Indiana University-Purdue University Indianapolis (IUPUI) / Objective: Nutritional assessment of infants in the Newborn Intensive Care Unit (NICU) depends on the performance of accurate, serial anthropometric measurements. In this Level IV NICU, nurses used tape measures more often than length boards making the length measurements inaccurate. The purpose of this study is to determine if an in-person, hands-on length board training program versus a self-instruction poster education, increases the use of length boards to measure length in NICU infants. Methods: Two nursing in-service education training sessions on how to correctly use a length board were held with the NICU staff over two separate two (2-week) periods. One session consisted of a self-direct education training method. The second education method was an in-person interactive learning experience with hands on practice. At the end of each education session, the participants completed the same four-question post-test. One month later, data was collected for one month following each of the training periods on the tool used to obtain linear measurements on infants in the NICU. Statistics: A 2x2 contingency table was constructed using the two qualitative variables of length board uses after the poster education versus length board uses after the live in-service education. Analysis was performed using SAS 9.4 ™ statistical software. Chi squared equals 93.980 with 1 degree of freedom. P-value <0.0001. Results: The month following the self-directed poster education, two hundred ninety-one (291) or 92% measurements were obtained using a tape measure and 19 (7%) obtained using a length board. The month following the interactive, in-service training, one hundred forty-eight (148) or 57% measurements were obtained using a tape measure and 105 (41%) with a length board. Thirty five percent (35%) more length measurements were obtained using a length board after the line in-service training (P-value <0.0001). Conclusion: Nurses in a Level IV Newborn Intensive Care Unit utilized length boards significantly more after a live in-service education than after a self-directed education.

No description available.

Branched-chain amino acids (BCAA) are a group of essential amino acids consisting of leucine, isoleucine, and valine. Leucine, in particular, has signaling functions affecting protein and energy metabolism. Plasma leucine concentration is positively correlated with obesity and associated metabolic disorders. We set out to test the hypothesis that metabolic dysfunction from high fat diets precedes dysfunctional BCAA metabolism. First, BCAA were supplemented to neonatal pigs for 4 weeks to evaluate whether the anabolic signaling function of leucine could increase muscle growth when fed for a longer duration than in previous studies. Neither normal pigs nor low birth weight pigs, which have naturally impaired muscle growth, grew better in response to BCAA supplementation, despite low birth weight pigs expressing less of the leucine sensing protein Sestrin2 in skeletal muscle. Furthermore, high plasma BCAA concentrations caused by the experimental diets had no effect on adiposity, liver fat accumulation, or expression of genes related to fatty acid synthesis, mitochondrial biogenesis, or energy expenditure in the pigs' livers. Having produced strong evidence that long term BCAA supplementation neither improves lean growth nor causes abnormal fat metabolism, we then tested whether fat supplementation changes BCAA metabolism. Pigs were fed milk replacer formula with either low energy (Control), or high energy from long-chain fatty acids (LCFA) or medium-chain fatty acids (MCFA) for 22 days. Although high fat diets did not increase plasma BCAA concentrations, the MCFA diet in particular caused metabolic changes which could lead to fatty liver disease and decreased oxidative BCAA disposal. Expression of fatty acid synthesizing genes were increased in the livers of pigs fed MCFA formula compared to Control and LCFA formula. Oxidation of α-ketoisocaproic acid was decreased in liver homogenate of pigs fed MCFA and LCFA formulas compared to Control. Additionally, hepatic oxidation of α-ketoisovalerate was decreased, and plasma concentration of α-ketoisovalerate was consequently increased, in pigs fed MCFA formula compared to Control, with LCFA formula causing intermediate results. In future research, it would be valuable to feed high MCFA formula for a longer period of time to determine whether nonalcoholic fatty liver disease will develop, and whether plasma BCAA concentrations will increase due to decreased oxidation. Overall, these studies concluded that long term BCAA supplementation does not increase muscle growth in neonatal pigs, but there is also no indication that they cause obesity or dysfunctional fat metabolism. On the other hand, high fat diets cause impairments in BCAA catabolism which may precede elevated plasma BCAA concentrations. / Doctor of Philosophy / Branched-chain amino acids (BCAA) are essential amino acids which are abundant in plant and animal proteins. In addition, the BCAA leucine has functions in protein and energy metabolism. Leucine consumption induces a signal to build new muscle protein. However, leucine concentration is also higher in blood plasma of obese individuals than in non-obese individuals, which has caused uncertainty regarding the safety of leucine consumption. In order to demonstrate that leucine does not cause obesity, we set out to test the hypothesis that high fat diets cause decreased breakdown of BCAA. In the first study, we tested whether one month of BCAA supplementation could increase muscle growth in neonatal pigs. Neither normal pigs nor low birth weight pigs, which have naturally impaired muscle growth, grew better in response to BCAA supplementation, despite low birth weight pigs expressing less of a leucine sensing protein in skeletal muscle. Furthermore, BCAA supplementation caused higher BCAA concentrations in blood plasma, but did not cause pigs to gain more fat, or cause any changes in liver fat metabolism. Having produced strong evidence that BCAA supplementation neither improves lean growth nor causes abnormal fat metabolism, we then tested whether fat supplementation changes BCAA metabolism. Pigs were fed milk replacer formula which was either low calorie (Control), or high calorie from animal fat, which is rich in long-chain fatty acids (LCFA) or high calorie from coconut oil, which is rich in medium-chain fatty acids (MCFA). Although high fat diets did not increase blood plasma BCAA concentrations, the MCFA formula in particular caused changes which could lead to fatty liver disease and decreased breakdown of BCAA. Genes which synthesize new fatty acids were increased in the livers of pigs fed MCFA formula compared to those fed LCFA and Control formulas. Furthermore, liver samples taken from pigs fed the MCFA and LCFA formulas were less able to fully break down metabolites of leucine compared to pigs fed the Control formula. In addition, liver samples from MCFA fed pigs were less able to fully break down metabolites of the BCAA valine, which led to higher concentrations of that metabolite in the blood plasma of pigs fed MCFA formula compared to pigs fed LCFA or Control formula. In the future, it would be valuable to feed a high MCFA formula for a longer period of time to determine whether nonalcoholic fatty liver disease will develop, and whether blood plasma BCAA concentrations will increase due to decreased breakdown. Overall, these studies concluded that long term BCAA supplementation does not increase muscle growth in neonatal pigs, but there is also no indication that they cause obesity or dysfunctional fat metabolism. On the other hand, high fat diets cause impairments in BCAA breakdown which may lead to elevated BCAA concentrations in blood plasma.

Many factors influence the efficiency of muscle growth including genetics, nutrition, and environment. The neonatal period is characterized as a time of rapid growth. Growth rate is reduced during neonatal nutrient restriction possibly due to altered satellite cell activity which can permanently alter growth potential. Therefore, optimal nutrition is important for maximizing the growth potential of the animal. Heat stress leads to changes in digestion and metabolism, thus alters nutrient availability to muscle. Heat stress is a prevalent problem in the agriculture industry resulting in great economic losses due to reduced growth, fertility, and increased morbidity. The use of functional feed additives is a potential strategy to mitigate these negative effects. The objective of this dissertation was to investigate nutritional strategies to improve growth in pigs during key malleable periods. Three nutritional studies were conducted to discern the optimal inclusion levels of calcium phosphate, energy, and protein in the diet to maximize neonatal muscle growth. Adequate dietary calcium phosphate was most efficient for satellite cell function which may be mediated by micro-RNA. Differentiation promoting miR-206 and correspondingly the fusion rate was highest in adequate calcium phosphate diets. Excess protein diets enhanced body and muscle growth, while deficient protein was detrimental to growth. Dietary protein treatments altered energy metabolism genes, and genes regulating protein degradation were upregulated in deficient protein diets. Dietary energy levels did not influence body weight, however feed efficiency improved with energy balance. Excess energy diets had the lowest fusion rates and the lowest differentiation promoting miR-1 expression. These data suggest that nutrient inclusion levels are important for satellite cell function and may mediate satellite cell activity through the expression of micro-RNAs. The final study sought to discern the ability of supplementation of an artificial high-intensity sweetener and capsicum oleoresin to mitigate the negative effects of heat stress on pig performance. Heat stress leads to increased body temperature and respiration and was detrimental to metabolic flexibility. Supplementation helped improve feed efficiency and maintain metabolic flexibility. These data indicate that supplementation may be an efficient strategy to mitigate heat stress. / Doctor of Philosophy / Muscle is an important tissue to consider when optimizing growing conditions in feed animals due to its function as a consumer good. Many factors influence the efficiency of muscle growth including genetics, nutrition, and environment. Fractional growth rates are highest during the neonatal period and animals require adequate nutrients to facilitate this growth. Nutrient restriction reduces growth rate and can lead to permanent changes the animals' body size and composition later in life. Therefore, optimal nutrition is important for maximizing the growth potential of the animal. While the nutrients in feed can be controlled to improve growth, other factors are more difficult to regulate. Heat stress is a prevalent problem in the agriculture industry resulting in great economic losses due to reduced growth, fertility, and increased morbidity. The use of functional feed additives is a potential strategy to alleviate these negative effects. The objective of this dissertation was to investigate nutritional strategies to improve growth in pigs during key malleable periods. Three nutritional studies were conducted to determine the optimal inclusion levels of calcium phosphate, energy, and protein in the diet to maximize neonatal muscle growth. Satellite cells are muscle-specific stem cells that help facilitate the growth of muscle. Altering the ability of satellite cells to proliferate and fuse impairs the ability of muscle to grow and repair. Adequate dietary calcium phosphate was most efficient for satellite cell function. Excess protein diets enhanced body and muscle growth, while deficient protein was detrimental to growth. Dietary protein treatments altered energy metabolism genes, and genes regulating protein degradation were upregulated in deficient protein diets. Dietary energy levels did not influence body weight, however, feed efficiency improved with energy balance. Satellite cells from excess energy diets had the lowest fusion rates. These data suggest that nutrient inclusion levels are important for satellite cell function and growth. The final study sought to discern the ability of the supplementation of an artificial high-intensity sweetener and capsicum oleoresin to mitigate the negative effects of heat stress on pig performance. Heat stress leads to increased body temperature and respiration and was detrimental to metabolic flexibility. Supplementation helped improve feed efficiency and maintain metabolic flexibility. These data indicate that supplementation may be an efficient strategy to mitigate heat stress.

Les prématurés subissent un stress oxydant qui résulte d’une défense antioxydante faible et/ou d’une charge oxydante. Des données suggèrent qu’un stress oxydant peut affecter le métabolisme énergétique et mener au syndrome métabolique. Hypothèse: Une faible défense antioxydante tôt dans la vie est suffisante pour affecter le métabolisme énergétique à long terme. Méthodes: Quatre groupes de cobayes (n=21) ont reçu entre leurs 3e et 7e jours de vie une diète standard (C-1sem, C-14sem) ou une diète déficiente (DC-1sem, DC-14sem). À 7 jours, les groupes C-1sem et DC-1sem ont été sacrifiés, le plasma et le foie collectés. Les groupes C-14sem et DC-14sem ont reçu la diète standard jusqu’à 14sem de vie. La glycémie et les triglycérides plasmatiques ont été mesurés à 1, 3, 11, et 13-14sem. La tolérance au glucose a été évaluée à 13sem. Les antioxydants hépatiques et les protéines régulant le métabolisme énergétique ont été analysés à 1 et 14sem. Résultats: Un statut redox oxydé du glutathion était associé avec la diète déficiente et était maintenu oxydé au moins jusqu’à 14sem (p<0.01). Les faibles niveaux de triglycérides plasmatiques et de glycémies, ainsi qu’une meilleure tolérance au glucose à 14sem (p<0.05) étaient associés avec un statut redox plus oxydé. Conclusion: Le faible taux de glutathion observé chez les prématurés a été reproduit dans notre modèle. Puisque nos données suggèrent un rôle protecteur d’un redox plus oxydé et que l’environnement redox est un important régulateur métabolique influençant le développement, il faudrait faire attention avant d’initier des traitements antioxydants agressifs chez les prématurés. / Preterm infants are faced to oxidative stress resulting from a low antioxidant defence and/or a high oxidant load. Datas suggest that an oxidative stress may impair energy metabolism leading to metabolic syndrome development. Hypothesis: A weak antioxidant defence early in life such as observed in preterm newborns is sufficient to impair energy metabolism later in life. Methods: Four groups of guinea pigs (n=21) received between their 3rd and 7th days of life a control diet (C-1week, C-14weeks) or antioxidant deficient diet (DC-1week, DC-14weeks). At 7 day-old, 1week-groups were sacrificed for plasma and liver sampling whereas 14week-groups were fed with the control diet until 14 week-old. Blood glucose and plasma triacylglycerol were determined at 1, 3, 11 and 13-14 week-old. Glucose tolerance test was performed at 13 week-old. Hepatic antioxidant defences and key proteins regulating lipid and glucose metabolism were measured at 1 and 14 weeks. Results: The oxidized redox status of glutathione associated with the neonatal deficient diet was maintained until at least 14 week-old (p<0.01). The low plasma triacylglycerol, low blood glucose and better tolerance to glucose at 14 weeks (p<0.05) were associated with an oxidized redox status. Conclusion: The low glutathione observed in newborn preterm infants has been reproduced in our animal model. Since the oxidized redox state observed here seems to be protective against impaired energy metabolism and since the cellular redox environment is known to be an important rheostat of metabolism influencing development, it suggests being careful before adopting aggressive antioxidant treatments in preterm infants.

Les prématurés subissent un stress oxydant qui résulte d’une défense antioxydante faible et/ou d’une charge oxydante. Des données suggèrent qu’un stress oxydant peut affecter le métabolisme énergétique et mener au syndrome métabolique. Hypothèse: Une faible défense antioxydante tôt dans la vie est suffisante pour affecter le métabolisme énergétique à long terme. Méthodes: Quatre groupes de cobayes (n=21) ont reçu entre leurs 3e et 7e jours de vie une diète standard (C-1sem, C-14sem) ou une diète déficiente (DC-1sem, DC-14sem). À 7 jours, les groupes C-1sem et DC-1sem ont été sacrifiés, le plasma et le foie collectés. Les groupes C-14sem et DC-14sem ont reçu la diète standard jusqu’à 14sem de vie. La glycémie et les triglycérides plasmatiques ont été mesurés à 1, 3, 11, et 13-14sem. La tolérance au glucose a été évaluée à 13sem. Les antioxydants hépatiques et les protéines régulant le métabolisme énergétique ont été analysés à 1 et 14sem. Résultats: Un statut redox oxydé du glutathion était associé avec la diète déficiente et était maintenu oxydé au moins jusqu’à 14sem (p<0.01). Les faibles niveaux de triglycérides plasmatiques et de glycémies, ainsi qu’une meilleure tolérance au glucose à 14sem (p<0.05) étaient associés avec un statut redox plus oxydé. Conclusion: Le faible taux de glutathion observé chez les prématurés a été reproduit dans notre modèle. Puisque nos données suggèrent un rôle protecteur d’un redox plus oxydé et que l’environnement redox est un important régulateur métabolique influençant le développement, il faudrait faire attention avant d’initier des traitements antioxydants agressifs chez les prématurés. / Preterm infants are faced to oxidative stress resulting from a low antioxidant defence and/or a high oxidant load. Datas suggest that an oxidative stress may impair energy metabolism leading to metabolic syndrome development. Hypothesis: A weak antioxidant defence early in life such as observed in preterm newborns is sufficient to impair energy metabolism later in life. Methods: Four groups of guinea pigs (n=21) received between their 3rd and 7th days of life a control diet (C-1week, C-14weeks) or antioxidant deficient diet (DC-1week, DC-14weeks). At 7 day-old, 1week-groups were sacrificed for plasma and liver sampling whereas 14week-groups were fed with the control diet until 14 week-old. Blood glucose and plasma triacylglycerol were determined at 1, 3, 11 and 13-14 week-old. Glucose tolerance test was performed at 13 week-old. Hepatic antioxidant defences and key proteins regulating lipid and glucose metabolism were measured at 1 and 14 weeks. Results: The oxidized redox status of glutathione associated with the neonatal deficient diet was maintained until at least 14 week-old (p<0.01). The low plasma triacylglycerol, low blood glucose and better tolerance to glucose at 14 weeks (p<0.05) were associated with an oxidized redox status. Conclusion: The low glutathione observed in newborn preterm infants has been reproduced in our animal model. Since the oxidized redox state observed here seems to be protective against impaired energy metabolism and since the cellular redox environment is known to be an important rheostat of metabolism influencing development, it suggests being careful before adopting aggressive antioxidant treatments in preterm infants.