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The effect of nitrogen intake, nitrogen source, calorie intake, body weight, adaptation time, research group and sex on the nitrogen balance of human adults was investigated. Data from studies reported in the literature were combined and analyzed statistically by multiple regression techniques. Analyses were made separately for six sources of nitrogen: egg, beef, rice, corn, wheat and wheat gluten. Nitrogen intake, caloric intake and body weight exerted significant effects on nitrogen balance (5% level of confidence) for six, three and two of the six nitrogen sources, respectively. Other variables were not significant at the 5% level. Although differences were not significant (5% level), the correlation between nitrogen intake and nitrogen balance was greatest for four of the six nitrogen sources when data were expressed as grams per square meter of body surface area (g/m2) as opposed to when they were expressed per kilogram body weight or per kilogram raised to the 0.73 power. Curvilinear relationships between intake and balance in the submaintenance range of intakes were evident for all protein sources except corn. The regression lines for several protein sources tended to converge at both lower and higher levels of intake . At levels of nitrogen intake below 1 g/m2, protein appeared to be utilized with near 100% efficiency, regardless of source. At levels of intake above 4.4 g/m2 , all nitrogen sources except wheat gluten gave nitrogen balances which did not differ significantly (5% level). In general, caloric intake exerted a positive but diminishing effect on nitrogen balance when nitrogen intake was held constant and caloric intake increased from maintenance to excessive levels. The mean amount of egg nitrogen required to achieve zero nitrogen balance decreased from 3. l g/m2 to 2.2 g/m2 as caloric intake increased from 1475 kilocalories per square meter of body surface area (kcal/m2) to 1760 kcal/m2. The findings are discussed in terms of present energy and protein requirements, the traditional concepts of the biological value of proteins, and the prediction of protein quality from amino acid composition.

L’exposition au régime maternel durant la période périnatale, induit des processus d’empreintes orientant à long terme le phénotype et la santé des individus. De plus, les orientations alimentaires, telles que celles concernant les protéines, évoluent quantitativement et qualitativement. Ces deux constats, encouragent la communauté scientifique à s’interroger sur les conséquences de ces variations de consommation en protéines sur les générations futures. Ce projet de thèse vise à évaluer chez la descendance femelle rat, les effets d’une alimentation maternelle variant par la teneur (riche versus normal) et la qualité (sources animales versus végétales) en protéines sur la modification des préférences alimentaires et sur les risques métaboliques.Deux études ont été réalisées chez le rat. Une première étude a évalué l’impact de l’excès de protéines à travers un régime hyperprotéique (HP) à base de protéines de lait pendant la gestation. Une seconde étude a évalué les effets d’un régime HP de source protéique spécifique (lait, pois ou dinde) pendant la gestation et d’un régime de source protéique spécifique (lait, pois ou dinde) pendant l’allaitement. Une fois sevrés et jusqu’à l’âge adulte (étude 1 : 15 semaines ; étude 2 : 10 semaines), les ratons femelles ont été soumis à des modèles de « dietary self-selection » (DSS) leur laissant la possibilité de choisir la composition en macronutriments, le niveau de consommation alimentaire et la source protéique (étude 2 uniquement). Indépendamment du régime maternel, ces deux études ont montré que lorsque les sources en macronutriments étaient séparées dans le modèle DSS, les ratons présentaient une hyperphagie liée à une consommation accrue de lipides au détriment des glucides.De plus, les résultats de la seconde étude ont montré que les ratons n’orientaient pas spécifiquement leur consommation de protéines vers la source protéique à laquelle ils avaient été exposés via le régime maternel périnatal. En revanche, les deux études ont montré que la consommation d’un régime HP pendant la gestation, quelle que soit la qualité des protéines le composant, induisait une augmentation de l’adiposité chez la descendance femelle adulte. Cette augmentation était majorée lorsque la descendance avait été soumise au régime de choix (DSS), leur permettant d’augmenter leur consommation de lipides au détriment des glucides.En conclusion, l’exposition périnatale à un régime HP de qualité variable en protéines augmente la sensibilité au surpoids chez la descendance femelle adulte rat. Nous avons évalué les relations entre ces données et : la sensibilité des voies centrales du contrôle de la prise alimentaire et de la récompense, la sensibilité des voies de contrôle du métabolisme énergétique périphérique et la composition et l’activité du microbiote de l’intestin.Ces travaux apportent un grand nombre de nouvelles données indiquant clairement qu’une alimentation équilibrée en quantité et en qualité de protéines pendant la grossesse, à travers le ratio protéines/glucides et le profil en acides aminés, pourrait jouer un rôle clé sur des paramètres phénotypiques de la descendance notamment lorsqu’elle est soumise à des choix alimentaires augmentés. / Abstract : Perinatal exposure to maternal diet induces programming processes of later individual phenotype and health. Additionally, food orientations like for protein, change in terms of quantity and quality. These observations enhance scientific community to evaluate consequences of protein consumption changes on future generations.This thesis project aims to determine the consequences of modifying protein quantity and quality in maternal diets on food preferences and metabolic risks in female rat offspring.Two studies were conducted in rats. The first study evaluated the impact of protein excess in the maternal diet during gestation, through a high-protein (HP) diet composed with cow milk protein. The second study evaluated effects of (i) a HP diet composed with different protein sources (cow milk, pea, or turkey) during gestation and (ii) these different protein sources (cow milk, pea, or turkey-derived) during lactation. From weaning to adulthood (study 1: 15 weeks after birth; study 2; 10 weeks after birth), female pups were subjected to “dietary self-selection” (DSS), which allowed them to choose their own macronutrient compositions, level of food intake and protein sources (second study only).Regardless of the maternal diet, these two studies showed that when DSS was composed with separate macronutrients, rats exhibited overfeeding and increased lipid intake coupled with a decreased carbohydrate intake. Moreover, the results of the second study indicated that rats did not orient their protein intake towards the maternal protein source to which they were exposed during perinatal period. Nevertheless, the two studies showed that the maternal HP diet during gestation caused an increased adiposity in female adult offspring, regardless of the maternal protein source. This increase was stronger when offspring were subjected to DSS condition, which allowed them to increase lipid intake and decrease carbohydrate intake.In conclusion, perinatal exposure to a HP diet varying in protein quantity and quality increases the risk of becoming overweight in female rat adult offspring. We assess the relationship between these data and the the sensitivity of central pathways of food intake and reward control, the sensitivity of energetic and peripheral metabolic pathways, and the gut microbiota composition and activity.This work provides new data indicating that a balanced diet in protein quantity and quality during gestation, through a protein/carbohydrate ratio and amino acid profile, could play a key role on offspring phenotypic parameters, especially when submitted to increased dietary options.

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Three experiments were conducted to determine the effect of different chemicals on the preservation of crab waste at room temperature. In Exp. 1, .2 and .4% NaOCI and H₂O₂ were used and the waste was stored for 17 d. In Exp. 2, NaCI (10%), NaNO₂ (1%), NaOCI (.4%), NaN₃ (.065%), KN0₃ (.1%), Tert butyl hydroperoxide (TBHP) (50 ppm), and I₂ (25 ppm) were used. After mixing with the chemicals the waste was stored for 21 d. In Exp. 3, the waste was treated with NaCI (100/0), NaNO₂(10/0) and NaN₃(.065%) and the mixtures were kept for 20, 30 and 40 d. In the first experiment the waste treated with .4% NaOCI preserved better than for the other treatments, with lower (P < .05) NH₃ and trimethylamine (TMA). In Exp. 2, treatment with NaCI, NaNO₂ and NaN₃ did not produce any change in the physical characters of the crab waste. The TMA, indole and NH₃ were lower (P < .05) and no H₂S was detected in the waste treated with those chemicals. In Exp. 3, treatment with NaCI did not alter the physical characteristics of crab waste. The waste had lower (P < .05) NH3, TMA and indole on d 20, 30 and 40 than those treated with NaNO₂ and NaN₃. / Ph. D.

Protein folding is the process in which polypeptides in their non-native states attain the unique folds of their native states. Adverse environmental conditions and genetic predisposition challenge the folding process and accelerate the production of proteotoxic misfolded proteins. Misfolded proteins are selectively recognized and removed from the cell by processes of protein quality control (PQC). In PQC molecular chaperones of the Heat shock protein 70 kDa (Hsp70) family play important roles by recognizing and facilitating the removal of misfolded proteins. Hsp70 function is dependent on cofactors that regulate the intrinsic ATPase activity of the chaperone. In this thesis I have used yeast genetic, cell biological and biochemical experiments to gain insight into the regulation of Hsp70 function in PQC by nucleotide-exchange factors (NEFs). Study I shows that the NEF Fes1 is a key factor essential for cytosolic PQC. A reverse genetics approach demonstrated that Fes1 NEF activity is required for the degradation of misfolded proteins associated with Hsp70 by the ubiquitin-proteasome system. Specifically, Fes1 association with Hsp70-substrate complexes promotes interaction of the substrate with downstream ubiquitin E3 ligase Ubr1. The consequences of genetic removal of FES1 (fes1Δ) are the failure to degrade misfolded proteins, the accumulation of protein aggregates and constitutive induction of the heat-shock response. Taken the experimental data together, Fes1 targets misfolded proteins for degradation by releasing them from Hsp70. Study II describes an unusual example of alternative splicing of FES1 transcripts that leads to the expression of the two alternative splice isoforms Fes1S and Fes1L. Both isoforms are functional NEFs but localize to different compartments. Fes1S is localized to the cytosol and is required for the efficient degradation of Hsp70-associated misfolded proteins. In contrast, Fes1L is targeted to the nucleus and represents the first identified nuclear NEF in yeast. The identification of distinctly localized Fes1 isoforms have implications for the understanding of the mechanisms underlying nucleo-cytoplasmic PQC. Study III reports on the mechanism that Fes1 employs to regulate Hsp70 function. Specifically Fes1 carries an N-terminal domain (NTD) that is conserved throughout the fungal kingdom. The NTD is flexible, modular and is required for the cellular function of Fes1. Importantly, the NTD forms ATP-sensitive complexes with Hsp70 suggesting that it competes substrates of the chaperone during Fes1-Hsp70 interactions. Study IV reports on methodological development for the efficient assembly of bacterial protein-expression plasmids using yeast homologous recombination cloning and the novel vector pSUMO-YHRC. The findings support the notion that Fes1 plays a key role in determining the fate of Hsp70-associated misfolded substrates and thereby target them for proteasomal degradation. From a broader perspective, the findings provide information essential to develop models that describe how Hsp70 function is regulated by different NEFs to participate in protein folding and degradation. / <p>At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 3: Manuscript.</p>

O Controle de qualidade de proteína (CQP) consiste na supervisão e no processamento de proteínas danificadas por meio de processos catalíticos (proteassoma e autofagia). Nesse estudo, caracterizamos o CQP, bem como os benefícios da ativação &#946;2-adrenérgica (&#946;2-AR) modulador positivo do CQP, em modelo animal de disfunção/atrofia muscular induzida por constrição crônica do nervo isquiático (CCI). Observamos que, apesar de um aumento na atividade catalítica, a atrofia está associada à um CQP insuficiente, detectado por um acúmulo de proteínas citotóxicas nessa musculatura. O tratamento com Formoterol (agonista &#946;2-AR) aumentou a atividade proteassomal e restaurou o fluxo de degradação via autofagia, resultando na melhora do CQP e da miopatia esquelética. A inibição da autofagia, mas não do proteassoma, foi capaz de abolir os efeitos do Formoterol na CCI. Nossos resultados sugerem uma nova contribuição da sinalização &#946;2-AR no quadro de miopatia esquelética, no qual sua ativação foi capaz de restaurar o CQP, contribuindo para a melhora do trofismo e função muscular. / The protein quality control (PQC) detects, repairs and disposes cytotoxic proteins through different proteolytic systems (proteasome and autophagy). Here, we characterized the PQC profile as well as the benefits of sustained &#946;2-adrenoceptor activation (&#946;2-AR) a positive PQC modulator, during skeletal muscle atrophy in a rat model of sciatic nerve constriction (SNC). PQC is disrupted in SNC rats, demonstrated by elevated proteasomal and lysosomal activities along with accumulation of cytotoxic proteins and pro-apoptotic factors. The &#946;2-AR activation (Formoterol) promotes a further increase in proteasomal activity, along with autophagic flux reestablishment. Of interest, sustained autophagy inhibition, but not proteasomal inhibition, is sufficient to abolish Formoterol effects on skeletal muscle PQC, mass and strength. These findings suggest a new contribution of &#946;2-AR signalling pathway to the pathophysiology of skeletal muscle where &#946;2-AR restores the impaired PQC, therefore contributing to a better skeletal muscle morphology and function.