Resting Energy Expenditure Is Elevated in Asthma.
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ABSTRACT:
SUBMITTER: Mey JT
PROVIDER: S-EPMC8064324 | biostudies-literature | 2021 Mar
REPOSITORIES: biostudies-literature
Publications
Resting Energy Expenditure Is Elevated in Asthma.
Mey Jacob T JT Matuska Brittany B Peterson Laura L Wyszynski Patrick P Koo Michelle M Sharp Jacqueline J Pennington Emily E McCarroll Stephanie S Micklewright Sarah S Zhang Peng P Aronica Mark M Hoddy Kristin K KK Champagne Catherine M CM Heymsfield Steven B SB Comhair Suzy A A SAA Kirwan John P JP Erzurum Serpil C SC Mulya Anny A
Nutrients 20210325 4
<b>Background:</b> Asthma physiology affects respiratory function and inflammation, factors that may contribute to elevated resting energy expenditure (REE) and altered body composition. <b>Objective:</b> We hypothesized that asthma would present with elevated REE compared to weight-matched healthy controls. <b>Methods:</b> Adults with asthma (<i>n</i> = 41) and healthy controls (<i>n</i> = 20) underwent indirect calorimetry to measure REE, dual-energy X-ray absorptiometry (DEXA) to measure body ...[more]
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| S-EPMC6300153 | 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.
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Project description:ContextPseudohypoparathyroidism type 1A (PHP1A) is caused by loss-of-function mutations on the maternally inherited GNAS allele and is associated with early-onset obesity, neurocognitive defects, and resistance to multiple hormones. The role of energy intake vs central regulation of energy expenditure in the pathophysiology of obesity remains unclear.ObjectiveThe aim of this study was to evaluate resting energy expenditure (REE) in participants with PHP1A.DesignWe assessed REE, biochemical, endocrine, and auxological status of 12 participants with PHP1A who had normal or elevated body mass index; controls were a cohort of 156 obese participants.SettingThis study took place at Children's Hospital in Philadelphia and Sick Children's Hospital in Toronto.Main outcome measuresREE as a percent of predicted REE was the outcome measure.ResultsPHP1A participants had normal endocrine status while receiving appropriate hormone replacement therapy, but had significantly decreased REE as a percent of predicted REE (using the modified Schofield equation).ConclusionOur results are consistent with REE being the principal cause of obesity in PHP1A rather than it being caused by excessive energy intake or endocrine dysfunction.
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Project description:PurposeThe purpose of this study was: 1) To compare Resting energy expenditure (REE) in adult males with Becker's Muscular Dystrophy (BeMD, n = 21, 39 ±12 years) and healthy controls (CTRL, n = 12, 37 ±12 years) 2) Determine whether other physiological parameters correlate with REE in BeMD, and 3) Compare current prediction methods of REE with measured REE.MethodsREE was calculated via indirect calorimetry using continuous, expired gas analysis following an overnight fast. Fat free mass (FFM) and fat mass were measured by bioelectrical impedance. B-mode ultrasound measured Tibialis Anterior (TA) and Gastrocnemius Medialis (GM) anatomical cross sectional area (ACSA). The Bone Specific Physical Activity Questionnaire measured physical activity.ResultsNo difference in REE was found between CTRL and BeMD groups (1913 ±203 & 1786 ±324 Kcal respectively). Other physiological comparisons showed increased fat mass (+54%), decreased TA ACSA (-42%), increased GM ACSA (+25%) as well as reduced respiratory function (FVC -28%; FEV1-27%) in BeMD adults compared to controls. REE estimated from prediction equations (Schofield's) in Muscular Dystrophy were different from measured REE (P<0.05, bias = -728kcal), while the Mifflin equation was no different from measured REE (r2 = 0.58, Bias = -8kcal). Within the present BeMD, REE predicted from FFM (REE = FFM x 34.57-270; r2 = 0.85) and body mass (REE = BM x 15.65 + 421.5; r2 = 0.66), were not different from measured REE (bias equals 0 and 0.2kcals, respectively).ConclusionsDespite no differences in REE between CTRL and BeMD adults, increased fat masses highlights the requirement for explicit nutritional guidelines, as well as maintenance of physical activity levels, where possible. Prediction equations are frequently used in clinical settings, however these have been shown to be less accurate in BeMD; therefore, the equations proposed here should be used where possible.
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