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At least 991 records · Page 55Linked to original sources
PubMed1999

The cyanogenic glucoside, prunasin (D-mandelonitrile-beta-D-glucoside), is a novel inhibitor of DNA polymerase beta.

A DNA polymerase beta (pol. beta) inhibitor has been isolated independently from two organisms; a red perilla, Perilla frutescens, and a mugwort, Artemisia vulgaris. These molecules were determined by spectroscopic analyses to be the cyanogenic glucoside, D-mandelonitrile-beta-D-glucoside, prunasin. The compound inhibited the activity of rat pol. beta at 150 microM, but did not influence the activities of calf DNA polymerase alpha and plant DNA polymerases, human immunodefficiency virus type 1 reverse transcriptase, calf terminal deoxynucleotidyl transferase, or any prokaryotic DNA polymerases, or DNA and RNA metabolic enzymes examined. The compound dose-dependently inhibited pol. beta activity, the IC(50) value being 98 microM with poly dA/oligo dT(12-18) and dTTP as the DNA template and substrate, respectively. Inhibition of pol. beta by the compound was competitive with the substrate, dTTP. The inhibition was enhanced in the presence of fatty acid, and the IC(50) value decreased to approximately 40 microM. In the presence of C(10)-decanoic acid, the K(i) value for substrate dTTP decreased by 28-fold, suggesting that the fatty acid allowed easier access of the compound to the substrate-binding site.

Amygdalin↗
PubMed1978

Differential susceptibility of Propionibacterium acnes, P. granulosum and P. avidum to free fatty acids.

The susceptibility of 98 Propionibacterium acnes, P. granulosum and P. avidum strains isolated from acne cases and appropriate reference strains to decanoic, dodecanoic, octadeca-9,12 dienoic, and octadeca-9,12,15 trienoic acids was investigated using minimal inhibitory concentration estimation by an agar dilution techique. The tested acids showed their relative antibacterial activity in the following order: C18:3 delta 9,12,15 greater than C18:2 delta 9,12 greater than C12:0 greater than C10:0 Differences between minimal inhibitory concentration values for P. acnes, and P. avidum versus P. granulosum strains were demonstrated in the cases of octadeca-9,12 dienoic, and octadeca-9,12,15 trienoic acids.

Decanoic Acids↗
PubMed2005

Food habits and appetite of elderly women at the time of a femoral neck fracture and after nutritional and anabolic support.

OBJECTIVE: To study appetite and food choices in lean elderly women at the time of a femoral neck fracture and after 6 months of nutritional and anabolic intervention. SUBJECTS AND METHODS: Forty-five nondemented women >70 years of age (mean +/- SD: 83 +/- 5 years) with a recent hip fracture and body mass index <24 kg/m2 (mean: 20.5 +/- 2.3) were interviewed about their appetite and dietary habits prior to fracture. The patients were randomized to treatment with a protein-rich liquid supplement (PR; 200 kcal and 20 g protein day(-1)) alone or in combination with nandrolone decanoate injections (PR/N) 25 mg i.m. every third week or to a control group (C). A second interview was conducted 6 months later. RESULTS: Reduced appetite before the fracture was reported by 60%. Half of the patients did not have dessert with any of their daily meals, one-third used low-fat margarines and one-third drank water with their meals. The estimated mean daily energy intake was 6.4 +/- 1.2 MJ (1541 +/- 304 kcal) indicating that three of four subjects did not meet their energy needs. At 6 months, 40% reported reduced appetite. There was no difference in the change of appetite between the three randomized groups. Still, half of the subjects appeared to not meet their energy needs. Protein intake increased in the PR and PR/N groups, in contrast to the controls (P = 0.002). CONCLUSION: Reduced appetite and insufficient energy intake was recorded in lean elderly women with a femoral neck fracture. Nutritional supplementation alone or in combination with an anabolic steroid increased protein intake without adversely affecting appetite.

Aged↗
PubMed1981

Steric course of reaction catalyzed by the enoyl acyl-carrier-protein reductase of Escherichia coli.

The steric course of the reaction catalyzed by Escherichia coli enoyl acyl-carrier-protein reductase was studied. 1. trans-2-[2-2H1]Decenoic and trans-2-[3-2H1]decenoic acids were synthesized and converted to the corresponding decenoyl thiol esters with CoA or acyl carrier protein. These deuterium-labeled decenoyl thiol esters were incubated with purified enoyl acyl-carrier-protein reductase in the presence of NADPH or NADH. 2. The unlabeled trans-2-decenoyl thiol esters were incubated with enoyl acyl-carrier-protein reductase in the presence of (4S)-[4-2H1]NADH. The unlabeled decenoyl thiol esters were also incubated with the enzyme in 2H2O. The decanoic acids formed in the above incubations were extracted and subjected to the action of acyl-CoA oxidase, which had been previously shown to catalyze the anti elimination of the pro-2R and pro-3R hydrogens of acyl-CoA. The resulting products, 2-decenoyl-CoAs, were converted to methyl esters and their deuterium contents were analyzed by gas chromatography/mass spectrometry. The results suggested that the reduction catalyzed by E. coli enoyl acyl-carrier-protein reductase occurs by a syn addition of hydrogen via a 2-Re, 3-Si attack on the double bond.

Acyl Carrier Protein↗
PubMed1986

Lipemic and lipoproteinemic effects of natural and synthetic androgens in humans.

Testosterone cypionate administration in weight-trained subjects reduced serum high-density lipoprotein cholesterol (HDL-C) levels without affecting the total cholesterol (Total-C)/HDL-C ratio. Nandrolone decanoate administration also reduced HDL-C levels, but elevated the Total-C/HDL-C ratio. These findings could not be attributed to changes in exercise patterns, dietary intake, or alcohol consumption. It is concluded that the synthetic androgen employed in this study produced a worsening of potential lipid-related risk factors for ischemic heart disease and that exogenous testosterone has a much less pronounced effect on such risk factors.

Adult↗
PubMed1981

The effect of an anabolic steroid on body composition in patients receiving intravenous nutrition.

In this controlled trial we investigated the effect of an anabolic steroid, in terms of the changes in body composition that occurred in ill surgical patients requiring intravenous nutrition. Glucose was the sole non-protein energy source. The study was conducted over a 14-day study period in two comparable groups of 13 patients. The changes in body weight, fat, protein and water were measured. The control group received a nutrient solution of hypertonic dextrose and amino acids (44.8 +/- 8.2 kcal/kg/day), and the comparative group received the same solution (44.3 +/- 5.2 kcal/kg/day) and 100 mg of an intramuscular injection of nandrolone decanoate at the commencement of the study and again one week later. Over the two-week study period both groups gained body weight. In the controls this was composed of fat (0.4 kg) and water 1.5 kg). In the anabolic steroid group, weight gain was mainly water, and fat gain did not occur. Neither group gained body protein. Diuretic therapy was required more often (21 patient days compared with 5 patients days; p less than 0.001) in the anabolic steroid group to control excessive water retention. Our study has shown no benefit from an anabolic steroid when given in combination with a 14-day course of intravenous nutrition. Water retention was more of a problem with this therapy.

Aged↗
PubMed2000

Fatty acid-induced cholecystokinin secretion and changes in intracellular Ca2+ in two enteroendocrine cell lines, STC-1 and GLUTag.

1. Fatty acid-induced cholecystokinin (CCK) secretion in humans and from the enteroendocrine cell line STC-1 depends critically on acyl chain length. 2. Therefore we have characterized the relationship between acyl chain length and the potency of the fatty acid to induce CCK secretion and changes in intracellular Ca2+ concentration ([Ca2+]i) in two enteroendocrine cell lines (STC-1 and GLUTag). We found that the potency of the fatty acid was directly proportional to its chain length and therefore inversely proportional to its solubility. 3. In both cell types, the fatty acid-induced rise in [Ca2+]i in response to decanoic acid (C10), dodecanoic acid (C12) and tetradecanoic acid (C14) was significantly reduced in Ca2+-free medium and largely blocked by nicardipine. Intracellular stores also contributed to the overall shape of the [Ca2+]i peak. Thus all the fatty acids tested caused the release of Ca2+ from stores and influx of extracellular Ca2+, presumably through L-type calcium channels. 4. To probe the site of fatty acid action, we studied the distribution of 14C-labelled dodecanoic acid. This label was rapidly and irreversibly accumulated by both cell types, where it became concentrated about 20-fold. Confocal microscopy of a fluorescent analogue of dodecanoic acid clearly demonstrated that it entered the cytosol and was not merely partitioning in the cell membrane. These data indicate that an intracellular action for fatty acid-induced CCK secretion cannot be eliminated. 5. Dodecanoic acid itself, and not a metabolite, is the agent responsible for triggering Ca2+ entry since a non-metabolizable form of dodecanoic acid (2-bromododecanoic acid) was also capable of inducing a rise in [Ca2+]i in both cell types. 6. In conclusion, the rise in [Ca2+]i in STC-1 and GLUTag cells evoked by medium- to long-chain fatty acids results from the triggering of a specific signalling pathway. Whether triggering occurs through activation of a membrane-bound receptor or at an intracellular site remains to be clarified.

Calcium↗
PubMed1996

Comparison of the inhibitory action on Saccharomyces cerevisiae of weak-acid preservatives, uncouplers, and medium-chain fatty acids.

This study was initiated to establish whether inhibition of growth of yeasts by medium-chain fatty acids resembled that caused by weak-acid preservatives or uncouplers. Unlike sorbic acid and 2,4-dinitrophenol, decanoic acid caused rapid cell death at its inhibitory concentration. This suggested a mode of action by medium-chain fatty acids, distinct from both weak-acid preservatives and uncouplers. Sorbic acid and 2,4-dinitrophenol both increased lag and doubling times, reduced cell yields and inhibitory concentrations of both were highly pH sensitive. The possibility is discussed as to whether weak-acid preservatives and uncouplers share common modes of inhibition.

2,4-Dinitrophenol↗
PubMed2004

5-Hydroxydecanoate is metabolised in mitochondria and creates a rate-limiting bottleneck for beta-oxidation of fatty acids.

5-Hydroxydecanoate (5-HD) blocks pharmacological and ischaemic preconditioning, and has been postulated to be a specific inhibitor of mitochondrial ATP-sensitive K(+) (K(ATP)) channels. However, recent work has shown that 5-HD is activated to 5-hydroxydecanoyl-CoA (5-HD-CoA), which is a substrate for the first step of beta-oxidation. We have now analysed the complete beta-oxidation of 5-HD-CoA using specially synthesised (and purified) substrates and enzymes, as well as isolated rat liver and heart mitochondria, and compared it with the metabolism of the physiological substrate decanoyl-CoA. At the second step of beta-oxidation, catalysed by enoyl-CoA hydratase, enzyme kinetics were similar using either decenoyl-CoA or 5-hydroxydecenoyl-CoA as substrate. The last two steps were investigated using l-3-hydroxyacyl-CoA dehydrogenase (HAD) coupled to 3-ketoacyl-CoA thiolase. V(max) for the metabolite of 5-HD (3,5-dihydroxydecanoyl-CoA) was fivefold slower than for the corresponding metabolite of decanoate (l-3-hydroxydecanoyl-CoA). The slower kinetics were not due to accumulation of d-3-hydroxyoctanoyl-CoA since this enantiomer did not inhibit HAD. Molecular modelling of HAD complexed with 3,5-dihydroxydecanoyl-CoA suggested that the 5-hydroxyl group could decrease HAD turnover rate by interacting with critical side chains. Consistent with the kinetic data, 5-hydroxydecanoyl-CoA alone acted as a weak substrate in isolated mitochondria, whereas addition of 100 mum 5-HD-CoA inhibited the metabolism of decanoyl-CoA or lauryl-carnitine. In conclusion, 5-HD is activated, transported into mitochondria and metabolised via beta-oxidation, albeit with rate-limiting kinetics at the penultimate step. This creates a bottleneck for beta-oxidation of fatty acids. The complex metabolic effects of 5-HD invalidate the use of 5-HD as a blocker of mitochondrial K(ATP) channels in studies of preconditioning.

Animals↗
PubMed1993

Biodegradation of a synthetic lubricant by Micrococcus roseus.

A bacterium that was able to utilize Emkarate 1550 (E1550), a synthetic lubricant ester, as the sole source of carbon was isolated. The isolate was tentatively identified as Micrococcus roseus. The components of the E1550 ester, octanoate, decanoate, and 1,1,1-tris(hydroxymethyl)propane (TMP), were detected in the culture medium of cells growing on the ester. The TMP tertiary alcohol accumulated during growth and was not utilized by this isolate. The detection of the components of the ester in the supernatant of cultures indicated that one of the first steps in its degradation was cleavage of the ester bonds. Esterase activity was significantly enhanced in cells grown on E1550 compared with esterase activity measured in cells grown on acetate.

Biodegradation, Environmental↗
PubMed1979

Cellular fatty acid composition of Francisella tularensis.

Several unusual fatty acids characterized strains of Francisella tularensis. Long-chain (C20-C26) acids and the hydroxy acids 2-hydroxy-decanoate, 3-hydroxy-hexadecanoate, and 3-hydroxy-octadecanoate appeared to be of special diagnostic value.

Decanoates↗
PubMed1979

Susceptibility of Staphylococcus aureus and group A, B, C, and G streptococci to free fatty acids.

The susceptibility of 242 strains of Staphylococcus aureus and 117 strains of streptococci of groups A, B, C, and G to decanoic, dodecanoic, octadeca-9,12-dienoic, and octadeca-9,12,15-trienoic acids was estimated by determination of minimal inhibitory concentrations. S. aureus strains appeared to be generally less susceptible to all four fatty acids than streptococcal strains of all groups. Dodecanoic acid was the most inhibitory fatty acid against both staphylococci and streptococci. Both saturated fatty acids used were more active than the unsaturated acids. Among the unsaturated acids, octadeca-9,12,15-trienoic acid appeared to be more inhibitory for Staphylococcus and Streptococcus strains than octadeca-9,12-dienoic acid. No differences in susceptibility to fatty acids among staphylococcal and streptococcal strains isolated from skin, throat, or other sites were found.

Decanoic Acids↗
PubMed1993

Muscle ultrastructure after strength training with placebo or anabolic steroid.

The influence of strength training on muscle fiber area, capillary ultrastructure, and capillary supply was studied in experienced male bodybuilders taking either anabolic steroids or a placebo. During 8 weeks, 13 subjects received a weekly injection of either placebo or nandrolone decanoate (starting dose 200 mg, followed by 100 mg weekly), in a double-blind, counterbalanced design. Before and after 8 weeks a needle biopsy was taken from the vastus lateralis muscle for studying morphometric characteristics of fibers and ultrastructure and morphometric characteristics of capillaries. The fiber cross-sectional area increased significantly only after steroid treatment. Capillary ultrastructure and capillary supply were not changed after the training period. In none of the measured parameters was any difference found between placebo and steroid treatment.

Adult↗
PubMed2001

Anabolic steroids increase exercise tolerance.

The influence of an anabolic androgenic steroid (AAS) on thymidine and amino acid uptake in rat hindlimb skeletal muscles during 14 days after a single exhaustive bout of weight lifting was determined. Adult male rats were divided randomly into Control or Steroid groups. Nandrolone decanoate was administered to the Steroid group 1 wk before the exercise bout. [3H]thymidine and [14C]leucine labeling were used to determine the serial changes in cellular mitotic activity, amino acid uptake, and myosin synthesis. Serum creatine kinase (CK) activity, used as a measure of muscle damage, increased 30 and 60 min after exercise in both groups. The total amount of weight lifted was higher, whereas CK levels were lower in Steroid than in Control rats. [3H]thymidine uptake peaked 2 days after exercise in both groups and was 90% higher in Control than in Steroid rats, reflecting a higher level of muscle damage. [14C]leucine uptake was approximately 80% higher at rest and recovered 33% faster postexercise in Steroid than in Control rats. In a separate group of rats, the in situ isometric mechanical properties of the plantaris muscle were determined. The only significant difference was a higher fatigue resistance in the Steroid compared with the Control group. Combined, these results indicate that AAS treatment 1) ameliorates CK efflux and the uptake of [3H]thymidine and enhances the rate of protein synthesis during recovery after a bout of weight lifting, all being consistent with there being less muscle damage, and 2) enhances in vivo work capacity and the in situ fatigue resistance of a primary plantarflexor muscle.

Anabolic Agents↗
PubMed2004

Cholecystokinin pathways modulate sensations induced by gastric distension in humans.

Ingested fat releases CCK, causes gastric relaxation, delays gastric emptying, and limits meal size; however, the mechanistic link among these actions has not been established. Fatty acid release of CCK is chain-length sensitive; dodecanoic acid (C12) induces greater CCK release than decanoic acid (C10). The effect of C12 or C10 on tolerance to subsequent intragastric infusion of liquid was determined in healthy subjects, with and without the CCK(1) receptor antagonist dexloxiglumide. Gastric wall relaxation after either fatty acid was assessed by graded volume distension and by barostat; gastric emptying was measured by gastric aspiration and by a [(13)C]octanoic acid breath technique. C12 released more CCK (mean plasma CCK after vehicle, 4.7 +/- 0.8 pM; C10, 4.8 +/- 0.3 pM; C12, 8 +/- 1.2 pM; P < 0.05 C12 vs. C10 or vehicle) and reduced the volume of water (and of 5 and 25% glucose solutions) delivered at maximum tolerance compared with C10 or vehicle (volume of water tolerated after vehicle, 1,535 +/- 164 ml; C10, 1,335 +/- 160 ml; C12, 842 +/- 103 ml; P < 0.05 C12 vs. C10 or vehicle); this effect was abolished by dexloxiglumide. Intragastric volumes were always similar at the limit of tolerance, and, whereas gastric relaxation occurred to similar degrees after the fatty acids, its duration was longer after C12, which also induced a longer delay in half-gastric emptying [t(1/2)(min) after vehicle, 53 +/- 2; C10, 67 +/- 3; C12, 88 +/- 7; P < 0.05 C12 vs. C10 or vehicle]. In conclusion, ingestion of a CCK-releasing fatty acid reduces the tolerated volume of liquid delivered into the stomach, primarily via a CCK(1) receptor-mediated delay in gastric emptying.

Adult↗
PubMed1975

Lipoate effect on carbohydrate and lipid metabolism and gastric H+ secretion.

Acid secretion (QH+) and oxygen consumption (Qo2) by frog gastric mucosae in vitro were sharply stimulated by lipoate. A rapid decline followed stimulation, subsequently falling below control values. Addition of only glucose or lactate had no effect on Qo2 or QH+. Pyruvate caused slight significant stimulation of Qo2. Any one of these compounds added to lipoate-treated mucosae increased the stimulatory effect of lipoate and markedly slowed the rate of decline subsequent to maximum stimulation. Various fatty acids had a moderate-to-high stimulatory effect on Qo2 and QH+. Lipoate added prior to the addition of fatty acids decreased the stimulatory effect of buryrate (minus 56%), decanoate (minus 87%), and palmitate (minus 60%). Propionate became an inhibitor in the presence of lipoate. Lipoate increased (plus 100%) the amount of glycogen oxidized and decreased (minus 69%) the amount of triglycerides oxidized. Lipoate-treated mucosae did not respond to histamine. Addition of glucose restored responsiveness. The results indicate that beta-oxidation of fatty acids plays a major role in the acid secretory process and is centrally involved in cyclic AMP and histamine stimulation of QH+.

Animals↗
PubMed2004

Effects of intraduodenal fatty acids on appetite, antropyloroduodenal motility, and plasma CCK and GLP-1 in humans vary with their chain length.

The gastrointestinal effects of intraluminal fats may be critically dependent on the chain length of fatty acids released during lipolysis. We postulated that intraduodenal administration of lauric acid (12 carbon atoms; C12) would suppress appetite, modulate antropyloroduodenal pressure waves (PWs), and stimulate the release of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) more than an identical dose of decanoic acid (10 carbon atoms; C10). Eight healthy males (19-47 yr old) were studied on three occasions in a double-blind, randomized fashion. Appetite perceptions, antropyloroduodenal PWs, and plasma CCK and GLP-1 concentrations were measured during a 90-min intraduodenal infusion of 1) C12, 2) C10, or 3) control (rate: 2 ml/min, 0.375 kcal/min for C12/C10). Energy intake at a buffet meal, immediately after completion of the infusion, was also quantified. C12, but not C10, suppressed appetite perceptions (P < 0.001) and energy intake (control: 4,604 +/- 464 kJ, C10: 4,109 +/- 588 kJ, and C12: 1,747 +/- 632 kJ; P < 0.001, C12 vs. control/C10). C12, but not C10, also induced nausea (P < 0.001). C12 stimulated basal pyloric pressures and isolated pyloric PWs and suppressed antral and duodenal PWs compared with control (P < 0.05 for all). C10 transiently stimulated isolated pyloric PWs (P = 0.001) and had no effect on antral PWs but markedly stimulated duodenal PWs (P = 0.004). C12 and C10 increased plasma CCK (P < 0.001), but the effect of C12 was substantially greater (P = 0.001); C12 stimulated GLP-1 (P < 0.05), whereas C10 did not. In conclusion, there are major differences in the effects of intraduodenal C12 and C10, administered at 0.375 kcal/min, on appetite, energy intake, antropyloroduodenal PWs, and gut hormone release in humans.

Adult↗
PubMed1987

Effect of anabolic steroids on skeletal muscle mass during hindlimb suspension.

The efficacy of anabolic steroid treatment [0.3 or 0.9 mg nandrolone decanoate (Deca-Durabolin) per day] was examined in the context of sparing rodent fast-twitch plantaris and slow-twitch soleus muscle weight, sparing subcellular protein, and altering isomyosin expression in response to hindlimb suspension. Female rats were assigned to four groups (7 rats/group for 6 wk): 1) normal control (NC), 2) normal steroid (NS), 3) normal suspension (N-SUS), and 4) suspension steroid (SUS-S). Compared with control values for the plantaris and soleus muscles, suspension induced 1) smaller body and muscle weight (P less than 0.05), 2) losses in myofibril content (mg/muscle, P less than 0.05), and 3) shifts in the relative expression (expressed as %of total isomyosin) of isomyosins which favored lesser slow myosin and greater fast myosin isotypes (P less than 0.05). Steroid treatment of suspended animals (SUS-S vs. N-SUS) partially spared body and muscle weight (P less than 0.05) and spared plantaris but not soleus myofibril content (mg/muscle, P less than 0.05). However, steroid treatment did not modify the isomyosin pattern induced by suspension. In normal rats (NS vs. NC), steroid treatment enhanced body and plantaris muscle weight but not soleus weight (P less than 0.05) and did not alter isomyosin expression in either muscle type. Collectively these data suggest that in young female rats anabolic steroids 1) enhance the body weight and the weight of a fast-twitch ankle extensor in normal rats, 2) ameliorate the loss in body weight, fast-twitch muscle weight and protein content and slow-twitch muscle weight associated with hindlimb suspension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗