Dose-response relationship between fat ingestion and oxidation: quantitative estimation using whole-body calorimetry and 13C isotope ratio mass spectrometry

Bj, Sonko; Am, Prentice; Coward, W. A.; Murgatroyd, P. R.; Goldberg, G R

doi:10.1038/sj.ejcn.1601112

Cited by 20 publications

(17 citation statements)

References 27 publications

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“…Greater fat intake would dilute the tracer and, thus, might have reduced recovery, but recovery tended to be largest after moderate exercise, which was the trial with the greatest intake. Second, data from Sonko et al (38) showed only a modest 11% relative decrease in labeled fatty-acid oxidation when the label was given with 50 grams of fat instead of 20 grams of fat, a much larger difference in fat intake than in our study. Finally, whole-body fat use during the entire chamber stay was greater during the moderate trial than the rest and heavy trials, but not the light trial, which was opposite of the intake statistics, suggesting that fat intake in our study was not the driving force in fat oxidation.…”

Section: Effect Of Exercise Intensity On Dietary-fat Usecontrasting

confidence: 47%

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

2003

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VOTRUBA, SUSANNE B., RICHARD L. ATKINSON, AND DALE A. SCHOELLER. Prior exercise increases dietary oleate, but not palmitate oxidation. Obes Res. 2003; 11:1509 -1518. Objective: Higher levels of physical activity have been associated with body weight maintenance, but previous work in our laboratory suggests that this is not purely related to energy balance. We hypothesize that this may be related to the partitioning of dietary fat between oxidation and storage. Research Methods and Procedures: Healthy women (age 24 Ϯ 1 years, BMI ϭ 21.2 Ϯ 0.4 kg/m 2 ) were recruited to participate in rest (n ϭ 10) or exercise sessions of light (n ϭ 11), moderate (n ϭ 10), and heavy (n ϭ 7) exercise. All exercises (1250 kJ above rest) were performed on a stationary cycle inside of a whole-body calorimeter. Results: Cumulative oxidation of [1-13 C]oleate was significantly greater after light (45 Ϯ 3%), moderate (54 Ϯ 4%), and heavy (51 Ϯ 4%) exercise than that with rest (33 Ϯ 3%) (p ϭ 0.0008). Cumulative oxidation of [d 31 ]palmitate did not differ among trials (12 Ϯ 2%, 14 Ϯ 1%, 17 Ϯ 2%, and 14 Ϯ 2% for rest, light, moderate, and heavy, respectively; p ϭ 0.30). Discussion: Exercise standardized for energy expenditure increases monounsaturated fat oxidation more than saturated fat oxidation and that the increase occurs regardless of intensity. Recommendations for physical activity for the purposes of weight control may be specific for dietary fat composition.

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Section: Effect Of Exercise Intensity On Dietary-fat Usecontrasting

confidence: 47%

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

2003

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“…This is assessed by using exogenous fatty acids labeled with C13 and integrated in the meal, and by measuring the C13 abundance in the expired air. [8][9][10] Since exogenous fat in the postprandial phase is mostly stored (in adipose tissue), the fraction oxidized is generally low, ranging from 10 to 20% of the exogenous fat intake, depending upon the conditions of measurements (duration) as well as the composition of the diet.…”

Section: àWhole Body Fat Oxidation ð1þmentioning

confidence: 99%

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Schütz

2004

Int J Obes

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The measurement of fat balance (fat input minus fat output) involves the accurate estimation of both metabolizable fat intake and total fat oxidation. This is possible mostly under laboratory conditions and not yet in free-living conditions. In the latter situation, net fat retention/mobilization can be estimated based on precise and accurate sequential body composition measurements. In case of positive balance, lipids stored in adipose tissue can originate from dietary (exogenous) lipids or from nonlipid precursors, mainly from carbohydrates (CHOs) but also from ethanol, through a process known as de novo lipogenesis (DNL). Basic equations are provided in this review to facilitate the interpretation of the different subcomponents of fat balance (endogenous vs exogenous) under different nutritional circumstances. One difficulty is methodological: total DNL is difficult to measure quantitatively in man; for example, indirect calorimetry only tracks net DNL, not total DNL. Although the numerous factors (mostly exogenous) influencing DNL have been studied, in particular the effect of CHO overfeeding, there is little information on the rate of DNL in habitual conditions of life, that is, large day-to-day fluctuations of CHO intakes, different types of CHO ingested with different glycemic indexes, alcohol combined with excess CHO intakes, etc. Three issues, which are still controversial today, will be addressed: (1) Is the increase of fat mass induced by CHO overfeeding explained by DNL only, or by decreased endogenous fat oxidation, or both? (2) Is DNL different in overweight and obese individuals as compared to their lean counterparts? (3) Does DNL occur both in the liver and in adipose tissue? Recent studies have demonstrated that acute CHO overfeeding influences adipose tissue lipogenic gene expression and that CHO may stimulate DNL in skeletal muscles, at least in vitro. The role of DNL and its importance in health and disease remain to be further clarified, in particular the putative effect of DNL on the control of energy intake and energy expenditure, as well as the occurrence of DNL in other tissues (such as in myocytes) in addition to hepatocytes and adipocytes.

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“…During this day, the subjects were allowed to engage in normal daily activities, with the exception of any vigorous activities or structured exercise. At 7:00 PM, they were asked to void, and a urine sample was stored to determine the basal body enrichment in H 2 18 O. After being weighed, a 0.4 g/kg estimated total body water dose of 10% H 2 18 O was given to the subjects.…”

Section: Protocolmentioning

confidence: 99%

“…When oxidized, 2 H-labeled fatty acid is metabolized to acetyl-CoA, releasing NADH molecules. The 2 H label is released as water, in part, when NADH molecules are oxidized in the respiratory chain.…”

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confidence: 99%

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Validation of deuterium-labeled fatty acids for the measurement of dietary fat oxidation during physical activity

Raman

Blanc²,

Adams

et al. 2004

Journal of Lipid Research

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Measurement of 13 C-labeled fatty acid oxidation is hindered by the need for acetate correction, measurement of the rate of CO 2 production in a controlled environment, and frequent collection of breath samples. The use of deuterium-labeled fatty acids may overcome these limitations. Herein, d 31 -palmitate was validated against [1-13 C]palmitate during exercise. Thirteen subjects with body mass index of 22.9 ؎ 3 kg/m 2 and body fat of 19.6 ؎ 11% were subjected to 2 or 4 h of exercise at 25% maximum volume oxygen consumption (VO 2max Stable isotopes have been used to quantify plasma and dietary fat oxidation in the past (1-3). When a 13 C-labeled fatty acid is dosed orally or by constant infusion, the 13 CO 2 in breath can be used to measure the tracer oxidized. The 13 C liberated during oxidative metabolism, however, is partly sequestered in the intermediates of the tricarboxylic acid (TCA) cycle ( ‫ف‬ 40%) and the bicarbonate pool (10%), causing fat oxidation to be underestimated. To correct for this sequestration, an additional dose of [1-13 C]acetate is administered. Acetate is converted to acetyl-CoA and is oxidized in the TCA cycle (4). Unfortunately, sequestration is variable and depends on the conditions under which it is measured; hence, estimation of acetate sequestration is essential (5). In addition, the use of 13 C-labeled fatty acid is further constrained by the need for frequent sampling of breath and the use of a metabolic cart or respiratory chamber to quantify the flux of CO 2 to calculate 13 C recovery accurately. These factors increase subject burden; thus, an alternative method to quantify fat oxidation in the body would be useful.One such method for the measurement of fat oxidation is the use of deuterium-labeled fatty acids (3, 6). When oxidized, 2 H-labeled fatty acid is metabolized to acetyl-CoA, releasing NADH molecules. The 2 H label is released as water, in part, when NADH molecules are oxidized in the respiratory chain. Oxidation of acetyl-CoA in the TCA cycle releases the rest of the deuterium label in the form of 2 Hlabeled water. This 2 H 2 O mixes with the body water and can be sampled in the urine (7). Urinary and insensible water losses are minimal (8); hence, the enrichment of label in urine can be used effectively to calculate the cumulative recovery of the label and hence the fat oxidized. Consequently, the need for measurement of CO 2 and flux is also eliminated.Deuterium-labeled palmitic acid has been validated against acetate-corrected 13 C-labeled palmitic acid during rest in humans by Votruba, Zeddun, and Schoeller (6), who dosed subjects at rest with 13 C-and d 31 -labeled palmitic acid and demonstrated that the cumulative recoveries for

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Dose-response relationship between fat ingestion and oxidation: quantitative estimation using whole-body calorimetry and 13C isotope ratio mass spectrometry

Cited by 20 publications

References 27 publications

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Validation of deuterium-labeled fatty acids for the measurement of dietary fat oxidation during physical activity

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