Energy expenditure-body size associations: molecular coordination.
Ontology highlight
ABSTRACT:
SUBMITTER: Heymsfield SB
PROVIDER: S-EPMC6375486 | biostudies-literature | 2018 Sep
REPOSITORIES: biostudies-literature
Publications
Energy expenditure-body size associations: molecular coordination.
European journal of clinical nutrition 20180905 9
Similar Datasets
Project description:Establishing if an adult's resting energy expenditure (REE) is high or low for their body size is a pervasive question in nutrition research. Early workers applied body mass and height as size measures and formulated the Surface Law and Kleiber's Law, although each has limitations when adjusting REE. Body composition methods introduced during the mid-20th century provided a new opportunity to identify metabolically homogeneous 'active' compartments. These compartments all show improved correlations with REE estimates over body mass-height approaches, but collectively share a common limitation: REE-body composition ratios are not 'constant' but vary across men and women and with race, age and body size. The now-accepted alternative to ratio-based norms is to adjust for predictors by applying regression models to calculate 'residuals' that establish if an REE is relatively high or low. The distinguishing feature of statistical REE-body composition models is a 'non-zero' intercept of unknown origin. The recent introduction of imaging methods has allowed development of physiological tissue-organ-based REE prediction models. Herein, we apply these imaging methods to provide a mechanistic explanation, supported by experimental data, for the non-zero intercept phenomenon and, in that context, propose future research directions for establishing between-subject differences in relative energy metabolism.
| S-EPMC3477241 | biostudies-literature
Project description:BackgroundTotal energy expenditure (TEE) data in patients with early-stage cancer are scarce, precluding an understanding of energy requirements.ObjectiveThe objective was to cross-sectionally characterize TEE in patients with colorectal cancer (CRC) and to compare measured TEE with energy recommendations. It was hypothesized that TEE would differ according to body mass, body composition, and physical activity level (PAL) and current energy recommendations would have poor individual-level accuracy.MethodsPatients with newly diagnosed CRC had resting energy expenditure (REE) measured by indirect calorimetry and TEE by doubly labeled water. Hypermetabolism was defined as REE > 110% of that predicted from the Mifflin St.-Jeor equation. Body composition was assessed via DXA. Physical activity was determined as the ratio of TEE to REE (TEE:REE) (PAL) and residual activity energy expenditure (RAEE). TEE was compared with energy recommendations of 25-30 kcal/d and Dietary Reference Intakes (DRIs) using Bland-Altman analyses. Patients were stratified according to median BMI, PAL, and sex-specific ratio of fat mass (FM) to fat-free mass (FFM).ResultsTwenty-one patients (M:F 14:7; mean ± SD BMI: 28.3 ± 4.9 kg/m2, age: 57 ± 12 y) were included. Most (n = 20) had stage II-III disease; 1 had stage IV. Approximately half (n = 11) were hypermetabolic; TEE was not different in those with hypermetabolism and REE as a percentage of predicted was not correlated with TEE. Mean ± SD TEE was 2473 ± 499 kcal/d (range: 1562-3622 kcal/d), or 29.7 ± 6.3 kcal/kg body weight (range: 20.4-48.5 kcal/kg body weight). Mean ± SD PAL was 1.43 ± 0.27. The energy recommendation of 25 kcal/kg underestimated TEE (-12.6% ± 16.5%, P = 0.002); all energy recommendations had wide limits of agreement (the smallest was DRI with measured PAL: -21.2% to 29.3%). Patients with higher BMI and FM:FFM had higher bias using kilocalories per kilogram recommendations; bias from several recommendations was frequently lower (i.e. underestimation) in patients with higher PAL and RAEE.ConclusionsTEE variability was not reflected in energy recommendations and error was related to body weight, body composition, and physical activity. This trial was registered at clinicaltrials.gov as NCT03131921.
| S-EPMC6669058 | biostudies-literature
Project description:ObjectivesTo examine if physical activity (PA) variety was associated with moderate- to vigorous-intensity PA (MVPA) energy expenditure and body mass index (BMI) at 18 months during an obesity intervention.MethodsParticipants with ≥ 10 minutes/week of MVPA at 6 months and complete PA data were included. Participants were classified into Variety (N = 30), ≥ 2 different activities/week, or Less Variety (N = 65), only 1 activity/week.ResultsWeekly MVPA-related energy expenditure was higher for Variety than Less Variety (3674.7 ± 1934.6 kcal/week vs 2197.3 ± 1841.4 kcal/week, p < .05) at 18 months, with no difference in BMI.ConclusionsGreater weekly PA variety during obesity treatment was related to greater 18-month MVPA energy expenditure.
| S-EPMC4828137 | biostudies-literature
Project description:Body mass in humans and animals is strongly associated with the rate of heat production as defined by resting energy expenditure (REE). Beginning with the ancient Greeks up to the present time, philosophers and scientists have endeavored to understand the nature and sources of bodily heat. Today we recognize that body mass consists of organs and tissues, each of which produces a specified amount of heat at rest. An individual organ's REE can now be estimated in vivo as the product of its assumed mass-specific metabolic rate and its imaging-derived mass; whole-body REE reflects the sum of organ and tissue metabolic rates. The sizes of organs and total body mass in adults are governed by two main factors, a person's stature or height, and their level of adiposity. With greater body size, as represented by adult height independent of adiposity, organs remain stable or increase in mass according to distinct "scaling" patterns. Similarly, with greater relative adiposity organs adaptively accommodate to the increase in imposed mechanical and metabolic loading conditions. Through a detailed analysis of these stature and adiposity effects, we show how classical statistical REE prediction models can be mechanistically understood at the anatomic body composition level.
| S-EPMC6410366 | biostudies-literature
Project description:SIRT1 is a NAD(+)-dependent enzyme that affects metabolism by deacetylating key transcriptional regulators of energy expenditure. Here, we tested whether deletion of PARP-2, an alternative NAD(+)-consuming enzyme, impacts on NAD(+) bioavailability and SIRT1 activity. Our results indicate that PARP-2 deficiency increases SIRT1 activity in cultured myotubes. However, this increase was not due to changes in NAD(+) levels, but to an increase in SIRT1 expression, as PARP-2 acts as a direct negative regulator of the SIRT1 promoter. PARP-2 deletion in mice increases SIRT1 levels, promotes energy expenditure, and increases mitochondrial content. Furthermore, PARP-2(-/-) mice were protected against diet-induced obesity. Despite being insulin sensitized, PARP-2(-/-) mice were glucose intolerant due to a defective pancreatic function. Hence, while inhibition of PARP activity promotes oxidative metabolism through SIRT1 activation, the use of PARP inhibitors for metabolic purposes will require further understanding of the specific functions of different PARP family members.
| S-EPMC3108571 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-04-20 | GSE230208 | GEO
Project description:Abstract Background: The uncoupling proteins (UCPs) belong to the mitochondrial inner membrane anion carrier superfamily and play an important role in energy homeostasis. UCP-1 is expressed mostly in brown adipose tissue (BAT) and act in the thermogenesis and regulation of energy expenditure. UCP-2 has a role in the metabolism of fatty acids direct and indirectly path insulin secretion. UCP-3 is specific of skeletal muscle and BAT and may affects the adaptive and translocation of fatty acids. Genetic polymorphisms in these proteins have been associated with obesity, as rs1800592 (-3826 A/G) in UCP-1 gene. The rs659366 (-866GA) UCP-2 has being associated with high expression of its RNAm, decrease of obesity risk, and increase of energy expenditure. The rs1800849 (-55CT) UCP-3 has been associated with low risk of type 2 Diabetes Mellitus, but its association with body mass index is controversial. Objective: To analyze the association of the polymorphisms rs1800592 UCP-1, rs659366 UCP-2, and rs1800849 UCP-3 with BMI and resting energy expenditure (REE). Material and Methods: We included 120 subjects with BMI>30kg/m2 and 100 subjects with BMI between18.5 -24.9 kg/m2, aged 20 to 50 years. Anthropometric data were recorded and the REE was measure for indirect calorimetric. Fasting glucose and lipid profile were assessed. Leptin, insulin and acylated-ghrelin were quantified by ELISA. Genomic DNA was extracted using comercial kit. Genotyping for three polymorphisms was performed by allelic discrimination using Taqman probes. Results: All the three polymorphisms of UCPs showed distribution in accordance with Hardy-Weinberg equilibrium. The weight, BMI, glucose, triglycerides, leptin, insulin, HOMA-IR, and REE levels were signitifcantly higher in obese subjects. There was a strong correlation between REE with BMI (r=0.42, p<0.00001) and with insulin levels (r=0.229, p=0.001) in all group. No differences in genotypic and allelic frequencies of rs1800592 UCP-1, rs659366 UCP-2 and rs180084 UCP-3 polymorphisms between obese and lean subjects. No differences among the genotypes rs1800592 UCP-1 and rs1800849 UCP-3 with metabolic variables. In rs659366 UCP-2 polymorhism, the REE and glucose concentrations were lower in carriers of rs659366AA genotype (F=3.11, p=0.046; F=2.97, p=0.053, respectively) in whole group. In obese subjects with rs659366AA UCP-2 genotype, the REE was significantly low (F=4.15, P=0.017). Conclusion. In this work the obese subjects with rs659366AA genotype had low REE. We found low glucose concentrations in the carries of rs659366 AA genotype.
| S-EPMC7209614 | biostudies-literature
Project description:BackgroundThere is a paucity of studies that have prospectively tested the energy surfeit theory of obesity with the use of objectively estimated energy intake and energy expenditure in humans. An alternative theory is that homeostatic regulation of body weight is more effective when energy intake and expenditure are both high (high energy flux), implying that low energy flux should predict weight gain.ObjectiveWe aimed to examine the predictive relations of energy balance and energy flux to future weight gain and tested whether results were replicable in 2 independent samples.DesignAdolescents (n = 154) and college-aged women (n = 75) underwent 2-wk objective doubly labeled water, resting metabolic rate, and percentage of body fat measures at baseline. Percentage of body fat was measured annually for 3 y of follow-up for the adolescent sample and for 2 y of follow-up for the young adult sample.ResultsLow energy flux, but not energy surfeit, predicted future increases in body fat in both studies. Furthermore, high energy flux appeared to prevent fat gain in part because it was associated with a higher resting metabolic rate.ConclusionCounter to the energy surfeit model of obesity, results suggest that increasing energy expenditure may be more effective for reducing body fat than caloric restriction, which is currently the treatment of choice for obesity. This trial was registered at clinicaltrials.gov as NCT02084836.
| S-EPMC4880998 | biostudies-literature
Project description:Metabolic processes that regulate muscle energy use are major determinants of bodily energy balance. Here, we find that sarcolemmal ATP-sensitive K(+) (K(ATP)) channels, which couple membrane excitability with cellular metabolic pathways, set muscle energy expenditure under physiological stimuli. Disruption of K(ATP) channel function provoked, under conditions of unaltered locomotor activity and blood substrate availability, an extra energy cost of cardiac and skeletal muscle performance. Inefficient fuel metabolism in K(ATP) channel-deficient striated muscles reduced glycogen and fat body depots, promoting a lean phenotype. The propensity to lesser body weight imposed by K(ATP) channel deficit persisted under a high-fat diet, yet obesity restriction was achieved at the cost of compromised physical endurance. Thus, sarcolemmal K(ATP) channels govern muscle energy economy, and their downregulation in a tissue-specific manner could present an antiobesity strategy by rendering muscle increasingly thermogenic at rest and less fuel efficient during exercise.
| S-EPMC2849280 | biostudies-literature
Project description:The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) control glucose homeostasis through well-defined actions on the islet beta cell via stimulation of insulin secretion and preservation and expansion of beta cell mass. We examined the importance of endogenous incretin receptors for control of glucose homeostasis through analysis of Glp1r(-/-), Gipr(-/-), and double incretin receptor knockout (DIRKO) mice fed a high-fat (HF) diet. DIRKO mice failed to upregulate levels of plasma insulin, pancreatic insulin mRNA transcripts, and insulin content following several months of HF feeding. Both single incretin receptor knockout and DIRKO mice exhibited resistance to diet-induced obesity, preservation of insulin sensitivity, and increased energy expenditure associated with increased locomotor activity. Moreover, plasma levels of plasminogen activator inhibitor-1 and resistin failed to increase significantly in DIRKO mice after HF feeding, and the GIP receptor agonist [D-Ala(2)]GIP, but not the GLP-1 receptor agonist exendin-4, increased the levels of plasma resistin in studies of both acute and chronic administration. These findings extend our understanding of how endogenous incretin circuits regulate glucose homeostasis independent of the beta cell via control of adipokine secretion and energy expenditure.
| S-EPMC1705821 | biostudies-literature