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At least 1,657 records · Page 92Linked to original sources
PubMed1992

Cholesterol concentration of egg yolk and blood plasma and performance of laying hens as influenced by dietary alpha-ketoisocaproic acid.

Experiments were conducted to determine the effect of supplemental alpha-ketoisocaproic acid (KIC) or Leu on layer performance and plasma and egg cholesterol levels. In the first experiment, 0, .09, or .27% KIC and .09 or .27% Leu were fed to 62-wk-old laying hens. In a second experiment, the same levels plus another level of .54% KIC and .54% Leu were fed to 32-wk-old hens for an 8-wk period. The basal diet or the basal diet supplemented with .27% KIC or .27% Leu were continued for 20 wk to determine the long-term effects of these supplements. In a third experiment, hens were fed 0, .1, .2, or .4% KIC for 8 wk. The addition of KIC and Leu to the hen diets did not affect percentage egg production, egg weight, shell thickness, or Haugh units. In Experiment 1, .27% KIC and .09% Leu significantly increased BW gain. Neither KIC or Leu significantly affected BW gain in Experiment 2 when measured at 8 or 28 wk. In the third experiment, diets supplemented with KIC increased significantly BW gain. In Experiment 1, .09% KIC and .09% Leu significantly reduced egg cholesterol at 4 wk. After 8 wk, .27% KIC reduced egg cholesterol significantly below the controls. No effect on plasma or egg cholesterol was observed in Experiments 2 and 3.

Animal Feed↗
PubMed1992

Growth and tissue lipid deposition of broilers fed alpha-ketoisocaproic acid.

Dietary alpha-ketoisocaproic acid (KIC) was studied for effects on growth, feed efficiency, tissue cholesterol (TC) content, and immune response to a Newcastle disease virus (NDV) vaccination in broilers. In two experiments, broiler chicks were fed diets supplemented with graded levels of KIC to .54% of the diet. Feed efficiency, fat deposition, BW gain, and plasma cholesterol levels were determined at 3 wk. In a third experiment, broilers were fed diets supplemented with 0, .1, .2, and .4% KIC throughout the starter (0 to 3 wk), grower (3 to 6 wk), and finisher (6 to 7 wk) periods. Abdominal fat and plasma and breast TC were measured at 7 wk. In Experiment 4, levels of KIC to .6% were fed to broilers to determine TC content and to measure the immune response to NDV vaccination. Feed efficiency, BW gain, and percentage abdominal fat were not affected by KIC in any of the broiler experiments. The addition of KIC to broiler diets resulted in a significant reduction in breast (Pectoralis major) TC. Biceps (Biceps femoralis) TC, adductor (Pubo-ishio-femoralis) TC, and plasma cholesterol content was not affected by KIC. Geometric mean titers to NDV were not improved by KIC. The data indicate that KIC has no effect on growth or abdominal fat deposition, but may have a role in TC homeostasis.

Adipose Tissue↗
PubMed1975

Intermediates in the penicillic acid biosynthesis in Penicillium cyclopium.

Feeding experiments using 14C-labelled precurosrs demonstrate the following sequence of the biological formation of penicillic acid in Penicillium cyclopium: orsellinic acid leads to 2-O-methylorsellinic acid leads to 1,4-dihydroxy-6-methoxy-2-methylbenzene leads 6-methoxy-2-methyl-benzoquinone(1,4)leads to penicillic acid.

Caproates↗
PubMed2004

Study on rat subcutaneous reaction to experimental polyurethane elastomers.

The purpose of the study was to investigate the biocompatibility of experimental elastomers, E580 and E590. The experimental elastomers and the control--a clinically used elastomer--were implanted into the subcutaneous tissue of rats. The tissue reactions were examined histologically on the 3rd, 7th, 14th, 28th, and 56th day after implantation. It was found that there were some irritant responses in the tissues adjacent to the implanted elastomers during the first week. However, the inflammatory tissue reaction subsided substantially from the second week onwards. The stable fibrous capsule surrounding the elastomer was formed after eight weeks. The tissue responses of the control, E580, and E590 were similar. The results suggested that the long-term tissue irritation of the experimental elastomers was so low such that they have the potential to be applied clinically.

Animals↗
PubMed2005

A synthetic TLR4 antagonist has anti-inflammatory effects in two murine models of inflammatory bowel disease.

Current evidence indicates that the chronic inflammation observed in the intestines of patients with inflammatory bowel disease is due to an aberrant immune response to enteric flora. We have developed a lipid A-mimetic, CRX-526, which has antagonistic activity for TLR4 and can block the interaction of LPS with the immune system. CRX-526 can prevent the expression of proinflammatory genes stimulated by LPS in vitro. This antagonist activity of CRX-526 is directly related to its structure, particularly secondary fatty acyl chain length. In vivo, CRX-526 treatment blocks the ability of LPS to induce TNF-alpha release. Importantly, treatment with CRX-526 inhibits the development of moderate-to-severe disease in two mouse models of colonic inflammation: the dextran sodium sulfate model and multidrug resistance gene 1a-deficient mice. By blocking the interaction between enteric bacteria and the innate immune system, CRX-526 may be an effective therapeutic molecule for inflammatory bowel disease.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1975

Biological studies of amiclenomycin.

The action of amiclenomycin (AM) in inhibiting growth of microorganisms is specific against mycobacteria in vitro, but the antibiotic does not show a therapeutic effect against tubercle bacilli in vivo. The action of AM is reversed by biotin, desthiobiotin (DTB) and 7,8-diaminopelargonic acid (DAPA), but not by 7-keto-8-aminopelargonic acid (KAPA), pimelic acid and glutaric acid. In the presence of AM, cultures of Mycobacterium smegmatis and Bacillus sphaericus accumulated KAPA, whereas the formation of DTB decreased. Therefore, AM is thought to inhibit KAPA-DAPA transamination in biotin biosynthesis. In M. smegmatic and B. sphaericus the conversions of KAPA to DAPA and of DTB to biotin were rate limiting in biotin synthesis. Accordingly, the synergistic antibiotic activity of AM, inhibiting the former, and actithiazic acid, inhibiting the latter reaction, would be simply explained.

Amino Acids, Diamino↗
PubMed1981

Microbial production of vitamin B12 antimetabolites. IV. Isolation and identification of 4-keto-5-amino-6-hydroxyhexanoic acid.

4-Keto-5-amino-6-hydroxyhexanoic acid was isolated from Bacillus cereus 102804 fermentations and found to inhibit the growth of Gram-positive and Gram-negative bacteria, when grown in a chemically defined medium. The mechanism appeared to be the inhibition of delta-aminolevulinic acid dehydratase. The Ki value of 4-keto-5-amino-6-hydroxyhexanoic acid in an enzyme preparation of Propionibacterium shermanii was 0.72 microM. Similar test conditions with 4-keto-5-aminohexanoic acid resulted in Ki of 12.1 microM. In both cases competitive inhibition was found. The structure of 4-keto-5-amino-6-hydroxyhexanoic acid was determined.

Aminocaproates↗
PubMed1976

Serum concentrations of individual monocarboxylic short-chain fatty acids C2-C6 in underweight children.

The serum concentrations of individual short-chain fatty acids containing 2-6 carbon atoms were studied in 12 underweight children. Mean n-butyric and iso-valeric acid levels were significantly elevated in underweight children, while those of n-valeric and iso-caproic acids were not significantly higher than in the control group. The level of total free fatty acids was also increased in the underweight group. A reduced enzymatic activity in fatty acid synthesis is supposed to be the factor underlying the impaired lipogenesis.

Adolescent↗
PubMed1998

Esterase activity and release of ethyl esters of medium-chain fatty acids by Saccharomyces cerevisiae during anaerobic growth.

During anaerobic fermentation, Saccharomyces cerevisiae releases large amounts of medium-chain fatty acids (MCFAs) and related ethyl esters which are very important for aromatic quality of fermented beverages. The physiological function of ester synthesis is not yet understood. As MCFAs are toxic, their conversion to esters has been proposed to be a detoxification mechanism. Esterases possess ester synthesizing ability. Throughout an anaerobic fermentation of a lipid-free synthetic medium carried out with a S. cerevisiae strain selected for wine making, we have monitored MCFA and ethyl ester production and, at the same time, measured growth and esterasic activity of intact cells. Because no correlation was found between the concentration of each fatty acid and its ethyl ester, there is no evidence that ester synthesis reduces the toxicity of MCFAs. Esterasic activity did not show any correlation with ester synthesis, but it was related to the release of MCFAs. A model is proposed in which ester synthesis is a consequence of the arrest of lipid biosynthesis resulting from a lack of oxygen. Under these conditions, an excess of acyl coenzyme A is produced, and acyl esters are formed as secondary products of reactions aimed at recovering free coenzyme A.

Anaerobiosis↗
PubMed1999

Role of the prostaglandin E receptor subtype EP1 in colon carcinogenesis.

Although the cyclooxygenase pathway of the arachidonic acid cascade has been suggested to play an important role in colon carcinogenesis, the molecular species of prostanoids and receptors involved have not been fully elucidated yet. We examined the development of aberrant crypt foci (ACFs), putative preneoplastic lesions of the colon, in two lines of knockout mice, each deficient in prostaglandin E receptors, EP1 and EP3, by treatment with the colon carcinogen, azoxymethane. Formation of ACFs was decreased only in the EP1-knockout mice to approximately 60% of the level in wild-type mice. Administration of 250, 500, or 1000 ppm of a novel selective EP1 antagonist, ONO-8711, in the diet to azoxymethane-treated C57BL/6J mice also resulted in a dose-dependent reduction of ACF formation. Moreover, when Min mice, having a nonsense mutation in the adenomatous polyposis coli gene, were given 500 ppm ONO-8711 in the diet, the number of intestinal polyps was significantly reduced to 57% of that in the basal diet group. These results strongly suggest that prostaglandin E2 contributes to colon carcinogenesis to some extent through its action at the EP1 receptor. Thus, EP1 antagonists may be good candidates as chemopreventive agents for colon cancer.

Animals↗