27 research outputs found
Nutrition and Growth
Nutrition plays a fundamental role in determining the growth of individuals. An appropriate growth progression is considered a harbinger of adequate nutrient intake and good health. On the other hand growth deceleration with or without short stature may indicate inadequate nutrition, even when there is no body weight deficit for height. Nutritional growth retardation (NGR) is most prevalent in populations at risk of poverty. However in affluent communities patients with NGR are often referred to the specialist because of short stature and delayed sexual development. The diagnosis may be overlooked and/or be established after exhaustive evaluations, if the pattern of weight progression over time is not considered. Patients with so-called idiopathic short stature may present diminished nutrient intake and decreased IGF-I levels, however their nutritional status and body weight progression patterns are usually not addressed by pediatric endocrinologists. NGR patients may cease to gain appropriate weight and fail to grow in height, even without exhibiting body weight deficits for height. They adapt to decreased nutrient intake by decreasing growth progression and thereby achieve equilibrium by decreasing the nutrient demands. This occurs by diminishing their metabolic rates and erythrocyte Na+, K+- ATPase activity, however they may not present alterations in other clinical biochemical markers of malnutrition. Therefore accurate weights and heights plotted on the growth chart over time are necessary to detect NGR. Nutritional rehabilitation is accompanied with catch up growth, though it may be difficult to change the dietary habits of adolescents who exhibit NGR
Obesity in Children
The prevalence of childhood obesity has increased dramatically during the past decades all over the world. The majority of obesity in adulthood has its origins in childhood which makes obesity a pediatric concern and the period when interventions should be done. Obesity is associated with increased morbidity and mortality in adult life and several adverse consequences in childhood like insulin resistance, type 2 diabetes, dyslipidemia, polycystic ovarian syndrome, pulmonary and orthopedic disorders and psychological problems. Both genetic and environmental factors play a role in the development of obesity. Prevention of obesity is critical, since effective treatment of this disease is limited. Food management and increased physical activity must be encouraged, promoted, and prioritized to protect children
Energy expenditures & physical activity in rats with chronic suboptimal nutrition
BACKGROUND: Sub-optimally nourished rats show reduced growth, biochemical and physiological changes. However, no one has assessed metabolic rate adaptations in rats subjected to chronic suboptimal nutrition (CSN). In this study energy expenditure (EE; kcal/100 g body weight) and physical activity (PA; oscillations in weight/min/kg body weight) were assessed in rats subjected to three levels of CSN. RESULTS: Body weight gain was diminished (76.7 ± 12.0 and 61.6 ± 11.0 g) in rats fed 70 and 60% of the ad-libitum fed controls which gained more weight (148.5 ± 32.3 g). The rats fed 80% gained weight similarly to controls (136.3 ± 10.5 g). Percent Fat-free body mass was reduced (143.8 ± 8.7 and 142.0 ± 7.6 g) in rats fed 70 and 60% of ad-libitum, but not in those fed 80% (200.8 ± 17.5 g) as compared with controls (201.6 ± 33.4 g). Body fat (g) decreased in rats fed 80% (19.7 ± 5.3), 70% (15.3 ± 3.5) and 60% (9.6 ± 2.7) of ad-libitum in comparison to controls (26.0 ± 6.7). EE and PA were also altered by CSN. The control rats increased their EE and PA during the dark periods by 1.4 ± 0.8 and 1.7 ± 1.1 respectively, as compared with light the period; whereas CSN rats fed 80 and 70% of ad-libitum energy intake had reduced EE and PA during the dark periods as compared with the light period EE(7.5 ± 1.4 and 7.8 ± 0.6 vs. 9.0 ± 1.2 and 9.7 ± 0.8; p < 0.05, respectively), PA(3.1 ± 0.8 and 1.6 ± 0.4 vs. 4.1 ± 0.9 and 2.4 ± 0.4; p < 0.05) and RQ (0.87 ± 0.04 and 0.85 ± 0.5; vs. 0.95 ± 0.03 and 0.91 ± 0.05 p < 0.05). In contrast, both light (7.1 ± 1.4) and dark period (6.2 ± 1.0) EE and PA (3.4 ± 0.9 and 2.5 ± 0.5 respectively) were reduced in rats fed 60% of ad-libitum energy intake. CONCLUSION: CSN rats adapt to mild energy restriction by reducing body fat, EE and PA mainly during the dark period while growth proceeds and lean body mass is preserved. At higher levels of energy restrictions there is decreased growth, body fat and lean mass. Moreover EE and PA are also reduced during both light and dark periods
Energy expenditure in chow-fed female non-human primates of various weights
<p>Abstract</p> <p>Background</p> <p>Until now no technology has been available to study energy metabolism in monkeys. The objective of this study was to determine daily energy expenditures (EE) and respiratory quotients (RQ) in female monkeys of various body weights and ages.</p> <p>Methods</p> <p>16 socially reared Bonnet Macaque female monkeys [5.5 ± 1.4 kg body weight, modified BMI (length measurement from head to base of the tail) = 28.8 ± 6.7 kg/crown-rump length, m<sup>2 </sup>and 11.7 ± 4.6 years] were placed in the primate Enhanced Metabolic Testing Activity Chamber (Model 3000a, EMTAC Inc. Santa Barbara, CA) for 22-hour measurements of EE (kcal/kg) and RQ (VCO<sub>2</sub>/VO<sub>2</sub>). All were fed monkey chow (4.03 kcal/g) ad-libitum under a 12/12 hour light/dark cycle. Metabolic data were corrected for differences in body weight. Results were divided into day (8-hours), dark (12 hours) and morning (2-hours) periods. Data analysis was conducted utilizing SPSS (Version 13).</p> <p>Results</p> <p>Modified BMI negatively correlated with 22-hour energy expenditure in all monkeys (r = -0.80, p < 0.01). The large variability of daily energy intake (4.5 to 102.0 kcal/kg) necessitated division into two groups, non-eaters (< 13 kcal/kg) and eaters (> 23 kcal/kg). There were reductions (p < 0.05) in both 22-hour and dark period RQs in the "non-eaters" in comparison to those who were "eaters". Monkeys were also classified as "lean" (modified BMI < 25) or "obese" (modified BMI > 30). The obese group had lower EE (p < 0.05) during each time period and over the entire 22-hours (p < 0.05), in comparison to their lean counterparts.</p> <p>Conclusion</p> <p>The EMTAC proved to be a valuable tool for metabolic measurements in monkeys. The accuracy and sensitivity of the instrument allowed detection of subtle metabolic changes in relation to energy intake. Moreover, there is an association between a reduction of energy expenditure and a gain in body weight.</p
Erratum to: Switching to Omnitrope® from Other Recombinant Human Growth Hormone Therapies: A Retrospective Study in an Integrated Healthcare System
Relationship between maternal obesity and infant feeding-interactions
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). METHODS: The amount of time four obese (BMI = 33.5 ± 5.3 kg/m(2)) and three normal weight (BMI = 23.1 ± 0.6 kg/m(2)) biological mothers, spent feeding and interacting with their infants, along with what they ingested, was recorded during 24-hour metabolic rate measurements in the EMTAC. The seven infants were 4.9 ± 0.7 months, 69 ± 3 cm, 7.5 ± 0.8 kg, 26 ± 3 % fat and 29 ± 25 percentile for weight for length. Energy and macronutrient intake (kcal/kg) were assessed. Maternal body composition was determined by air displacement plethysmorgraphy and that of the infants by skin-fold thicknesses. Pearson correlations and independent t-tests were utilized for statistical analysis (p < 0.05). RESULTS: Infants born to obese biological mothers consumed more energy (87.6 ± 18.9 vs. 68.1 ± 17.3) and energy as carbohydrate (25 ± 6 vs.16 ± 3; p < 0.05) than their normal weight counterparts. Most of the increased intake was due to complementary feedings. Twenty-four hour infant energy intake increased with both greater maternal body weight (r = 0.73;p < 0.06) and percent body fat. Furthermore, obese biological mothers spent less total time interacting (570 ± 13 vs. 381 ± 30 minutes) and feeding (298 ± 32 vs.176 ± 22 minutes) (p < 0.05) their infants than their normal weight counterparts. Twenty-four hour interaction time negatively correlated with both maternal body weight (r = -0.98; p < 0.01) and percent body fat (r = -0.92; p < 0.01). Moreover, infants of obese mothers slept more (783 ± 38 vs. 682 ± 32 minutes; p < 0.05) than their normal weight counterparts. However, there were no differences in total 24-hour energy expenditure, resting and sleeping metabolic rates (kcal/kg) for infants born to obese and normal weight biological mothers. CONCLUSION: Greater maternal body weight and percent body fat were associated with greater infant energy intakes. These infants were fed less frequently and consumed more carbohydrates in a shorter period of time as compared to infants from normal weight biological mothers. These variations in feeding patterns may predispose certain infants to obesity