PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 3103088

Glutamine oxidation by developing rat small intestine.

R E Kimura
View original source ↗Export metadata ↓

Abstract

Glutamine has been reported to be a major oxidative substrate in adult rat small intestine. The significance of glutamine by developing rat jejunal tissue slices and isolated mitochondria was determined. Jejunum slices from suckling rats actively oxidized glutamine at rates significantly greater than adult slices. Increasing the glutamine concentration (0.5-4 mM) in the assay increased glutamine by jejunum of suckling pups by 30% compared to a 100% increase in adult jejunum. Glutamine oxidation by isolated jejunal mitochondria was similar in suckling and adult rat. Glutamine oxidation by jejunum of suckling rat was increased in the presence of 5 mM glucose whereas adult glutamine oxidation was not affected by exogenous glucose. Glutamine inhibited glucose oxidation by jejunum of both suckling and adult rats. In adult jejunal homogenates alanine aminotransferase activity was 2-fold greater than in suckling animals. In the presence of 10 mM aminooxyacetate, a known inhibitor of alanine aminotransferase, glutamine oxidation by jejunum of suckling rat was inhibited by 95%, suggesting that alanine aminotransferase is a major metabolic pathway for the oxidation of glutamine.

Explore related subjects

3-Hydroxybutyric AcidAlanine TransaminaseAminooxyacetic AcidAnimalsCarbon DioxideCycloserineFemaleGlucoseGlutamineHydroxybutyratesIntestine, SmallMaleMitochondriaOxidation-ReductionRatsRats, Inbred StrainsJournal ArticleResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R E Kimura. 1987. Glutamine oxidation by developing rat small intestine.. https://doi.org/10.1203/00006450-198702000-00021

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Beta-hydroxy-beta-methylbutyrate supplementation in critically ill trauma patients.

BACKGROUND: Negative nitrogen balance and skeletal muscle loss are common in critically injured patients and may contribute to morbidity, mortality and resource utilization. Juven, an enteral supplement which is a combination of beta-hydroxy-beta-methylbutyrate (HMB), arginine (ARG), and glutamine (GLN) has been shown to restore muscle in cachetic acquired immunodeficiency syndrome (AIDS) and cancer patients. More recently HMB has been shown to attenuate cancer-induced muscle loss by decreasing muscle proteolysis. The purpose of this study was to analyze whether HMB alone or in combination with ARG and GLN would have a similar effect on critically injured trauma patients. We hypothesized that nitrogen balance would be improved and muscle proteolysis decreased with HMB and HMB/ARG/GLN supplementation. METHODS: There were 100 adult trauma patients with Injury Severity Score (ISS) >18 were enrolled in this prospective, randomized, blinded study. All patients received standard tube feeds and one of three iso-nitrogenous supplements; HMB, HMB/ARG/ GLN, or placebo (PLAC) for 28 days. Urine, serum, and clinical data were collected for 72 patients receiving at least 7 days of supplementation during the first 14 days of treatment. Urinary 3-methylhistidine (3-MH) was used as a proxy for muscle proteolysis. RESULTS: The three groups were similar in age, gender, mechanism, and severity of injury, with the average ISS being 31.9. Utilizing covariant (ISS) repeated measure (days 1-14) mixed model (SAS) analysis, there was a significant treatment effect (p = 0.05) on nitrogen balance (g/d). Change in nitrogen balance from the first 7 days to the last 7 days was -4.3 for the HMB and -5.6 g/d HMB/ARG/GLN groups compared with -8.9 g/d for the PLAC group. 3-MH to creatinine ratios were not different in the PLAC group as compared with the HMB/ARG/GLN and HMB groups (Treatment Effect, p = 0.80). CONCLUSIONS: These data suggest that supplementation with HMB alone may improve nitrogen balance in critically injured adult patients and that this effect is not a result of lowered muscle protein turnover as originally hypothesized.

3-Hydroxybutyric Acid↗
PubMed2007

The bacterial storage compound poly-beta-hydroxybutyrate protects Artemia franciscana from pathogenic Vibrio campbellii.

Infections caused by antibiotic-resistant luminescent Vibrios can cause dramatic losses in aquaculture. In this study, the short-chain fatty acid beta-hydroxybutyrate and its polymer poly-beta-hydroxybutyrate were investigated as possible new biocontrol agents. beta-Hydroxybutyrate was shown to completely inhibit the growth of pathogenic Vibrio campbelli at 100 mM. Moreover, the addition of 100 mM of this fatty acid to the culture water of Artemia nauplii infected with the V. campbelli strain significantly increased the survival of the nauplii. As Artemia is a non-selective and particle filter feeder, we also investigated whether poly-beta-hydroxybutyrate particles could be used to protect Artemia from the pathogenic V. campbellii. The addition of 100 mg l(-1) poly-beta-hydroxybutyrate or more to the Artemia culture water offered a preventive and curative protection from the pathogen as a significantly enhanced survival was noticed. If added as a preventive treatment, a complete protection of infected nauplii (no significant mortality compared with uninfected nauplii) was observed at 1000 mg l(-1) poly-beta-hydroxybutyrate. Our data indicate that the use of poly-beta-hydroxybutyrate might constitute an ecologically and economically sustainable alternative strategy to fight infections in aquaculture.

3-Hydroxybutyric Acid↗