Practical aspects of indirect calorimetry in laboratory animals

Even, Patrick C.; Mokhtarian, Asghar; Pele, Agnes

doi:10.1016/0149-7634(94)90056-6

Cited by 90 publications

(93 citation statements)

References 36 publications

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“…This hypothesis is strengthened by our observations that body weight loss is equal between genotypes during 48-h starvation and that pmch Ϫ/Ϫ rats show a refeeding deficit compared with pmch ϩ/ϩ rats during 72-h refeeding. The lower absolute EE values might be related to the lower caloric intake due to a lower thermic effect of food (12).…”

Section: E483mentioning

confidence: 99%

Pmchexpression during early development is critical for normal energy homeostasis

Mul

Berg³

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Mul JD, Yi CX, van den Berg SAA, Ruiter M, Toonen PW, van der Elst MCJ, Voshol PJ, Ellenbroek BA, Kalsbeek A, la Fleur SE, Cuppen E. Pmch expression during early development is critical for normal energy homeostasis. Am J Physiol Endocrinol Metab 298: E477-E488, 2010. First published November 24, 2009 doi:10.1152/ajpendo.00154.2009.-Postnatal development and puberty are times of strong physical maturation and require large quantities of energy. The hypothalamic neuropeptide melanin-concentrating hormone (MCH) regulates nutrient intake and energy homeostasis, but the underlying mechanisms are not completely understood. Here we use a novel rat knockout model in which the MCH precursor Pmch has been inactivated to study the effects of loss of MCH on energy regulation in more detail. Pmch Ϫ/Ϫ rats are lean, hypophagic, osteoporotic, and although endocrine parameters were changed in pmch Ϫ/Ϫ rats, endocrine dynamics were normal, indicating an adaptation to new homeostatic levels rather than disturbed metabolic mechanisms. Detailed body weight growth and feeding behavior analysis revealed that Pmch expression is particularly important during early rat development and puberty, i.e., the first 8 postnatal weeks. Loss of Pmch resulted in a 20% lower set point for body weight that was determined solely during this period and remained unchanged during adulthood. Although the final body weight is diet dependent, the Pmch-deficiency effect was similar for all diets tested in this study. Loss of Pmch affected energy expenditure in both young and adult rats, although these effects seem secondary to the observed hypophagia. Our findings show an important role for Pmch in energy homeostasis determination during early development and indicate that the MCH receptor 1 system is a plausible target for childhood obesity treatment, currently a major health issue in first world countries. melanin-concentrating hormone; hypothalamus; childhood obesity; rat knockout model CHILDHOOD OBESITY IS NOW WIDELY recognized as a severe public health issue (43). Treatment with drugs aimed at neural systems involved in the determination of the energy balance could potentially result in a lower energy balance during puberty as well as later in adulthood. Therefore, neuropeptides involved in body weight regulation during early development and puberty are attractive targets for anti-childhood obesity drugs.The neuronal metabolic systems in humans and primates develop prenatally, while in rodents these systems develop during the first 3 postnatal weeks (5, 21). This results in the activation and optimization of neuronal systems during early rodent development. A second important metabolic period is puberty, a period of major growth, hormonal changes, and sexual maturation. In the rat, puberty is characterized by different responses of young-adolescent [postnatal day (PND) 40] and young-adult (PND 60) male rats to environmental cues like stress and cold (17,18). In addition to these age-dependent behavioral differences, the amount of food consumed durin...

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Section: E483mentioning

confidence: 99%

Pmchexpression during early development is critical for normal energy homeostasis

Mul

Berg³

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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“…(Even et al 2 provide an equivalent equation -equation (7) of their paper. There is, however, an error in this equation: F in CO 2 should be replaced by F out O 2 , as correctly used in their equation (6).)…”

Section: Measurement Of Respiratory Quotientmentioning

confidence: 99%

“…There are some excellent articles that provide such information [1][2][3][4][5][6] and there would be little point in repeating them. There does, however, appear to be a need for an article that introduces those who work with animal models of obesity, and perhaps others, to the mathematics of indirect calorimetry and the limitations of its interpretation.…”

Section: Introductionmentioning

confidence: 99%

Some mathematical and technical issues in the measurement and interpretation of open-circuit indirect calorimetry in small animals

et al. 2006

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Indirect calorimetry is increasingly used to investigate why compounds or genetic manipulations affect body weight or composition in small animals. This review introduces the principles of indirect (primarily open-circuit) calorimetry and explains some common misunderstandings. It is not widely understood that in open-circuit systems in which carbon dioxide (CO 2 ) is not removed from the air leaving the respiratory chamber, measurement of airflow out of the chamber and its oxygen (O 2 ) content paradoxically allows a more reliable estimate of energy expenditure (EE) than of O 2 consumption. If the CO 2 content of the exiting air is also measured, both O 2 consumption and CO 2 production, and hence respiratory quotient (RQ), can be calculated. Respiratory quotient coupled with nitrogen excretion allows the calculation of the relative combustion of the macronutrients only if measurements are over a period where interconversions of macronutrients that alter their pool sizes can be ignored. Changes in rates of O 2 consumption and CO 2 production are not instantly reflected in changes in the concentrations of O 2 and CO 2 in the air leaving the respiratory chamber. Consequently, unless air-flow is high and chamber size is small, or rates of change of O 2 and CO 2 concentrations are included in the calculations, maxima and minima are underestimated and will appear later than their real times. It is widely appreciated that bigger animals with more body tissue will expend more energy than smaller animals. A major issue is how to compare animals correcting for such differences in body size. Comparison of the EE or O 2 consumption per gram body weight of lean and obese animals is misleading because tissues vary in their energy requirements or in how they influence EE in other ways. Moreover, the contribution of fat to EE is lower than that of lean tissue. Use of metabolic mass for normalisation, based on interspecific scaling exponents (0.75 or 0.66), is similarly flawed. It is best to use analysis of covariance to determine the relationship of EE to body mass or fat-free mass within each group, and then test whether this relationship differs between groups.

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“…The collection of V O2 and V CO2 data allowed for the estimation of energy expenditure (kcal/min), glucose oxidation (Gox, g/min), and lipid oxidation (Lox, g/min) according to classic formulas (12,38): energy expenditure ϭ 3.91 V O2 ϩ 1.10 V CO2; Gox ϭ 4.57 V CO2 Ϫ 3.23 V CO2; and Lox ϭ 1.69 V O2 Ϫ 1.69 V CO2. Energy expenditure, Gox, and Lox were converted into watts (J/s) assuming 1 kcal ϭ 4.18 kJ, 15.65 J/g for glucose, and 39.6 J/g for lipids.…”

Section: Animalsmentioning

confidence: 99%

“…Energy expenditure, Gox, and Lox were converted into watts (J/s) assuming 1 kcal ϭ 4.18 kJ, 15.65 J/g for glucose, and 39.6 J/g for lipids. Protein oxidation was not used in the calculations because it was considered negligible over a short time period, under a standard high carbohydrate diet, and in the postingestive state, that is, when other fuels are usually preferred (3,12,38). Moreover, to limit energy expenditure related to thermoregulation, the temperature in the metabolic cage was set at 26°C Ϯ 1.…”

Section: Animalsmentioning

confidence: 99%

Effects of intracerebroventricular and intra-accumbens melanin-concentrating hormone agonism on food intake and energy expenditure

Guesdon¹,

Paradis²,

Samson³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Guesdon B, Paradis É , Samson P, Richard D. Effects of intracerebroventricular and intra-accumbens melanin-concentrating hormone agonism on food intake and energy expenditure. Am J Physiol Regul Integr Comp Physiol 296: R469 -R475, 2009. First published January 7, 2009 doi:10.1152/ajpregu.90556.2008.-The brain melanin-concentrating hormone (MCH) system represents an anabolic system involved in energy balance regulation through influences exerted on the homeostatic and nonhomeostatic controls of food intake and energy expenditure. The present study was designed to further delineate the effect of the MCH system on energy balance regulation by assessing the actions of the MCH receptor 1 (MCHR1) agonism on both food intake and energy expenditure after intracerebroventricular (third ventricle) and intra-nucleus-accumbens-shell (intraNAcSH) injections of a MCHR1 agonist. Total energy expenditure and substrate oxidation were assessed following injections in male Wistar rats using indirect calorimetry. Food intake was also measured. Pair-fed groups were added to evaluate changes in thermogenesis that would occur regardless of the meal size and its thermogenic response. Using such experimental conditions, we were able to demonstrate that acute MCH agonism in the brain, besides its orexigenic effect, induced a noticeable change in the utilization of the main metabolic fuels. In pair-fed animals, MCH significantly reduced lipid oxidation when it was injected in the third ventricle. Such an effect was not observed following the injection of MCH in the NAcSH, where MCH nonetheless strongly stimulated appetite. The present results further delineate the influence of MCH on energy expenditure and substrate oxidation while confirming the key role of the NAcSH in the effects of the MCH system on food intake. brain; feeding behavior; substrate oxidation; energy balance IN THE BRAIN, SEVERAL INTERCONNECTED neurons receiving inputs from peripheral and central signals exert complex controls on food intake and energy expenditure, which are the two inescapable determinants of energy balance (6,13,23,31). In recent years, a few groups of investigators have directed their attention to one of the regulatory determinants of energy balance, namely the melanin-concentrating hormone (MCH) system. MCH-containing neurons are concentrated within the lateral hypothalamus (LH) and the adjacent zona incerta from where they project to the rest of the brain (7), in a pattern that generally conforms to the distribution of the MCH receptor 1 (MCHR1, the functional MCH receptor in rats and mice) (17).Evidence that the MCH system is involved in body weight regulation has emerged from various sources (24, 29). Hypothalamic expression of MCH mRNA is upregulated during starvation in lean mice, as well as in genetically obese ob/ob mice (30), and MCH overexpression leads to obesity and to an increased susceptibility to high-fat feeding (19). In addition, acute or chronic intracerebroventricular administration of MCH or MCHR1 agonists stimulate feeding in r...

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Practical aspects of indirect calorimetry in laboratory animals

Cited by 90 publications

References 36 publications

Pmchexpression during early development is critical for normal energy homeostasis

Pmchexpression during early development is critical for normal energy homeostasis

Some mathematical and technical issues in the measurement and interpretation of open-circuit indirect calorimetry in small animals

Effects of intracerebroventricular and intra-accumbens melanin-concentrating hormone agonism on food intake and energy expenditure

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