet or their oxidation in isolated hepatocytes. The 2,4-dienoyl-CoA reductase, therefore, does not seem to be a regulatory enzyme in the metabolism of dietary polyunsaturated fatty acids. It is concluded that an induction of the peroxisomal beta-oxidation system most likely is involved in the reported increases in ketogenesis from very long chain polyunsaturated fatty acids.

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“…In contrast the activity of urate oxidase, a known peroxisomal enzyme, was unchanged. Thus DCQVA apparently has characteristic features shared by various peroxisome proliferators [1,[6][7][8][9][10]]. This is a first observation of a naturally occurring metabolite of cholic acid that is a peroxisome proliferator.…”

Section: Discussionmentioning

confidence: 99%

“…Similar effects are evoked by high-fat diets [3,4] or diabetes [5], which cause intracellular accumulation of fatty acids. Induction of peroxisome proliferation is associated with the induction of several fatty acid-metabolizing enzymes, notably those involved in peroxisomal fl-oxidation and in microsomal w-oxidation [6], as well as mitochondrial 2,4-dienoyl-CoA reductase (EC 1.3.1.34) [7][8][9][10], which plays an essential role in the fl-oxidation of unsaturated fatty acids [11]. Thus it has been hypothesized that a physiological role of peroxisome proliferation is in regulating fatty acid homeostasis and that the intracellular accumulation of fatty acids is the stimulus for triggering peroxisome proliferation [1].…”

Section: Introductionmentioning

confidence: 99%

Induction of peroxisomal β-oxidation by a microbial catabolite of cholic acid in rat liver and cultured rat hepatocytes

Nishimaki-Mogami

Takahashi

Toyoda

et al. 1993

Biochemical Journal

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The capability of (4R)-4-(2,3,4,6,6a beta,7,8,9,9a alpha,9b beta-decahydro-6a beta-methyl-3-oxo-1H-cyclopental[f]quinolin-7 beta-yl)valeric acid (DCQVA), a catabolite of cholic acid produced by enterobacteria, to induce peroxisome proliferation in vivo and in vitro was studied. Rats given 0.3% DCQVA in the diet for 2 weeks showed marked increases in peroxisomal beta-oxidation, mitochondrial 2,4-dienoyl-CoA reductase and microsomal laurate omega-oxidation activities in the liver compared with control rats given the diet without DCQVA. Cultured rat hepatocytes treated with DCQVA for 72 h also exhibited greatly enhanced beta-oxidation activity. The increased activity was concentration-dependent and the effective concentrations were comparable with those of clofibric acid that produced the same degree of induction in the assay. The results demonstrate that DCQVA is a potent peroxisome proliferator that occurs naturally in rat intestine.

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Increased 4‐enoyl‐CoA reductase activity in liver mitochondria of rats fed high‐fat diets and its effect on fatty acid oxidation and the inhibitory action of pent‐4‐enoate

Cited by 21 publications

References 15 publications

Reciprocal responses to dietary diacylglycerol of hepatic enzymes of fatty acid synthesis and oxidation in the rat

Reciprocal responses to dietary diacylglycerol of hepatic enzymes of fatty acid synthesis and oxidation in the rat

The effect of feeding fish oils, vegetable oils and clofibrate on the ketogenesis from long chain fatty acids in hepatocytes

Induction of peroxisomal β-oxidation by a microbial catabolite of cholic acid in rat liver and cultured rat hepatocytes

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