scholarly journals Urinary Metabolomics Validates Metabolic Differentiation Between Renal Cell Carcinoma Stages and Reveals a Unique Metabolic Profile for Oncocytomas

Metabolites ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 155 ◽  
Author(s):  
Oluyemi S. Falegan ◽  
Shanna A. Arnold Egloff ◽  
Andries Zijlstra ◽  
M. Eric Hyndman ◽  
Hans J. Vogel
Keyword(s):  
Metabolic Profile ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Benign Lesions ◽  
Cross Sectional ◽  
Acid Cycle ◽  
Chromophobe Rcc ◽  
Cross Sectional Imaging ◽  
Sectional Imaging ◽  
Tricarboxylic Acid Cycle Intermediates

Renal cell carcinoma (RCC) is a heterogeneous malignancy which often develops and progresses asymptomatically. Benign oncocytomas are morphologically similar to malignant chromophobe RCC and distinguishing between these two forms on cross-sectional imaging remains a challenge. Therefore, RCC-specific biomarkers are urgently required for accurate and non-invasive, pre-surgical diagnosis of benign lesions. We have previously shown that dysregulation in glycolytic and tricarboxylic acid cycle intermediates can distinguish benign lesions from RCC in a stage-specific manner. In this study, preoperative fasting urine samples from patients with renal masses were assessed by ¹H nuclear magnetic resonance (NMR). Significant alterations in levels of tricarboxylic acid cycle intermediates, carnitines and its derivatives were detected in RCC relative to benign masses and in oncocytomas vs. chromophobe RCC. Orthogonal Partial Least Square Discriminant Analysis plots confirmed stage discrimination between benign vs. pT1 (R2 = 0.42, Q2 = 0.27) and benign vs. pT3 (R2 = 0.48, Q2 = 0.32) and showed separation for oncocytomas vs. chromophobe RCC (R2 = 0.81, Q2 = 0.57) and oncocytomas vs. clear cell RCC (R2 = 0.32, Q2 = 0.20). This study validates our previously described metabolic profile distinguishing benign tumors from RCC and presents a novel metabolic signature for oncocytomas which may be exploited for diagnosis before cross-sectional imaging.

scholarly journals Triheptanoin partially restores levels of tricarboxylic acid cycle intermediates in the mouse pilocarpine model of epilepsy

2013 ◽  
Vol 129 (1) ◽  
pp. 107-119 ◽  
Author(s):  
Mussie G. Hadera ◽  
Olav B. Smeland ◽  
Tanya S. McDonald ◽  
Kah Ni Tan ◽  
Ursula Sonnewald ◽  
...  
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Cycle ◽  
Pilocarpine Model ◽  
Tricarboxylic Acid Cycle Intermediates

scholarly journals Metabolic phases during the development of granulation tissue

1967 ◽  
Vol 105 (1) ◽  
pp. 333-341 ◽  
Author(s):  
Kirsti Lampiaho ◽  
E. Kulonen
Keyword(s):  
Granulation Tissue ◽  
Collagen Synthesis ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Pentose Phosphate ◽  
Acid Cycle ◽  
Short Period ◽  
Tricarboxylic Acid Cycle Intermediates ◽  
Observation Period

1. The metabolism of incubated slices of sponge-induced granulation tissue, harvested 4–90 days after the implantation, was studied with special reference to the capacity of collagen synthesis and to the energy metabolism. Data are also given on the nucleic acid contents during the observation period. Three metabolic phases were evident. 2. The viability of the slices for the synthesis of collagen was studied in various conditions. Freezing and homogenization destroyed the capacity of the tissue to incorporate proline into collagen. 3. Consumption of oxygen reached the maximum at 30–40 days. There was evidence that the pentose phosphate cycle was important, especially during the phases of the proliferation and the involution. The formation of lactic acid was maximal at about 20 days. 4. The capacity to incorporate proline into collagen hydroxyproline in vitro was limited to a relatively short period at 10–30 days. 5. The synthesis of collagen was dependent on the supply of oxygen and glucose, which latter could be replaced in the incubation medium by other monosaccharides but not by the metabolites of glucose or tricarboxylic acid-cycle intermediates.

The Ethylmalonyl-CoA Pathway for Methane-based Biorefineries: A Case Study of Using Methylosinus trichosporium OB3b, an Alpha-proteobacterial Methanotroph, for Producing 2-Hydroxyisobutyric Acid and 1,3-Butanediol from Methane

2021 ◽  
Author(s):  
Dung Hoang Anh Mai ◽  
Thu Thi Nguyen ◽  
Eun Yeol Lee
Keyword(s):  
Carbon Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Methylosinus Trichosporium Ob3b ◽  
Methylosinus Trichosporium ◽  
Acid Cycle ◽  
Hydroxyisobutyric Acid ◽  
Tricarboxylic Acid Cycle Intermediates ◽  
Alpha Proteobacteria

The ethylmalonyl-CoA pathway is one of three known anaplerotic pathways that replenish tricarboxylic acid cycle intermediates and plays a major role in the carbon metabolism of many alpha-proteobacteria including Methylosinus...

13C isotopomer model for estimation of anaplerotic substrate oxidation via acetyl-CoA

1996 ◽  
Vol 271 (4) ◽  
pp. E788-E799 ◽  
Author(s):  
F. M. Jeffrey ◽  
C. J. Storey ◽  
A. D. Sherry ◽  
C. R. Malloy
Keyword(s):  
Biochemical Analysis ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acetyl Coa ◽  
Acid Cycle ◽  
Propionate Metabolism ◽  
13C Nuclear Magnetic Resonance ◽  
Isotopomer Analysis ◽  
Tricarboxylic Acid Cycle Intermediates ◽  
Anaplerotic Pathway

A previous model using 13C nuclear magnetic resonance isotopomer analysis provided for direct measurement of the oxidation of 13C-enriched substrates in the tricarboxylic acid cycle and/or their entry via anaplerotic pathways. This model did not allow for recycling of labeled metabolites from tricarboxylic acid cycle intermediates into the acetyl-CoA pool. An extension of this model is now presented that incorporates carbon flow from oxaloacetate or malate to acetyl-CoA. This model was examined using propionate metabolism in the heart, in which previous observations indicated that all of the propionate consumed was oxidized to CO2 and water. Application of the new isotopomer model shows that 2 mM [3-13C]propionate entered the tricarboxylic acid cycle as succinyl-CoA (an anaplerotic pathway) at a rate equal to 52% of tricarboxylic acid cycle turnover and that all of this carbon entered the acetyl-CoA pool and was oxidized. This was verified using standard biochemical analysis; from the rate (mumol.min-1.g dry wt-1) of propionate uptake (4.0 +/- 0.7), the estimated oxygen consumption (24.8 +/- 5) matched that experimentally determined (24.4 +/- 3).

Tricarboxylic acid cycle activity in perfused rat lungs after O2 exposure

1992 ◽  
Vol 262 (4) ◽  
pp. L495-L501 ◽  
Author(s):  
D. J. Bassett ◽  
S. S. Reichenbaugh
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Enzyme Inactivation ◽  
Pyridine Nucleotides ◽  
Acid Cycle ◽  
Metabolic Conditions ◽  
Steady State Levels ◽  
14Co2 Production ◽  
Tricarboxylic Acid Cycle Intermediates

O2-induced impairment of mitochondrial energy generation was examined in intact lungs isolated from rats after 18-30 h exposure to either air or 100% O2 in vivo. Mitochondrial metabolic rates were determined by separate measurements of 14CO2 production from [1-14C]pyruvate and [U-14C]palmitate, perfused under normal and stimulated metabolic conditions brought about by perfusion with the uncoupler of oxidative phosphorylation, 2,4-dinitrophenol (DNP). In the absence of DNP, O2 exposure did not significantly alter 14CO2 productions from either substrate. DNP increased lung pyruvate and palmitate catabolism to CO2 twofold in air-exposed lungs but did not alter 14CO2 production in lungs isolated from O2-exposed rats. These data demonstrated an O2-induced impairment of maximal mitochondrial metabolism of both pyruvate and palmitate that could not be explained by alterations in tissue free coenzyme A or by loss of pyridine nucleotides. However, comparisons of the steady-state levels of tricarboxylic acid cycle intermediates between O2- and air-exposed lungs did identify isocitrate dehydrogenase as a possible site of O2-induced enzyme inactivation.

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