scholarly journals Luminescence spectroscopy of singlet oxygen enables monitoring of oxygen consumption in biological systems consisting of fatty acids

2013 ◽  
Vol 15 (27) ◽  
pp. 11386 ◽  
Author(s):  
Anita Gollmer ◽  
Johannes Regensburger ◽  
Tim Maisch ◽  
Wolfgang Bäumler

1974 ◽  
Vol 58 (3) ◽  
pp. 660-666 ◽  
Author(s):  
Kiyoshi Goda ◽  
Tokuji Kimura ◽  
Arthur L. Thayer ◽  
Kenneth Kees ◽  
A. Paul Schaap


1976 ◽  
Vol 37 (1) ◽  
pp. 167 ◽  
Author(s):  
William J. Rogers ◽  
Richard O. Russell ◽  
Roger E. Moraski ◽  
Huey G. McDaniel ◽  
Charles E. Rackley




1957 ◽  
Vol 35 (1) ◽  
pp. 511-525 ◽  
Author(s):  
Richard F. Passey ◽  
Donald Fairbairn

While ascaris eggs developed to the vermiform stage (10 days) both lipids and carbohydrates (glycogen and trehalose) decreased in amount. During the next 15 days, in which the embryo became infective, lipids continued to decrease, but at a greater rate, whereas carbohydrate was completely resynthesized. Examination of the possible sources of the required carbon revealed that protein, non-protein nitrogenous compounds, phosphorus compounds, metabolic acids, glycerol, and volatile acids occurring in the triglycerides were not adequate and that carbon dioxide was not extensively fixed. Direct evidence for the conversion of triglyceride acids to carbohydrate was furnished by the increase in lipid-free dry weight, which corresponded closely with the increase in carbohydrate. Moreover, the amount of lipid carbon which disappeared was equal to the sum of the carbon dioxide and carbohydrate carbon which appeared, and oxygen consumption was insufficient to account for the complete combustion of lipid carbon. It was concluded that the carbon of partially oxidized fragments of fatty acids, possibly acetylcoenzyme A, was incorporated into glycogen and trehalose, and hence that ascaris eggs in this stage of their development were able to bring about a net conversion of fat to carbohydrate.







Author(s):  
Luke V. Lutkus ◽  
Sam S. Rickenbach ◽  
Theresa M. McCormick


2019 ◽  
Vol 149 (12) ◽  
pp. 2120-2132 ◽  
Author(s):  
Elizabeth R Axton ◽  
Laura M Beaver ◽  
Lindsey St. Mary ◽  
Lisa Truong ◽  
Christiana R Logan ◽  
...  

ABSTRACT Background Dietary nitrate improves exercise performance by reducing the oxygen cost of exercise, although the mechanisms responsible are not fully understood. Objectives We tested the hypothesis that nitrate and nitrite treatment would lower the oxygen cost of exercise by improving mitochondrial function and stimulating changes in the availability of metabolic fuels for energy production. Methods We treated 9-mo-old zebrafish with nitrate (sodium nitrate, 606.9 mg/L), nitrite (sodium nitrite, 19.5 mg/L), or control (no treatment) water for 21 d. We measured oxygen consumption during a 2-h, strenuous exercise test; assessed the respiration of skeletal muscle mitochondria; and performed untargeted metabolomics on treated fish, with and without exercise. Results Nitrate and nitrite treatment increased blood nitrate and nitrite levels. Nitrate treatment significantly lowered the oxygen cost of exercise, as compared with pretreatment values. In contrast, nitrite treatment significantly increased oxygen consumption with exercise. Nitrate and nitrite treatments did not change mitochondrial function measured ex vivo, but significantly increased the abundances of ATP, ADP, lactate, glycolytic intermediates (e.g., fructose 1,6-bisphosphate), tricarboxylic acid (TCA) cycle intermediates (e.g., succinate), and ketone bodies (e.g., β-hydroxybutyrate) by 1.8- to 3.8-fold, relative to controls. Exercise significantly depleted glycolytic and TCA intermediates in nitrate- and nitrite-treated fish, as compared with their rested counterparts, while exercise did not change, or increased, these metabolites in control fish. There was a significant net depletion of fatty acids, acyl carnitines, and ketone bodies in exercised, nitrite-treated fish (2- to 4-fold), while exercise increased net fatty acids and acyl carnitines in nitrate-treated fish (1.5- to 12-fold), relative to their treated and rested counterparts. Conclusions Nitrate and nitrite treatment increased the availability of metabolic fuels (ATP, glycolytic and TCA intermediates, lactate, and ketone bodies) in rested zebrafish. Nitrate treatment may improve exercise performance, in part, by stimulating the preferential use of fuels that require less oxygen for energy production.



2010 ◽  
Vol 299 (3) ◽  
pp. E475-E485 ◽  
Author(s):  
Nicolai M. Doliba ◽  
Wei Qin ◽  
Sergei A. Vinogradov ◽  
David F. Wilson ◽  
Franz M. Matschinsky

Fatty acids, acetylcholine, and GLP-1 enhance insulin secretion in a glucose-dependent manner. However, the interplay between glucose, fatty acids, and the neuroendocrine regulators of insulin secretion is not well understood. Therefore, we studied the acute effects of PA (alone or in combination with glucose, acetylcholine, or GLP-1) on isolated cultured mouse islets. Two different sets of experiments were designed. In one, a fixed concentration of 0.5 mM of PA bound to 0.15 mM BSA was used; in the other, a PA ramp from 0 to 0.5 mM was applied at a fixed albumin concentration of 0.15 mM so that the molar PA/BSA ratio changed within the physiological range. At a fixed concentration of 0.5 mM, PA markedly inhibited acetylcholine-stimulated insulin release, the rise of intracellular Ca2+, and enhancement of cAMP production but did not influence the effects of GLP-1 on these parameters of islet cell function. 2-ADB, an IP3 receptor inhibitor, reduced the effect of acetylcholine on insulin secretion and reversed the effect of PA on acetylcholine-stimulated insulin release. Islet perfusion for 35–40 min with 0.5 mM PA significantly reduced the calcium storage capacity of ER measured by the thapsigargin-induced Ca2+ release. Oxygen consumption due to low but not high glucose was reduced by PA. When a PA ramp from 0 to 0.5 mM was applied in the presence of 8 mM glucose, PA at concentrations as low as 50 μM significantly augmented glucose-stimulated insulin release and markedly reduced acetylcholine's effects on hormone secretion. We thus demonstrate that PA acutely reduces the total oxygen consumption response to glucose, glucose-dependent acetylcholine stimulation of insulin release, Ca2+, and cAMP metabolism, whereas GLP-1's actions on these parameters remain unaffected or potentiated. We speculate that acute emptying of the ER calcium by PA results in decreased glucose stimulation of respiration and acetylcholine potentiation of insulin secretion.



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