Birth weight predicted baseline muscular efficiency, but not response of energy expenditure to calorie restriction: An empirical test of the predictive adaptive response hypothesis

2015 ◽  
Vol 28 (4) ◽  
pp. 484-492 ◽  
Author(s):  
Megan Workman ◽  
Jack Baker ◽  
Jane B. Lancaster ◽  
Christine Mermier ◽  
Joe Alcock
PEDIATRICS ◽  
1989 ◽  
Vol 83 (5) ◽  
pp. 706-716
Author(s):  
Judith A. Ernst ◽  
Karyl A. Rickard ◽  
Patricia R. Neal ◽  
Pao-Lo Yu ◽  
Tjien O. Oei ◽  
...  

The effect of nonnutritive sucking during gavage feeding on nutritional outcome and gastrointestinal transit time was evaluated in 18 premature appropriate for gestational age infants whose birth weights were \g=le\1,400 g and gestational ages were \g=le\30 weeks. Infants were randomized to a treatment (nonnutritive sucking infants received a pacifier for 30 minutes with each feeding, 12 times per day until they reached a weight of 1,500 g, eight times per day thereafter) or control (no pacifier) group. The nine nonnutritive sucking (five girls, four boys) and nine control (five girls, four boys) infants were treated for 14 days. Infants were without medical complications and were fed a single premature formula by intermittent gastric gavage at exactly 120 kcal/kg/d throughout the study period. Weight gain, linear growth, subscapular and triceps skinfold, and arm circumference accretions were assessed weekly. Serum proteins (albumin, prealbumin, retinol-binding protein, and transferrin) were measured weekly. Gastrointestinal transit times were measured weekly using carmine red markers. In contrast to previous studies, these data indicate no apparent effect of nonnutritive sucking on growth outcome, serum proteins, or gastrointestinal transit time in growing, very low birth weight infants when nutrient intake was controlled. In a subgroup of eight boys (four nonnutritive sucking, four control), energy and fat excretions were determined from 72-hour fecal collections and energy expenditure was estimated from six-hour cumulative heart rate measurements. Neither excretion of fat and calories nor estimated energy expenditure was affected significantly by nonnutritive sucking in this subgroup of baby boys. Fat excretion correlated well (r = .987) with energy excretion.


1987 ◽  
Vol 110 (5) ◽  
pp. 753-759 ◽  
Author(s):  
Karl F. Schulze ◽  
Mark Stefanski ◽  
Julia Masterson ◽  
Regina Spinnazola ◽  
Rajasekhar Ramakrishnan ◽  
...  

2017 ◽  
Author(s):  
Amy J. Osborne ◽  
Peter K. Dearden

AbstractThe Developmental Origins of Health and Disease (DOHaD) hypothesis predicts that early-life environmental exposures can be detrimental to later-life health, and that mismatch between the pre- and postnatal environment may contribute to the growing non-communicable disease (NCD) epidemic. Within this is an increasingly recognised role for epigenetic mechanisms; epigenetic modifications can be influenced by, e.g., nutrition, and can alter gene expression in mothers and offspring. Currently, there are no whole-genome transcriptional studies of response to nutritional alteration. Thus, we sought to explore how nutrition affects the expression of genes involved in epigenetic processes in Drosophila melanogaster. We manipulated Drosophila food macronutrient composition at the F0 generation, mismatched F1 offspring back to a standard diet, and analysed the transcriptome of the F0 – F3 generations by RNA-sequencing. At F0, the altered (high protein, low carbohydrate, HPLC) diet increased expression of genes involved in epigenetic processes, with coordinated downregulation of genes involved in immunity, neurotransmission and neurodevelopment, oxidative stress and metabolism. Upon reversion to standard nutrition, mismatched F1 and F2 generations displayed multigenerational inheritance of altered gene expression. By the F3 generation, gene expression had reverted to F0 (matched) levels. These nutritionally-induced gene expression changes demonstrate that dietary alteration can upregulate epigenetic genes, which may influence the expression of genes with broad biological functions. Further, the multigenerational inheritance of the gene expression changes in F1 and F2 mismatched generations suggests a predictive adaptive response (PAR) to maternal nutrition. Our findings may help to understand the interaction between maternal diet and future offspring health, and have direct implications for the current NCD epidemic.


2011 ◽  
Vol 300 (4) ◽  
pp. E735-E745 ◽  
Author(s):  
Matthew D. Bruss ◽  
Airlia C. S. Thompson ◽  
Ishita Aggarwal ◽  
Cyrus F. Khambatta ◽  
Marc K. Hellerstein

Calorie restriction (CR) reduces the rate of cell proliferation in mitotic tissues. It has been suggested that this reduction in cell proliferation may mediate CR-induced increases in longevity. However, the mechanisms that lead to CR-induced reductions in cell proliferation rates remain unclear. To evaluate the CR-induced physiological adaptations that may mediate reductions in cell proliferation rates, we altered housing temperature and access to voluntary running wheels to determine the effects of food intake, energy expenditure, percent body fat, and body weight on proliferation rates of keratinocytes, liver cells, mammary epithelial cells, and splenic T-cells in C57BL/6 mice. We found that ∼20% CR led to a reduction in cell proliferation rates in all cell types. However, lower cell proliferation rates were not observed with reductions in 1) food intake and energy expenditure in female mice housed at 27°C, 2) percent body fat in female mice provided running wheels, or 3) body weight in male mice provided running wheels compared with ad libitum-fed controls. In contrast, reductions in insulin-like growth factor I were associated with decreased cell proliferation rates. Taken together, these data suggest that CR-induced reductions in food intake, energy expenditure, percent body fat, and body weight do not account for the reductions in global cell proliferation rates observed in CR. In addition, these data are consistent with the hypothesis that reduced cell proliferation rates could be useful as a biomarker of interventions that increase longevity.


2003 ◽  
Vol 89 (4) ◽  
pp. 533-537 ◽  
Author(s):  
Jacqueline Bauer ◽  
Kathrin Maier ◽  
Gerald Hellstern ◽  
Otwin Linderkamp

The aim of the present study was to obtain serial values of O2 consumption (VO2), CO2 production (VCO2) and energy expenditure (EE) in healthy but extremely-low-birth-weight infants (birth weight <1000 g), during the first 5 weeks after birth. A total of seventeen spontaneously breathing and appropriate-for-gestational-age (birth weight and body length above the 10th and below the 90th percentile) preterm infants with gestational age 25–28 weeks and birth weight 590–990 g were enrolled in the study. Calorimetry was performed using an open-circuit calorimeter on days 6, 12, 18, 24, 30 and 36 of postnatal life. During the 5 weeks of observation, VO2 increased from 4·7 (SD 0·5) TO 9·1 (sd 1·0) ml/kg per min, VCO2 from 4·5 (sd 0·4) to 8·3 (SD 0·6) ml/kg per min and EE from 115 (sd 12) to 310 (sd 71) kJ/kg per d. The energy intake was always higher than EE, even at days 6 and 12. The RER decreased from 0·99 (sd 0·09) at day 12 to 0·91 (SD 0·05) at day 30. On all study days, there were highly significant positive correlations between energy intake and weight gain, EE and weight gain, and EE and energy intake (P<0·05). Multiple regression analysis showed that on most study days EE was more affected by energy intake than by weight gain. We conclude that in healthy preterm infants with birth weight <1000 g, EE increases by about 150 % in the first 5 weeks after birth, and that the EE values are related to energy intake and weight gain independent of postnatal age.


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