Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.49 (glucose-6-phosphate dehydrogenase)
 7,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of hepatic fatty acid oxidation enzymes in rats fed linseed and perilla oils rich in alpha-linolenic acid (alpha-18:3) were compared with those in the animals fed safflower oil rich in linoleic acid (18:2) and saturated fats (coconut or palm oil). Mitochondrial and peroxisomal palmitoyl-CoA (16:0-CoA) oxidation rates in the liver homogenates were significantly higher in rats fed linseed and perilla oils than in those fed saturated fats and safflower oil. The fatty oxidation rates increased as dietary levels of alpha-18:3 increased. Dietary alpha-18:3 also increased the activity of fatty acid oxidation enzymes except for 3-hydroxyacyl-CoA dehydrogenase. Unexpectedly, dietary alpha-18:3 caused great reduction in the activity of 3-hydroxyacyl-CoA dehydrogenase measured with short- and medium-chain substrates but not with long-chain substrate. Dietary alpha-18:3 significantly increased the mRNA levels of hepatic fatty acid oxidation enzymes including carnitine palmitoyltransferase I and II, mitochondrial trifunctional protein, acyl-CoA oxidase, peroxisomal bifunctional protein, mitochondrial and peroxisomal 3-ketoacyl-CoA thiolases, 2, 4-dienoyl-CoA reductase and delta3, delta2-enoyl-CoA isomerase. Fish oil rich in very long-chain n-3 fatty acids caused similar changes in hepatic fatty acid oxidation. Regarding the substrate specificity of beta-oxidation pathway, mitochondrial and peroxisomal beta-oxidation rate of alpha-18:3-CoA, relative to 16:0- and 18:2-CoAs, was higher irrespective of the substrate/albumin ratios in the assay mixture or dietary fat sources. The substrate specificity of carnitine palmitoyltransferase I appeared to be responsible for the differential mitochondrial oxidation rates of these acyl-CoA substrates. Dietary fats rich in alpha-18:3-CoA relative to safflower oil did not affect the hepatic activity of fatty acid synthase and glucose 6-phosphate dehydrogenase. It was suggested that both substrate specificities and alterations in the activities of the enzymes in beta-oxidation pathway play a significant role in the regulation of the serum lipid concentrations in rats fed alpha-18:3.
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PMID:Effect of dietary alpha-linolenic acid on the activity and gene expression of hepatic fatty acid oxidation enzymes. 1123 6

The aim of the present study was to investigate the effects of photoperiod and feeding level on lipid metabolism in ovine perirenal and subcutaneous adipose tissues (AT) and in skeletal and cardiac muscles. Twenty dry non-pregnant ovariectomised ewes were divided into two groups and subjected to either 8 h or 16 h light/d, and underfed at 22 % energy requirements for 7 d. Half of the ewes in each group were slaughtered and the remaining ewes were refed at 190 % energy requirements for 14 d, until slaughtering. Refeeding increased (2.6-4.3-fold) malic enzyme (ME), fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH) and glycerol-3-phosphate dehydrogenase (G3PDH) activities in subcutaneous AT as well as lipoprotein lipase (LPL) activity in perirenal (3.5-fold) and subcutaneous (10-fold) AT and to a lesser extent (1.4-fold) in the skeletal longissimus thoracis and cardiac muscles. Moreover, variations of LPL mRNA level followed variations of LPL activity: refeeding increased perirenal AT- and cardiac muscle-mRNA levels (7.4- and 2-fold respectively). The main finding of this study is that, for a given level of food intake, long days (compared with short days) increased the LPL activity in the longissimus thoracis muscle and, in refed ewes, the activities of LPL and ME in subcutaneous AT. Furthermore, long days increased LPL mRNA level in cardiac muscle and perirenal AT. Thus, our results show that there are direct effects of photoperiod on sheep AT lipogenic potential, as well as on muscle LPL activity, which are not caused by changes in nutrient availability.
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PMID:Effects of photoperiod and feeding level on adipose tissue and muscle lipoprotein lipase activity and mRNA level in dry non-pregnant sheep. 1129 75

Activities of enzymes involved in hepatic fatty acid oxidation and synthesis among rats fed sesame (Sesamum indicum L.) differing in lignan content (sesamin and sesamolin) were compared. Sesame seeds rich in lignans from two lines, 0730 and 0732, lines established in this laborary, and those from a conventional cultivar (Masekin) were employed. Seeds from the 0730 and 0732 lines contained sesamin and sesamolin at amounts twice those from Masekin. Sesame seeds were added at levels of 200 g/kg to the experimental diets. Sesame increased both the hepatic mitochondrial and the peroxisomal fatty acid oxidation rate. Increases were greater with sesame rich in lignans than with Maskin. Noticeably, peroxisomal activity levels were >3 times higher in rats fed diets containing sesame seeds from the 0730 and 0732 lines than in those fed a control diet without sesame. The diet containing Masekin seed caused only a 50% increase in the value, however. Diets containing seeds from the 0730 and 0732 lines, compared to the control and Masekin diets, also significantly increased the activity of hepatic fatty acid oxidation enzymes including acyl-CoA oxidase, carnitine palmitoyltranferase, 3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase. In contrast, diets containing sesame lowered the activity of enzymes involved in fatty acid synthesis including fatty acid synthase, glucose-6-phosphate dehydrogenase, ATP-citrate lyase, and pyruvate kinase. No significant differences in enzyme activities were, however, seen among diets containing sesame from Masekin cultivar and lines 0730 and 0732. Serum triacylglycerol concentrations were lower in rats fed diets containing sesame from lines 0730 and 0732 than in those fed the control or Masekin diet. It is apparent that sesame rich in lignans more profoundly affects hepatic fatty acid oxidation and serum triacylglycerol levels. Therefore, consumption of sesame rich in lignans results in physiological activity to alter lipid metabolism in a potentially beneficial manner.
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PMID:Effect of sesame seeds rich in sesamin and sesamolin on fatty acid oxidation in rat liver. 1136 49

The putative hypolipidemic effect of garlic remains controversial. To gain further insight into the effect of garlic on lipid metabolism, the present study determined the inhibitory effects of water-soluble organosulfur compounds present in garlic on triglyceride (TG) and fatty acid synthesis in cultured rat hepatocytes. When incubated at 0.05 to 4.0 mmol/L with cultured hepatocytes, S-allyl cysteine (SAC) and S-propyl cysteine (SPC) decreased [2-14C]acetate incorporation into triglyceride in a concentration-dependent fashion achieving a maximal inhibition at 4.0 mmol/L of 43 and 51%, respectively. The rate of [2-14C]acetate incorporation into phosphlipids was depressed to a similar extent by SAC and SPC. SPC, SAC, S-ethyl cysteine (SEC), and gamma-glutamyl-S-methyl cysteine decreased [2-14C]acetate incorporation into fatty acid synthesis by 81, 59, 35, and 40%, respectively, at 2.0-4.0 mmol/L concentrations. Alliin, gamma-glutamyl-S-allyl cysteine, gamma-glutamyl-S-propyl cysteine S-allyl-N-acetyl cysteine, S-allylsulfonyl alanine, and S-methyl cysteine had no effect on fatty acid synthesis. The activities of lipogenic enzymes, fatty acid synthase (FAS), and glucose-6-phosphate dehydrogenase (G6PDH) were measured in cultured hepatocytes treated with the inhibitors. The activity of FAS in cells treated with 4.0 mmol/L SAC and SPC, respectively, was 32 and 27% lower than that of nontreated cells. Neither SAC nor SPC affected G6PDH activity. The results indicate that SAC, SEC, and SPC inhibit lipid biosynthesis in cultured rat hepatocytes, and further suggest that these S-alk(en)yl cysteines of garlic impair triglyceride synthesis in part due to decreased de novo fatty acid synthesis resulting from inhibition on FAS. Whether tissue concentrations of active garlic components can achieve levels required to inhibit TG synthesis in vivo warrants further investigation.
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PMID:Water-soluble organosulfur compounds of garlic inhibit fatty acid and triglyceride syntheses in cultured rat hepatocytes. 1138 92

Recently, we have found that despite the significant reduction of body weight after multiple starvation-refeeding cycles, white adipose tissue (WAT) exhibits surprisingly high rates of lipogenesis and lipogenic enzyme activities. The purpose of this study was to determine the response of WAT lipogenic enzyme mRNAs of rats subjected to multiple cycles of 3 days fasting and 3 days of refeeding. Despite the body weight reduction, significant increase of lipogenic enzymes (ie, fatty acid synthase [FAS], acetyl-coenzyme A [CoA] carboxylase [ACC], adenosine triphosphate (ATP)-citrate lyase [ACL], NADP-linked malic enzyme [ME], and glucose 6-phosphate dehydrogenase [G6PDH]) mRNAs in WAT was found after multiple cycles of starvation-refeeding of rats on standard laboratory diet. These findings, together with the results published recently, indicate that multiple cycles of starvation-refeeding cause the increased lipogenesis in WAT by upregulation of the lipogenic enzymes gene expression.
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PMID:Increase of lipogenic enzyme mRNA levels in rat white adipose tissue after multiple cycles of starvation-refeeding. 1139 54

This work was designed to study the effect of different lipid sources on hepatic lipogenic enzyme activity in rats fed ad libitum or energy-controlled diets. Male Wistar rats were fed diets containing 40% of energy as fat (olive oil, sunflower oil, palm oil, or beef tallow) for 4 wk. In experiment 1 rats had free access to food, and in experiment 2 rats were fed a controlled amount of food. In both experiments, rats fed the olive oil diets had higher activities of glucose-6-phosphate dehydrogenase, malic enzyme, fatty acid synthase, and acetyl-CoA carboxylase (P < 0.05) than rats fed the other fats. It is unlikely that this effect could be attributed to the stimulation by insulin or triiodothyronine because serum values did not differ among the groups. Enzymatic activities were positively and significantly correlated with liver triacylglycerol content, but not with serum triacylglycerol levels. No interaction between lipid source and feeding protocol was found. Oleic acid and components in olive oil other than fatty acids, such as phytosterols, may account for the effects of dietary fat on lipogenic enzyme activity.
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PMID:Differential effects of diets that provide different lipid sources on hepatic lipogenic activities in rats under ad libitum or restricted feeding. 1139 5

Male Sprague-Dawley rats were fed a cholesterol-free (Exp. 1) or cholesterol-supplemented (Exp. 2) diet containing 20% casein (control group) or 15% defatted squid and 5% casein (defatted squid group), as protein, for 14 d. Serum and hepatic cholesterol concentrations were lower in rats fed defatted squid than in those fed casein in both cholesterol-free (-20%, P < 0.05 and -15%, P < 0.05, respectively) and cholesterol-supplemented (-25%, P < 0.05 and -15%, P < 0.05, respectively) diets. Hepatic triglyceride concentration was lower in the defatted squid than in the control groups in both cholesterol-free (-51%, P< 0.05) and cholesterol-supplemented diets (-38%, P < 0.01). The activities of cytosolic fatty acid synthase and the NADPH-generating enzymes, malic enzyme and glucose-6-phosphate dehydrogenase, in the liver were lower in the defatted squid than in the control groups in both cholesterol-free (-21%, P< 0.01, -33%, P < 0.05, and -33%, P < 0.01, respectively) and cholesterol-supplemented diets (-34%, P < 0.05, -57%, P < 0.05, and -67%, P < 0.05, respectively). The activity of mitochondrial carnitine palmitoyltransferase in the liver was comparable between the control and defatted squid groups. The activity of Mg2+-dependent phosphatidate phosphohydrolase in the liver cytosol was lower in the defatted squid (-9%, P < 0.05) than in the control groups only in the cholesterol-free diet. Fecal excretion of total steroids was stimulated by the feeding of defatted squid in both cholesterol-free (+77%, P < 0.005) and cholesterol-supplemented diets (+29%, P < 0.01). These results suggest that the nonlipid fraction of squid exerts a hypocholesterolemic effect by increasing the excretion of total steroids in feces. The fraction also induces a triglyceride-lowering activity in the liver by decreasing hepatic lipogenesis.
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PMID:Effects of dietary defatted squid on cholesterol metabolism and hepatic lipogenesis in rats. 1143 57

Eicosapentaenoic and docosahexaenoic acids were distributed mainly in the sn-1 and 3 positions of seal oil triacylglycerols and in the sn-2 position of fish oil triacylglycerols. Seal oil-rich or fish oil-rich fats having constant polyunsaturated (PUFAs)/monounsaturated/saturated fatty acids and n-6/n-3 PUFAs ratios were fed to hamsters for 3 weeks. The control fat contained linoleic acid as the sole PUFA. The concentration of triacylglycerols in the liver was significantly lower in the fish oil group than in the control group. Phospholipid concentration in serum was lower and that in the liver was higher in the seal oil group compared with the fish oil group. The activities of fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), and the malic enzyme were significantly lower in both the fish and seal oil groups than in the control group. Dietary seal oil more effectively reduced arachidonic acid content in liver phosphatidylcholine and phosphatidylethanolamine and serum phosphatidylcholine than fish oil. These results showed that different intramolecular distribution of n-3 PUFAs influenced glycerolipid metabolism and arachidonic acid content in serum and liver phospholipids of hamsters.
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PMID:Effect of dietary seal and fish oils on lipid metabolism in hamsters. 1157 80

The effect of sesamin, one of the most abundant lignans in sesame seed, on hepatic fatty acid synthesis was examined in rats. Rats were fed experimental diets containing varying amounts (0, 0.1 and 0.2% for Exp. 1 and 0, 0.2 and 0.4% for Exp. 2, respectively) of sesamin for 15 days. The activity and gene expression of enzymes involved in fatty acid synthesis including acetyl-CoA carboxylase, fatty acid synthase, ATP-citrate lyase and glucose-6-phosphate dehydrogenase decreased as the dietary level of sesamin increased in Exp. 1 and in rats fed the 0.2% sesamin diet they were approximately one-half those in animals fed a sesamin-free diet. In Exp. 2, the 0.2% sesamin diet lowered these parameters to one-half the level for a sesamin-free diet, but no further reduction was seen in animals fed the 0.4% sesamin diet. Dietary sesamin dose-dependently decreased the sterol regulatory element binding protein-1 (SREBP-1) mRNA level, and the value in rats fed a 0.4% sesamin diet was approximately one-half that in those fed a sesamin-free diet. The protein content of the membrane-bound precursor form of SREBP-1 decreased as dietary sesamin increased and was 37% lower in rats fed the 0.4% sesamin diet than in those fed a sesamin-free diet. Dietary sesamin exerted a more marked influence on the protein content of the mature nuclear form of SREBP-1. Diets containing 0.2 and 0.4% sesamin lowered the amount of mature SREBP-1 protein to less than one-fifth of that in the animals fed a sesamin-free diet. It was suggested that the dietary sesamin-dependent decrease in lipogenic enzyme gene expression is due to the suppression of the gene expression of SREBP-1 as well as the proteolysis of the membrane-bound precursor form of this transcriptional factor to generate the mature form.
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PMID:Sesamin, a sesame lignan, decreases fatty acid synthesis in rat liver accompanying the down-regulation of sterol regulatory element binding protein-1. 1175 Aug 82

Two treatments, fasting/refeeding and administration of liver X receptor (LXR) agonists, elevate the mRNA for sterol regulatory element-binding protein-1c (SREBP-1c) and enhance lipid synthesis in liver. These treatments do not affect the mRNA for SREBP-1a, an alternative transcript from the same gene. Through homologous recombination, we eliminated the exon encoding SREBP-1c from the mouse genome, leaving the SREBP-1a transcript intact. On a normal diet, livers of SREBP-1c(-/-) mice manifested reductions in multiple mRNAs encoding enzymes of fatty acid and triglyceride synthesis, including acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). In contrast, SREBP-1c(-/-) livers showed a compensatory increase in hepatic SREBP-2 mRNA, accompanied by increased mRNA levels for cholesterol biosynthetic enzymes. In fasted/refed animals, ACC and FAS mRNAs rose, but not to the same extent as in wild-type livers. The refeeding-induced increase in SREBP-1c(-/-) mice was greater than in mice lacking SREBP cleavage-activating protein (SCAP), in which all nuclear SREBPs are absent. Thus, SREBP-2 and/or SREBP-1a can substitute partially for SREBP-1c in permitting an insulin-mediated increase in ACC and FAS mRNAs. In contrast, mRNAs for several other lipogenic enzymes (glucose-6-phosphate dehydrogenase, malic enzyme, glycerol-3-phosphate acyltransferase, and stearoyl-CoA desaturase-1) showed a complete failure of the normal inductive response to refeeding, indicating specific reliance on SREBP-1c. Moreover, these mRNAs, as well as multiple other lipogenic mRNAs, showed a markedly blunted response to the LXR agonist T090137, indicating an essential role of SREBP-1c in the LXR response.
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PMID:Diminished hepatic response to fasting/refeeding and liver X receptor agonists in mice with selective deficiency of sterol regulatory element-binding protein-1c. 1178 83


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