Comprehensive Assessment of the Components of Energy Expenditure in Infants Using a New Infant Respiratory Chamber

Cole, Conrad R.; Rising, Russell; Hakim, Amin; Danon, Marco; Mehta, Rajeev; Choudhury, Shahana A.; Sundaresh, Mamatha; Lifshitz, Fima

doi:10.1080/07315724.1999.10718857

Cited by 17 publications

(43 citation statements)

References 17 publications

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“…Energy expenditure (kcal/min) was continuously calculated during metabolic testing according to the method of Jequier [25] and summarized every five minutes as described previously [26]. At the conclusion of each metabolic test, all metabolic data were corrected for parental interaction, prior to the calculation of resting (RMR; kcal/kg/day) and sleeping metabolic rates (SMR; kcal/kg/d) as described previously [15].…”

Section: Methodsmentioning

confidence: 99%

Relationship between maternal obesity and infant feeding-interactions

Rising¹,

Lifshitz

2005

Nutr J

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Background: There are no data regarding the relationship between maternal adiposity and interaction and feeding of infants and possible contribution to childhood obesity. In this study we determined the relationship between maternal body weight and composition and infant feeding patterns and maternal-infant interaction during 24-hour metabolic rate measurements in the Enhanced Metabolic Testing Activity Chamber (EMTAC).

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Section: Methodsmentioning

confidence: 99%

Relationship between maternal obesity and infant feeding-interactions

Rising¹,

Lifshitz

2005

Nutr J

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“…Previous studies using an infant respiratory chamber directly quantitated energy expenditure and basal metabolic rates in infants from 3 to 4 mo of age and found some differences from World Health Organization figures, particularly in those with HIV or other causes of growth retardation (20,21). When measured over longer times (24 h) the energy expenditure in active infants was underestimated by the Schofield equation (16,20,21). However, there were no differences between inferred and directly measured resting metabolic rates (21).…”

mentioning

confidence: 87%

“…There are little data to support the scientific notion that energy expenditure and basic metabolic rate are the same in infants and in older children (16,17). Previous studies using an infant respiratory chamber directly quantitated energy expenditure and basal metabolic rates in infants from 3 to 4 mo of age and found some differences from World Health Organization figures, particularly in those with HIV or other causes of growth retardation (20,21). When measured over longer times (24 h) the energy expenditure in active infants was underestimated by the Schofield equation (16,20,21).…”

mentioning

confidence: 89%

“…When measured over longer times (24 h) the energy expenditure in active infants was underestimated by the Schofield equation (16,20,21). However, there were no differences between inferred and directly measured resting metabolic rates (21). We made the assumptions that the data from Schofield and Wier equations could be used to determine the derived CUMPD from the raw data of 13 CO 2 enrichment over baseline (DOB).…”

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confidence: 99%

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Screening Newborns for Galactosemia Using Total Body Galactose Oxidation to CO2 in Expired Air

Barbouth

Velazquez

Konopka³

et al. 2007

Pediatr Res

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Classic galactosemia is caused by impaired galactose-1-phosphate uridyltransferase (GALT EC 2.7.712). If discovered and treated within the first days of life, the acute problems of hepatocellular damage, sepsis, and death are prevented. However, chronic problems such as ataxia, tremor, dyspraxic speech, and ovarian failure may occur. To determine whether screening newborns before discharge from the nursery for GALT deficiency is feasible and whether acute and chronic signs could be prevented by earlier intervention, we developed a simplified "breath test." We quantitated total body oxidation of 13 C-D-galactose to 13 CO 2 in expired air by normal newborns between 2 h and 2 mo of age and compared their results to older children with GALT deficiency. We found no differences in total body galactose oxidation (TBGO) among normal newborns up to 48 h of age, but a 2-fold rise in TBGO developed during their first 2 wk of life. Older children with galactosemia had significantly less oxidative capacity than normal newborns. We conclude that newborn breath testing for total body galactose oxidation is feasible before discharge from nursery. It has potential utility for both preventing acute neonatal toxicity and determining the mechanisms producing long-term complications such as ovarian failure, dyspraxia, ataxia, and tremors. C lassic galactosemia is an autosomal recessive disorder caused by a deficiency of galactose-1-phosphate uridyltransferase (GALT EC 2.7.7.12). The biochemical phenotype is characterized by accumulation of galactose, galactose-1-phosphate, and galactitol in cells, and of excess excretion of galactitol and galactose (1-4). The disease incidence is approximately 1:30,000 live births in the United States (2). If untreated in the first 2 wk of life, poor feeding, jaundice, hepatic failure, Escherichia coli sepsis, and death may occur. We have personal experience with families whose newborns had died (http://www.savebabies.org/diseasedescriptions/galactosemia. php, formally known as, "Tyler for Life Foundation" and personal experience).Despite population-based newborn screening and dietary intervention within 2-3 wk of life, the clinical outcome of patients with classic galactosemia is variable. Long-term complications include premature ovarian failure, dyspraxic speech, short stature, learning disabilities, and cataracts (5-7). In one ex post facto study, outcome was not related to time of treatment (5).Most states in the United States screen for galactosemia by the Beutler Method, which measures GALT in dried blood on filter paper through enzyme-linked fluorescence of NADPH production from glucose-1-phosphate. Some states use total galactose quantization (8,9). The median time for results to be received by a referring physician from public health laboratories is poorly documented nationally but from personal experience varies between 4 and 30 d (9).It is not clear whether this prolonged exposure to excess galactose-1-phosphate produces the chronic effects of galactosemia during fetal developm...

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“…The main analytical unit of this instrument was developed to be suitable for various applications in both humans and animals for comprehensive measurements of energy expenditure and physical activity [53,54]. For this study, the EMTAC was retrofitted with a 72 liter plexiglass rodent enclosure (Figure 2).…”

Section: Resultsmentioning

confidence: 99%

Exogenous recombinant human growth hormone effects during suboptimal energy and zinc intake

Rising¹,

Scaglia²,

Cole

et al. 2005

Nutr Metab (Lond)

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BackgroundEnergy and Zinc (Zn) deficiencies have been associated with nutritional related growth retardation as well as growth hormone (GH) resistance. In this study, the relationship between suboptimal energy and/or Zn intake and growth in rats and their response to immunoreactive exogenous recombinant human GH (GHi), was determined.ResultsRats treated with GHi and fed ad-libitum energy and Zn (100/100) had increased IGFBP-3 (p < 0.05) as compared with NSS (215 ± 23 vs. 185 ± 17 ng/ml) along with similar body weight gain. Rats treated with GHi and fed suboptimal energy and full Zn (70/100) had significantly increased weight gain (109.0 ± 18.2 vs. 73.8 ± 11.0 g) and serum IGF-I levels (568 ± 90 vs. 420 ± 85 ng/ml), along with decreased total body water (TBW; 61.0 ± 1.6 vs. 65.7 ± 2.1%) as compared to NSS controls. However, body weight gain was reduced (p < 0.05) as compared with rats fed ad-libitum energy. Growth hormone treated rats fed only suboptimal Zn (100/70), had increased weight gain (217.5 ± 13.2 vs. 191.6 ± 17.9 g; p < 0.05) compared to those given NSS. These rats gained weight in similar amounts to those fed full Zn. Rats treated with GHi and fed both suboptimal energy and Zn (70/70) showed similar results to those fed suboptimal energy with appropriate Zn (70/100), along with significant increases in IGFBP-3 levels (322 ± 28 vs. 93 ± 28 ng/ml). All restricted rats had reduced 24-h EE (kcal/100 g BW) and physical activity index (oscillations/min/kg BW) and GHi did not overcome these effects.ConclusionThese results suggest that GHi enhances weight gain in rats with suboptimal energy and Zn intake but does not modify energy expenditure or physical activity index. Suboptimal Zn intake did not exacerbate the reduced growth or decrease in energy expenditure observed with energy restriction.

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Comprehensive Assessment of the Components of Energy Expenditure in Infants Using a New Infant Respiratory Chamber

Cited by 17 publications

References 17 publications

Relationship between maternal obesity and infant feeding-interactions

Relationship between maternal obesity and infant feeding-interactions

Screening Newborns for Galactosemia Using Total Body Galactose Oxidation to CO2 in Expired Air

Exogenous recombinant human growth hormone effects during suboptimal energy and zinc intake

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