Mismatch between lipid mobilization and oxidation: glycerol kinetics in running African goats

1993 ◽  
Vol 264 (4) ◽  
pp. R797-R803 ◽  
Author(s):  
J. M. Weber ◽  
T. J. Roberts ◽  
C. R. Taylor
Keyword(s):  
Fatty Acid ◽  
Aerobic Capacity ◽  
Indirect Calorimetry ◽  
Treadmill Exercise ◽  
Large Fraction ◽  
O2 Consumption ◽  
Glycerol Release ◽  
Intense Exercise ◽  
Lipid Mobilization ◽  
Relative Contribution

Glycerol kinetics and total fatty acid (FA) oxidation of trained African pygmy goats were measured by continuous infusion of [2-3H]glycerol and indirect calorimetry during treadmill exercise at 40, 60, and 85% maximal O2 consumption (VO2max). Our main goals were 1) to determine whether rates of FA mobilization and utilization are eventually matched as exercise intensity increases, thereby minimizing reesterification to supply more FA to working muscles, and 2) to test the hypothesis that lipolytic rate is proportional to aerobic capacity by comparing low-aerobic goats with published values from highly aerobic dogs and humans. Mean rate of glycerol release in the circulation (Ra glycerol) was 3.83 +/- 0.11 at rest, 7.69 +/- 0.88 at 40% VO2max, reached a maximum of 15.32 +/- 0.95 at 60% VO2max, and returned to 10.53 +/- 0.76 mumol.kg-1 x min-1 at 85% VO2max. Lipolytic rate did not match total FA oxidation, implying that Ra glycerol cannot be used as an index of FA utilization, even during intense exercise. A large fraction of total FA released by lipolysis was reesterified at 60 and 85% VO2max, showing that FA mobilization does not limit whole animal FA oxidation at these intensities. Comparing goat, dog, and human responses reveals that mammalian lipolytic rate is scaled with aerobic capacity. High- and low-aerobic species exercising at the same %VO2max mobilize FA in exact proportion with their metabolic rate, suggesting that the relative contribution of FA to total energy provision is independent of VO2max.

scholarly journals Design of the oxygen and substrate pathways. III. Partitioning energy provision from carbohydrates.

1996 ◽  
Vol 199 (8) ◽  
pp. 1659-1666 ◽  
Author(s):  
J M Weber ◽  
T J Roberts ◽  
R Vock ◽  
E R Weibel ◽  
C R Taylor
Keyword(s):  
Total Energy ◽  
Aerobic Capacity ◽  
Indirect Calorimetry ◽  
Glucose Oxidation ◽  
Muscle Cells ◽  
Carbohydrate Oxidation ◽  
Total Carbohydrate ◽  
Relative Contribution ◽  
Glycogen Stores

This paper quantifies maximal fluxes through the pathway supplying carbohydrates to the mitochondria of muscle cells. Continuous infusions of D-[3-(3)H]glucose together with indirect calorimetry were used to investigate the partitioning of the supply of carbohydrates through the two branches of the pathway: from circulating glucose and from glycogen stores within the muscle cells to the mitochondria. The relative contribution of circulating glucose to total carbohydrate oxidation was small, accounting for only 13% and 23% of the carbohydrate oxidized at exercise intensities approaching MO2max in dogs and goats, respectively. Unexpectedly, maximal rates of circulating glucose oxidation were nearly the same in the two species (when expressed in absolute terms; dog:goat ratio = 1.2), despite the 2.2-fold difference in aerobic capacity. We conclude that the glycogen stores in the muscle cells are the major source of substrates at maximal rates of oxidation, supplying 60-70% of the total energy. Furthermore, it is this branch of the carbohydrate pathway that is adapted to the large difference in aerobic capacity between dogs and goats.

scholarly journals Omega-3 fatty acid blood levels are inversely associated with cardiometabolic risk factors in HFpEF patients: the Aldo-DHF randomized controlled trial

2021 ◽  
Author(s):  
Katharina Lechner ◽  
Johannes Scherr ◽  
Elke Lorenz ◽  
Benjamin Lechner ◽  
Bernhard Haller ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Aerobic Capacity ◽  
Cardiometabolic Risk ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Blood Levels ◽  
Omega 3 ◽  
Maximal Aerobic Capacity ◽  
Omega 3 Fatty Acid ◽  
Neurohumoral Activation

Abstract Objectives To evaluate associations of omega-3 fatty acid (O3-FA) blood levels with cardiometabolic risk markers, functional capacity and cardiac function/morphology in patients with heart failure with preserved ejection fraction (HFpEF). Background O3-FA have been linked to reduced risk for HF and associated phenotypic traits in experimental/clinical studies. Methods This is a cross-sectional analysis of data from the Aldo-DHF-RCT. From 422 patients, the omega-3-index (O3I = EPA + DHA) was analyzed at baseline in n = 404 using the HS-Omega-3-Index® methodology. Patient characteristics were; 67 ± 8 years, 53% female, NYHA II/III (87/13%), ejection fraction ≥ 50%, E/e′ 7.1 ± 1.5; median NT-proBNP 158 ng/L (IQR 82–298). Pearson’s correlation coefficient and multiple linear regression analyses, using sex and age as covariates, were used to describe associations of the O3I with metabolic phenotype, functional capacity, echocardiographic markers for LVDF, and neurohumoral activation at baseline/12 months. Results The O3I was below (< 8%), within (8–11%), and higher (> 11%) than the target range in 374 (93%), 29 (7%), and 1 (0.2%) patients, respectively. Mean O3I was 5.7 ± 1.7%. The O3I was inversely associated with HbA1c (r = − 0.139, p = 0.006), triglycerides-to-HDL-C ratio (r = − 0.12, p = 0.017), triglycerides (r = − 0.117, p = 0.02), non-HDL-C (r = − 0.101, p = 0.044), body-mass-index (r = − 0.149, p = 0.003), waist circumference (r = − 0.121, p = 0.015), waist-to-height ratio (r = − 0.141, p = 0.005), and positively associated with submaximal aerobic capacity (r = 0.113, p = 0.023) and LVEF (r = 0.211, p < 0.001) at baseline. Higher O3I at baseline was predictive of submaximal aerobic capacity (β = 15.614, p < 0,001), maximal aerobic capacity (β = 0.399, p = 0.005) and LVEF (β = 0.698, p = 0.007) at 12 months. Conclusions Higher O3I was associated with a more favorable cardiometabolic risk profile and predictive of higher submaximal/maximal aerobic capacity and lower BMI/truncal adiposity in HFpEF patients. Graphic abstract Omega-3 fatty acid blood levels are inversely associated with cardiometabolic risk factors in HFpEF patients. Higher O3I was associated with a more favorable cardiometabolic risk profile and aerobic capacity (left) but did not correlate with echocardiographic markers for left ventricular diastolic function or neurohumoral activation (right). An O3I-driven intervention trial might be warranted to answer the question whether O3-FA in therapeutic doses (with the target O3I 8–11%) impact on echocardiographic markers for left ventricular diastolic function and neurohumoral activation in patients with HFpEF. This figure contains modified images from Servier Medical Art (https://smart.servier.com) licensed by a Creative Commons Attribution 3.0 Unported License.

The Effects of Cold and Prostaglandin E1 on Lipid Mobilization in the Chicken

1971 ◽  
Vol 49 (5) ◽  
pp. 394-398 ◽  
Author(s):  
W. D. Wagner ◽  
R. A. Peterson ◽  
R. J. Cenedella
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Cold Exposure ◽  
Prostaglandin E1 ◽  
Plasma Free Fatty Acid ◽  
Prostaglandin E ◽  
Elevated Plasma ◽  
Lower Plasma ◽  
Lipid Mobilization ◽  
Plasma Ffa

Plasma free fatty acid (FFA) levels and the effects of prostaglandin E1 (PGE1) were studied in cold-acclimated and cold-exposed chickens and compared to controls. Chickens cold-acclimated at 4–7 or 8–11 °C for 4 weeks had significantly elevated plasma FFA when compared to the controls at 19–21 °C. Although PGE1 had no effect on the basal level of FFA of controls, a significantly lower plasma FFA was seen after injection of either 10 or 30 μg PGE1/kg in cold-acclimated chickens. Chickens cold-exposed to 2–3 °C for 4 h demonstrated significant elevations of plasma FFA when compared to controls. Only 30 μg PGE1/kg significantly depressed the plasma FFA in the cold-exposed birds. No inhibition of basal FFA release was seen in control animals. From these experiments, it is concluded that chickens mobilize FFA extensively under cold-exposure and that this stimulated lipolysis is inhibited by PGE1.

405 REGULATION OF PLASMA FREE FATTY ACID METABOLISM DURING INTENSE EXERCISE

1994 ◽  
Vol 26 (Supplement) ◽  
pp. S72
Author(s):  
C. A. Raguso ◽  
A. R. Coggan ◽  
L. S. Sidossis ◽  
A. Gastaldelli ◽  
R. R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Plasma Free Fatty Acid ◽  
Intense Exercise ◽  
Free Fatty Acid Metabolism

Fatty acid, tricarboxylic acid cycle metabolites, and energy metabolism in vascular smooth muscle

1994 ◽  
Vol 267 (2) ◽  
pp. H764-H769 ◽  
Author(s):  
J. T. Barron ◽  
S. J. Kopp ◽  
J. Tow ◽  
J. E. Parrillo
Keyword(s):  
Smooth Muscle ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Lactate Production ◽  
Tca Cycle ◽  
High Energy ◽  
Tricarboxylic Acid ◽  
O2 Consumption

The influence of octanoate on O2 consumption, tricarboxylic acid (TCA) cycle intermediates, and high-energy phosphates was examined in intact resting porcine carotid artery to investigate the role of fatty acid in energy metabolism and its integration with glucose metabolism in vascular smooth muscle. Incubation of resting arteries with octanoate (0.5 mM), which was previously shown to inhibit aerobic glycolysis (6), inhibited lactate production by 64% and increased O2 consumption by 30%. The increase in O2 consumption with octanoate was approximately equal to that calculated to account for the ATP production lost by inhibition of aerobic lactate production by octanoate. In glucose-free medium, the level of high-energy phosphate was reduced but was restored when octanoate was included in the incubation medium. This was associated with an increase in O2 consumption. These results suggest that the energy requirements of resting carotid artery can be largely met by the oxidative metabolism of fatty acid. Octanoate induced anaplerosis of the TCA cycle, as indicated by a 70% increase in the level of citrate. Extracellular glucose was necessary for octanoate-induced anaplerosis, probably by providing the extra carbon via pyruvate carboxylation, whereas a coupled transamination involving aspartate was a less important anaplerotic mechanism.

Fatty acid kinetic responses to running above or below lactate threshold

1995 ◽  
Vol 79 (2) ◽  
pp. 439-447 ◽  
Author(s):  
J. A. Kanaley ◽  
C. D. Mottram ◽  
P. D. Scanlon ◽  
M. D. Jensen
Keyword(s):  
Fatty Acid ◽  
Endurance Training ◽  
Fatty Acid Oxidation ◽  
Indirect Calorimetry ◽  
Lactate Threshold ◽  
Exercise Group ◽  
Acid Oxidation ◽  
Running Exercise ◽  
Marathon Training ◽  
Energy Demands

During running exercise above the lactate threshold (LT), it is unknown whether free fatty acid (FFA) mobilization can meet the energy demands for fatty acid oxidation. This study was performed to determine whether FFA availability is reduced during running exercise above compared with below the LT and to assess whether the level of endurance training influences FFA mobilization. Twelve marathon runners and 12 moderately trained runners ran at a workload that was either above or below their individual LT. Fatty acid oxidation (indirect calorimetry) and FFA release ([1–14C]palmitate) were measured at baseline, throughout exercise, and at recovery. The plasma FFA rate of appearance increased during exercise in both groups; running above or below the LT, but the total FFA availability for 30 min of exercise was greater (P < 0.01) in the below LT group (marathon, 23 +/- 2 mmol; moderate, 21 +/- 2 mmol) than in the above LT group (18 +/- 3 and 13 +/- 3 mmol, respectively). Total fatty acid oxidation (indirect calorimetry) greatly exceeded circulating FFA availability, regardless of training or exercise group (P < 0.01). No statistically significant exercise intensity or training differences in fatty acid oxidation were found (above LT: marathon, 71 +/- 12, moderate, 64 +/- 17 mmol/30 min; below LT: marathon 91 +/- 12, moderate, 60 +/- 5 mmol/30 min). In conclusion, during exercise above or below LT, circulating FFA cannot meet the oxidative needs and intramuscular triglyceride stores must be utilized. Further marathon training does not enhance effective adipose tissue lipolysis during exercise compared with moderate endurance training.

scholarly journals Phenolic Compounds Reduce the Fat Content in Caenorhabditis elegans by Affecting Lipogenesis, Lipolysis, and Different Stress Responses

2020 ◽  
Vol 13 (11) ◽  
pp. 355
Author(s):  
Paula Aranaz ◽  
David Navarro-Herrera ◽  
María Zabala ◽  
Ana Romo-Hualde ◽  
Miguel López-Yoldi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Phenolic Compounds ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Lipid Mobilization ◽  
C Elegans ◽  
Unfolded Protein ◽  
Reducing Activity ◽  
Protein Response

Supplementation with bioactive compounds capable of regulating energy homeostasis is a promising strategy to manage obesity. Here, we have screened the ability of different phenolic compounds (myricetin, kaempferol, naringin, hesperidin, apigenin, luteolin, resveratrol, curcumin, and epicatechin) and phenolic acids (p-coumaric, ellagic, ferulic, gallic, and vanillic acids) regulating C. elegans fat accumulation. Resveratrol exhibited the strongest lipid-reducing activity, which was accompanied by the improvement of lifespan, oxidative stress, and aging, without affecting worm development. Whole-genome expression microarrays demonstrated that resveratrol affected fat mobilization, fatty acid metabolism, and unfolded protein response of the endoplasmic reticulum (UPRER), mimicking the response to calorie restriction. Apigenin induced the oxidative stress response and lipid mobilization, while vanillic acid affected the unfolded-protein response in ER. In summary, our data demonstrates that phenolic compounds exert a lipid-reducing activity in C. elegans through different biological processes and signaling pathways, including those related with lipid mobilization and fatty acid metabolism, oxidative stress, aging, and UPR-ER response. These findings open the door to the possibility of combining them in order to achieve complementary activity against obesity-related disorders.

Profiling substrate fluxes in the isolated working mouse heart using 13C-labeled substrates: focusing on the origin and fate of pyruvate and citrate carbons

2004 ◽  
Vol 286 (4) ◽  
pp. H1461-H1470 ◽  
Author(s):  
Maya Khairallah ◽  
François Labarthe ◽  
Bertrand Bouchard ◽  
Gawiyou Danialou ◽  
Basil J. Petrof ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Ex Vivo ◽  
Heart Function ◽  
Acid Oxidation ◽  
Mouse Heart ◽  
Relative Contribution ◽  
Cardiac Functions ◽  
Lactate And Pyruvate

The availability of genetically modified mice requires the development of methods to assess heart function and metabolism in the intact beating organ. With the use of radioactive substrates and ex vivo perfusion of the mouse heart in the working mode, previous studies have documented glucose and fatty acid oxidation pathways. This study was aimed at characterizing the metabolism of other potentially important exogenous carbohydrate sources, namely, lactate and pyruvate. This was achieved by using 13C-labeling methods. The mouse heart perfusion setup and buffer composition were optimized to reproduce conditions close to the in vivo milieu in terms of workload, cardiac functions, and substrate-hormone supply to the heart (11 mM glucose, 0.8 nM insulin, 50 μM carnitine, 1.5 mM lactate, 0.2 mM pyruvate, 5 nM epinephrine, 0.7 mM oleate, and 3% albumin). The use of three differentially 13C-labeled carbohydrates and a 13C-labeled long-chain fatty acid allowed the quantitative assessment of the metabolic origin and fate of tissue pyruvate as well as the relative contribution of substrates feeding acetyl-CoA (pyruvate and fatty acids) and oxaloacetate (pyruvate) for mitochondrial citrate synthesis. Beyond concurring with the notion that the mouse heart preferentially uses fatty acids for energy production (63.5 ± 3.9%) and regulates its fuel selection according to the Randle cycle, our study reports for the first time in the mouse heart the following findings. First, exogenous lactate is the major carbohydrate contributing to pyruvate formation (42.0 ± 2.3%). Second, lactate and pyruvate are constantly being taken up and released by the heart, supporting the concept of compartmentation of lactate and glucose metabolism. Finally, mitochondrial anaplerotic pyruvate carboxylation and citrate efflux represent 4.9 ± 1.8 and 0.8 ± 0.1%, respectively, of the citric acid cycle flux and are modulated by substrate supply. The described 13C-labeling strategy combined with an experimental setup that enables continuous monitoring of physiological parameters offers a unique model to clarify the link between metabolic alterations, cardiac dysfunction, and disease development.

Oxygen consumption and hemodynamic responses during graded treadmill exercise in the dog

1984 ◽  
Vol 57 (2) ◽  
pp. 601-607 ◽  
Author(s):  
G. A. Ordway ◽  
D. L. Floyd ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Maximal Exercise ◽  
Treadmill Exercise ◽  
Work Load ◽  
Dynamic Exercise ◽  
O2 Consumption ◽  
Treadmill Test ◽  
O2 Uptake ◽  
Hemodynamic Variables ◽  
Linear Relationships ◽  
H 20

A description is given of a technique that provides a relatively simple means by which O2 consumption and hemodynamic variables can be measured in exercising dogs. We used a multistage submaximal treadmill test to study the responses of 10 foxhounds to dynamic exercise. They were also studied during maximal treadmill exercise. O2 consumption increased from 16.3 +/- 1.7 ml O2 X min-1 X kg-1 at rest to 92.9 +/- 9.7 ml O2 X min-1 X kg-1 at a work load of 6.4 km/h, 20% grade and to 111.9 +/- 9.6 ml O2 X min-1 X kg-1 during maximal exercise. Cardiac output (CO) increased from 6.11 +/- 0.45 l/min at rest to 16.91 +/- 1.46 and 17.66 +/- 0.60 l/min at 6.4 km/h, 20% grade and maximal exercise, respectively. Arteriovenous O2 difference increased from 5.8 +/- 0.3 vol% at rest to 12.0 +/- 0.4 and 13.2 +/- 0.7 vol% at 6.4 km/h, 20% grade and maximal exercise, respectively. Heart rate (HR) increased from 116 +/- 7 beats/min at rest to 250 +/- 8 beats/min at 6.4 km/h, 20% grade and to 278 +/- 6 beats/min during maximal exercise. O2 uptake, CO, and arteriovenous O2 difference increased with the onset of exercise, appeared to level at lower work intensities (6.4 km/h, 4 and 8% grade), and increased significantly at each of the higher work intensities (6.4 km/h, 12, 16, and 20% grade). Additionally, we observed linear relationships between O2 consumption and HR (HR = 1.35 X VO2 + 120.5; r = 0.87; P less than 0.001) and between O2 consumption and CO (CO = 5.91 X VO2 + 216.6; r = 0.96; P less than 0.001). Further, the linear relationship between O2 consumption and CO demonstrated in the present study is similar to that observed in humans.

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