The basis of direct and indirect calorimetry and their potentials

Schütz, Y.

doi:10.1002/dmr.5610110406

Cited by 53 publications

(29 citation statements)

References 71 publications

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“…19 However, the conclusion that de novo lipogenesis is reduced by BCaSKF based on RQ values is valid under these circumstances (that is, RQ b 1.0) 20 and is further evidenced by drug-induced substantial decreases in hepatic and adipose tissue lipogenic enzyme activities (Table 4). However, additional mechanisms are operative in the BCaSKF induced reduction in serum FFA.…”

Section: Dopaminergic Agonists Improve Diabetes In Obaob Micementioning

confidence: 96%

Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists

et al. 1999

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OBJECTIVE: We previously reported that a two week treatment with SKF 38393 (SKF, a dopamine D 1 receptor agonist), plus bromocriptine (BC, a dopamine D 2 receptor agonist) acted synergistically to normalize hyperphagia, body fat, hyperglycaemia and hyperlipidaemia in obaob mice. The present study further investigates the biochemical mechanisms triggered by this drug treatment. DESIGN: Six week old female C57BLa6J obaob mice were divided into three groups and treated for two weeks with either BC and SKF, vehicle (control), or vehicle and pair fed to match the drug-treated group's daily food intake. RESULTS: BCaSKF treatment reduced food consumption by 55%, and treated mice weighed less than either pair fed or ad libitum fed controls after two weeks of treatment. Moreover, oxygen consumption was increased by 2.4-fold and the respiratory quotient (RQ) decreased from 1.23 to 0.96 (indicating a reduction in de novo lipogenesis) by drug treatment relative to ad libitum fed controls, but these parameters were unaffected by pair feeding control mice. The treatment also reduced blood glucose and free fatty acids (FFA) relative to pair fed and ad libitum fed controls. BCaSKF treatment (but not pair feeding) concurrently reduced lipolysis, lipogenic enzyme activities and hepatic gluconeogenic enzyme activities. Treatment also increased hepatic concentrations of glycogen and xylulose-5-phosphate (X-5-P), a key stimulator of glycolysis. Finally, BCaSKF, but not pair feeding, reduced the circulating concentrations of thyroxine and corticosterone, two hormones known to increase lipolysis, lipogenesis and hyperglycaemia. Drug treatment also increased serum dehydroepiandrosterone (DHEA) sulfate concentrations, an inhibitor of body fat store accumulation. CONCLUSION: These ®ndings demonstrate that BCaSKF treatment not only normalizes hyperphagia of obaob mice, but also redirects several metabolic and endocrine activities, independent of its effects on feeding to improve the obese-diabetic syndrome in obaob mice.

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Section: Dopaminergic Agonists Improve Diabetes In Obaob Micementioning

confidence: 96%

Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists

et al. 1999

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“…The use of ammonia alone (as the end product) was justified because the use of urea as the end product requires blood sampling at the beginning and end of the test to correct for the 15 N remaining in the urea pool.…”

Section: Assessment Of Protein Turnovermentioning

confidence: 99%

“…Details of the method were described previously by Fern et al (16,17). The 15 N enrichment of ammonia was corrected for background isotopic 15 N abundance in urine (typically 0.366 atom%) as measured in the first predose urine sample.…”

Section: Assessment Of Protein Turnovermentioning

confidence: 99%

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Whole-body protein turnover and resting energy expenditure in obese, prepubertal children2

Schütz

Rueda-Maza

Zaffanello

et al. 1999

The American Journal of Clinical Nutrition

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Background: Obesity is becoming more frequent in children; understanding the extent to which this condition affects not only carbohydrate and lipid metabolism but also protein metabolism is of paramount importance. Objective: We evaluated the kinetics of protein metabolism in obese, prepubertal children in the static phase of obesity. Design: In this cross-sectional study, 9 obese children (x -± SE: 44 ± 4 kg, 30.9 ± 1.5% body fat) were compared with 8 lean (28 ± 2 kg ,16.8 ± 1.2% body fat), age-matched (8.5 ± 0.2 y) control children. Whole-body nitrogen flux, protein synthesis, and protein breakdown were calculated postprandially over 9 h from 15 N abundance in urinary ammonia by using a single oral dose of [ 15 N]glycine; resting energy expenditure (REE) was assessed by indirect calorimetry (canopy) and body composition by multiple skinfold-thickness measurements. Results: Absolute rates of protein synthesis and breakdown were significantly greater in obese children than in control children (x -± SE: 208 ± 24 compared with 137 ± 14 g/d, P < 0.05, and 149 ± 20 compared with 89 ± 13 g/d, P < 0.05, respectively). When these variables were adjusted for fat-free mass by analysis of covariance, however, the differences between groups disappeared. There was a significant relation between protein synthesis and fat-free mass (r = 0.83, P <0.001) as well as between protein synthesis and REE (r = 0.79, P < 0.005). Conclusions: Obesity in prepubertal children is associated with an absolute increase in whole-body protein turnover that is consistent with an absolute increase in fat-free mass, both of which contribute to explaining the greater absolute REE in obese children than in control children. Am J Clin Nutr 1999;69:857-62. KEY WORDSEnergy metabolism, resting metabolic rate, protein metabolism, whole-body protein turnover, protein synthesis, fat-free mass, obesity, children INTRODUCTIONAlthough much research has been conducted on human obesity in the past decades, more investigations have been performed of adult obesity than of childhood onset obesity. It is well known, however, that many obese adults were obese when they were young (1-5). Therefore, important issues to explore are whether the metabolic disturbances encountered in adult obesity (blunted postprandial thermogenesis, increased lipid oxidation, impaired glucose tolerance, and insulin resistance) can be observed at younger ages and to assess the magnitude of these disturbances and the age of onset.The postabsorptive resting metabolic rate of obese children was explored previously by several investigators (6-8). When expressed as an absolute value, the rate of resting energy expenditure (REE) was found to be greater in obese than in nonobese children or adolescents (6-8), confirming results observed in obese adolescents (9) and obese adults (10). The small increase in fat-free mass (FFM) accompanying the large inflation in adipose tissue in obese children explains the greater REE in these children than in lean children. However, this constitutes an e...

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“…RQ, the amount of carbon dioxide released per liter of oxygen consumed, depends upon the type of fuel preferentially oxidized in the body. RQ equal to 1 signifies that majority of calories are derived from glucose oxidation, while RQ close to 0.7 or below signifies oxidation of fat (14). In the fed state, there was no significant difference in the RQ between animals of all 3 genotypes ( Figure 1A).…”

Section: Icam-1 or Cd18 Deficiency Diminishes The Physiologic Change mentioning

confidence: 95%

ICAM-1 and β2 Integrin Deficiency Impairs Fat Oxidation and Insulin Metabolism during Fasting

Babić

Wang

Lai

et al. 2004

Mol Med

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Intercellular adhesion molecule 1 (ICAM-1) and β2 integrins play critical roles in immune responses. ICAM-1 may also participate in regulation of energy balance because ICAM-1-deficient mice become obese on a high-fat diet. We show that mice deficient in these adhesion receptors are unable to respond to fasting by up-regulation of fatty acid oxidation. Normal mice, when fasted, exhibit reduced circulating neutrophil counts and increased ICAM-1 expression and neutrophil recruitment in liver. Mice lacking ICAM-1 or β2 integrins fail to show these responses-instead they become hypoglycemic with steatotic livers. Fasting ICAM-1-deficient mice reduce insulin more slowly than wild-type mice. This produces fasting hyperinsulinemia that prevents activation of adenosine mono-phosphate (AMP)-activated protein kinase in muscles and liver, which results in decreased import of long chain fatty acids into mitochondria. Thus, we show a new role for immune cells and their adhesion receptors in regulating metabolic response to fasting.

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The basis of direct and indirect calorimetry and their potentials

Cited by 53 publications

References 71 publications

Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists

Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists

Whole-body protein turnover and resting energy expenditure in obese, prepubertal children2

ICAM-1 and β2 Integrin Deficiency Impairs Fat Oxidation and Insulin Metabolism during Fasting

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