published_or_final_version / Chemistry / Master / Master of Philosophy

Thesis (M. Phil.)--University of Hong Kong, 1990.

Orientador: Felix Guillermo Reyes Reyes / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Engenharia de Alimentos / Made available in DSpace on 2018-08-17T15:50:36Z (GMT). No. of bitstreams: 1 Maluly_HellenDeaBarros_D.pdf: 1502288 bytes, checksum: 2755d6e579f948905440f6ae2d7bbd17 (MD5) Previous issue date: 2011 / Resumo: Tem sido relatado que a administração de glutamato monossódico (MSG) por via parenteral e oral possui um efeito lesivo sobre o núcleo arqueado do hipotálamo provocando alterações na regulação do apetite e, como conseqüência, obesidade e distúrbios relacionados à síndrome metabólica, que são caracterizados por alterações no metabolismo de carboidratos (resistência à glicose e insulina), dislipidemia e doença cardiovascular. Este estudo teve como objetivo avaliar possíveis alterações metabólicas e cardiovasculares quando da exposição oral ao MSG em níveis de até 5,0% na dieta. O estudo foi realizado com ratos diabéticos e não diabéticos. A utilização de animais diabéticos se justifica por serem susceptíveis a indução de possíveis distúrbios metabólicos. Foi avaliado o perfil metabólico característico da condição diabética, incluindo eletrocardiograma, testes bioquímicos, determinação de aminoácidos livres no soro dos animais e a possível alteração histológica de órgãos que são afetados pela condição diabética (fígado, rins e coração). Concluiu-se que o uso de MSG na concentração de até 5,0% na dieta, não alterou os parâmetros estudados, tanto nos animais não diabéticos, como nos diabéticos. As alterações observadas em animais diabéticos refletiram aos distúrbios característicos desta enfermidade, independente da adição de MSG na dieta / Abstract: It has been reported that the parenteral or oral administration of monosodium glutamate (MSG) has an deletereous effect on the arcuate nucleus of the hypothalamus, inducing alterations in the control of appetite that can lead to obesity and disorders related to the metabolic syndrome, such as alterations in carbohydrate metabolism (glucose and insulin resistance), dyslipidemia and cardiovascular disease. This study aimed to evaluate possible metabolic and cardiovascular alterations as a consequence to oral exposure to MSG at levels up to 5.0% in the diet. The study was carried out using diabetic and non-diabetic rats, the use of diabetic animals being justified by their susceptibility to the induction of possible metabolic disorders. The metabolic profile characteristic of the diabetic condition was evaluated, including electrocardiogram, biochemical tests, determination of amino acids in the serum and the possible histological alteration in the organs that are affected by this condition (liver, kidneys and heart). In conclusion, the use of MSG at levels up to 5.0% in the diet did not change the parameters studied in both: non diabetic and diabetic animals. The alterations observed in the diabetic animals reflected the metabolic changes characteristic of this disease, regardless the addition of MSG to the diet / Doutorado / Doutor em Ciência de Alimentos

A glândula pineal sintetiza o hormônio melatonina à noite e este regula diversos sistemas fisiológicos, adaptando-os às exigências de cada momento do dia. O objetivo deste trabalho foi o de analisar o perfil noturno da síntese de melatonina na glândula pineal de ratos, em diferentes idades, tratados com glutamato monossódico (MSG) no período neonatal. Ratos Wistar, machos e fêmeas, receberam injeções de MSG (4mg/g/dia) ou de solução salina (0,9%) do 2º ao 8º dia pós-natal. Foram avaliados o peso corporal e dos tecidos adiposos, o comprimento naso-anal,o perfil noturno da síntese de melatonina e da atividade da enzima AANAT, o GTT e o ITT. O MSG induziu um aumento no peso dos tecidos adiposos, sem aumento do peso corporal. Não foi observada hiperglicemia, nem intolerância à glicose, mas sim resistência insulínica. A ritmicidade circadiana da melatonina e da AANAT foi preservada, mas houve um aumento de ambos no ZT 15. As alterações na síntese de melatonina parecem decorrer das lesões hipotalâmicas provocadas pelo MSG, pela redução do NPY, aumento da insulina ou da noradrenalina. / The pineal gland synthesizes melatonin exclusively at night. Melatonin is a temporal synchronizer of several physiological functions, adapting the organism to the diurnal environmental changes. The purpose of this work was to analyze the effects of neonatal monosodium glutamate (MSG) administration on the nocturnal profile of melatonin synthesis in the pineal gland. Wistar rats, males and females, were injected neonatally with MSG (4mg/g/day) or saline solution (0.9%) from the 2nd to 8th post-natal day. Body weight and adipose tissue weight, naso-anal length, nocturnal melatonin and AANAT activity profiles, GTT and ITT were analyzed. MSG induced a great increase in adipose depots without increase in body weight. It did not induce hyperglycemia nor glucose intolerance, but induced insulin resistance. Circadian rhythmicity of melatonin synthesis and AANAT activity was not altered, but there was an increase at ZT 15 in both. It seems that melatonin synthesis changes could be related to hypothalamic lesions, through a reduction in NPY or insulin/norepinephrine elevation.

Made available in DSpace on 2017-07-21T19:59:54Z (GMT). No. of bitstreams: 1 PALLOMA HOCAYEN.pdf: 1571020 bytes, checksum: 2b66eed389dee29aecb38d9310ca585e (MD5) Previous issue date: 2012-05-09 / In recent years diabetes has been gaining huge proportions, due to changes in the habits of life, poor diet and physical inactivity are key factors in disease development. To this end, various species of plants have been used etnofarmacologicamente or in clinical trials or to treat and combat the symptoms of Diabetes Mellitus. The present study used the methanol extract of the plant Bracharis dracunculifolia (rosemary field) belonging to the Asteraceae family, with the objective of evaluating the effect of his administration on hypothalamic obesity in animal model of MSG. The methodology was based on the preparation of the extract metabolic B. dracunculifolia by means of drying processes, spraying, orbital agitation of the extract in methanol, filtration and addition of rotaevaporação toxicity test of the extract in the brine shrimp. To obtain MSG animals, were used in newborn animals still injection of monosodium glutamate (MSG) for five consecutive days at a dose of 4 mg / g body weight to induce obesity. Treatment with methanol extract was carried out on animals at 180 days of life, for 30 days. Weight was evaluated, consumption of water and feed throughout the experiment. And after the animals have been sacrificed held in the isolation of pancreatic islets which were incubated with increasing concentrations of glucose (5.6 mM, 8.3 mM, 16.7 mM). The results obtained in the study demonstrated low toxicity of the extract of B. dracunculifolia. The MSG animals had proven by induction of obesity increased Lee index, and higher levels of visceral and subcutaneous fat compared to controls. The MSG animals weighed less, consumed less water and less food and had impaired glucose tolerance. The biochemical parameters did not obtain significant differences, except for triglycerides which showed to be higher in MSG animals, not having succeeded in restoring the extract this parameter. In the isolation of pancreatic islets, MSG animals that received the extract of B. dracunculifolia showed a significant secretion of insulin by the islets isolated, noting that the concentration of 8.3 mM and 16.7 mM was obtained increased secretion of insulin. It is concluded that the methanol extract of B. dracunculifolia obtained significant effect on insulin secretion in pancreatic islet cell isolation, noting the results obtained in the group MSG (MP), which were hyperinsulinemia because of a possible enhancement of oxidative stress, especially the high antioxidant content present in the extract B. dracunculifolia used in the study. / Nos últimos anos o Diabetes vem ganhando grandes proporções, devido a mudanças nos hábitos de vida das pessoas, má alimentação e sedentarismo, que são fatores centrais no desenvolvimento da doença. Para tanto, várias espécies de plantas vêm sendo utilizadas etnofarmacologicamente ou em ensaios clínicos para tratar e ou combater os sintomas do Diabetes Mellitus. O presente estudo utilizou o extrato metanólico da planta Bracharis dracunculifolia (alecrim do campo), pertencente a família Asteraceae, com o objetivo de avaliar o efeito de sua administração na obesidade hipotalâmica em modelo de animais MSG. A metodologia se baseou na preparação do extrato metabólico de B. dracunculifolia, por meio de processos de secagem, pulverização, agitação orbital do extrato em metanol, filtragem e rotaevaporação além do teste de toxicidade do extrato frente a Artemia salina. Para a obtenção de animais MSG, foram aplicados nos animais ainda neonatos injeção de glutamato monossódico (MSG), durante cinco dias consecutivos, na dose de 4mg/g de peso corporal, para indução da obesidade. O tratamento com o extrato metanólico foi realizado nos animais aos 180 dias de vida, durante 30 dias. Foi avaliado o peso, consumo de água e ração durante todo o experimento. E após os animais terem sido sacrificados realizou-se o isolamento de ilhotas pancreáticas, que foram incubadas em concentrações crescentes de glicose (5,6mM; 8,3mM; 16,7mM). Os resultados obtidos no estudo demonstraram baixa toxicidade do extrato de B. dracunculifolia. Os animais MSG obtiveram indução da obesidade comprovada pelo aumento do Índice de Lee, e maior teor de gorduras viscerais e subcutânea em relação aos controles. Os animais MSG apresentaram menor peso, consumiram menos água e menos ração e apresentaram intolerância a glicose. Os parâmetros bioquímicos não obtiveram diferenças significativas, com exceção dos triglicerídeos que apresentou-se maior nos animais MSG, não tendo o extrato conseguido restaurar este parâmetro. No isolamento de ilhotas pancreáticas, os animais MSG que receberam o extrato de B. dracunculifolia apresentaram uma secreção significativa de insulina pelas ilhotas isoladas, ressaltando que na concentração de 8,3mM e 16,7mM foi obtida maior secreção de insulina. Conclui-se que o extrato metanólico de B. dracunculifolia obteve efeito significativo da secreção de insulina, no isolamento de ilhotas pancreáticas, ressaltando os resultados obtidos no grupo MSG (MP), que se apresentaram hiperinsulinêmicos, devido a uma possível melhora do stress oxidativo, destacando-se o alto teor antioxidante presente no extrato de B. dracunculifolia utilizado no estudo.

Made available in DSpace on 2017-07-10T14:17:08Z (GMT). No. of bitstreams: 1 Josineia Coradini.pdf: 1285807 bytes, checksum: bfae8484a476d39e0d4df7db2833f2c3 (MD5) Previous issue date: 2014-02-10 / Currently, obesity is considered a common nutritional disorder. It's one of the most relevant public health problems in modern society and a possible risk factor for carpal tunnel syndrome, the pathology that is most closely related to compression of the median nerve. This experimental study with a quantitative and qualitative approach aimed to evaluate the influence of the exercise of swimming on peripheral nerve regeneration in control and obese rates submitted to compressive lesion of the median nerve. Wistar neonates rats along their first 5 days of life received MSG subcutaneous injections (4g/Kg from their body weight at the day). The control group received hyperosmotic saline solution. 48 Wistar rats were used, divided into 6 groups: G1 (control), G2 (control with lesion), G3 (control with lesion + swimming), G4 (obese), G5 (obese with lesion) and G6 (obese with lesion + swimming). The nerve compression was induced through a surgical procedure. The treatment with swimming started on the 3rd day after surgery, and was applied 5 times per week with progressive durations. Before the lesion, the animals were submitted to nociceptive and strength assessments. These tests were repeated on the 3rd postoperative day and also during treatment on the 7th, 14th and 21st day. At the end of treatment, the animals were anesthetized and the median nerve was removed, processed for embedment in paraffin and prepared for protein analysis of BDNF and GAP-43. The data revealed that the pain threshold in the medial region, near the nerve compression, was lower in the second and third assessment when compared to the other assessments, and that groups G5 and G6 were the ones that showed lower nociceptive thresholds in the assessments. In the analysis of grip strength at the first evaluation, all groups are equal, but in the other reviews the G1 and G4 show themselves significantly different from the others. The G1 and G4 groups present organized structures, with myelin sheaths marked by osmium tetroxide. The other groups have a large tissue disorganization, with considerable loss of myelin sheath, however, it was possible verify recovery areas of the nerve fiber, by the the myelin sheath formation in groups G3 and G6. BDNF protein expression is higher in groups G3 and G6 when compared to G1 and G4 groups. The GAP-43 protein was only higher in G3 when compared to G1 and G4 groups. The exercise of swimming was able to enabling the axon regeneration process both in control rats and in obese ones, without difference between these groups, but It was not effective in improving the functionality of the affected limb as well as in the increase of the proteins studied / Atualmente a obesidade é considerada uma desordem nutricional comum, sendo um dos mais relevantes problemas de saúde pública na sociedade moderna e um possível fator de risco para síndrome do túnel do carpo, a qual é a patologia mais relacionada à compressão do nervo mediano. Esta pesquisa é de caráter experimental com abordagem quantitativa e qualitativa tendo como objetivo avaliar a influência do exercício de natação como terapia na regeneração nervosa periférica de ratos controles e obesos, submetidos à lesão compressiva do nervo mediano. Ratos Wistar neonatos durante os primeiros cinco dias de vida receberam injeções subcutâneas de MSG.(4g/kg de peso corporal ao dia). O grupo controle recebeu solução salina hiperosmótica. Foram utilizados 48 ratos machos da linhagem Wistar, divididos em 6 grupos: G1 (controle), G2 (controle com lesão), G3 (controle com lesão + natação), G4 (obesos), G5 (obesos com lesão), G6 (obesos com lesão + natação). A compressão nervosa foi realizada por meio de procedimento cirúrgico. O tratamento com natação iniciou no 3º dia de pós- operatório, sendo realizado 5 vezes por semana com duração progressiva. Anteriormente à lesão, os animais foram submetidos a uma avaliação nociceptiva e de força, que se repetiu no 3º dia de pós-operatório e também durante o tratamento no 7º, 14º e 21º dia. Ao fim do tratamento, com os animais anestesiados, o nervo mediano foi retirado e processado para emblocamento em parafina e preparado para análise proteica do BDNF e GAP-43. O limiar de dor na região medial, próximo a compressão nervosa, foi menor na segunda e na terceira avaliação quando comparadas as demais avaliações, e os grupos G5 e G6 apresentaram menor limiar nociceptivo nas avaliações. Na análise da força de preensão no momento da primeira avaliação todos os grupos foram iguais entre si, porém nas outras avaliações os grupos G1 e G4 mostraram-se significativamente diferentes dos demais. Os grupos G1 e G4 apresentaram as estruturas de forma organizada, com bainhas de mielinas marcadas pelo tetroxido de ósmio. Já os demais grupos apresentaram uma grande desorganização tecidual, com diminuição considerável da bainha de mielina, entretanto, foi possível verificar áreas de recuperação da fibra nervosa, pela formação da bainha de mielina nos grupos G3 e G6. A expressão proteica de BDNF foi maior nos grupos G3 e G6 quando comparado aos grupos G1 e G4. A proteína GAP-43 somente foi maior no grupo G3 quando comparado aos grupos G1 e G4. O exercício de natação foi capaz que potencializar o processo de regeneração axonal tanto em ratos controle quanto em ratos obesos, não ocorrendo distinção entre estes grupos, porém não foi eficaz na melhora da funcionalidade do membro acometido como também no aumento das proteínas estudadas

Research on obesity, weight loss, and food addiction (FA) suggested a strong relationship between use of food additives and the brain's addictive response to food. Previous researchers have examined (FA) and have identified certain food additives such as monosodium glutamate (MSG) and high fructose corn syrup (HFCS) as contributors to food addiction and overeating. Social cognitive theory (SCT) has also been effective in addressing addictive behaviors such as drug addiction, alcohol addiction, and smoking cessation (Bricker et al., 2010). However, researchers had not examined food addiction, social cognitive theory, and obesity in the same study. The purpose of this quantitative, quasi-experimental study was to compare the effects of SCT-based health information and non-SCT-based health information on FA among obese and overweight women. The Yale Food Addiction Scale (YFAS) was used to measure changes in FA and food addiction symptoms among 84 obese and overweight women who received SCT-based health information and non-SCT-based health information. Total scores from pretests and posttests were analyzed using analysis of covariance. Between-group differences on the symptom count posttest scores of the YFAS were analyzed using analysis of variance. Scores were used to determine the difference in FA and FA symptoms between nonrandomized groups. Although the results were not statistically significant, almost 60% (n = 50) of participants experienced a favorable decrease in FA symptoms and experienced weight loss. Findings may provide a basis for determining additional options for health professionals to address obesity and FA patterns.

Posttraumatic stress disorder (PTSD) is a severe anxiety disorder characterised by hypothalamic-pituitary-adrenal (HPA)-axis abnormalities, hyperarousal, anxiety, flashbacks of trauma memories and avoidance. Increasing evidence is now accumulating that the disorder is also associated with shrinkage of the hippocampus and cognitive dysfunction that may have its origin in stress-induced excitotoxicity. Animal studies have indeed highlighted a potential role of the excitotoxic glutamatenitric oxide (NO) pathway in the stress response. Since PTSD appears to be an illness that progresses and worsens over time after an initial severe traumatic event, this study has used an animal model that emphasises repeated trauma to investigate the effect of stress on hippocampal NO synthase (NOS) activity, the release of the nitrogen oxide metabolites of NO (NOx), and also the evoked release of cGMP. Furthermore, the modulation and dependency of these responses on glutamate, NO and cGMP activity using drugs selective for these targets, will also be investigated. Rats (n=10/group) were exposed to repeated stress together with saline or drug administration immediately after the stress procedure and continuing for one week post-stress. The animals were then sacrificed for assay of hippocampal NOS activity, NO, and cGMP accumulation. Animals received either the glutamate-NMDA receptor antagonist, memantine (MEM;5mg/kg ip/d), the neuronal NOS selective inhibitor, 7- nitroindazole monosodium salt (7-NINA;20mg/kg ip/d), the cGMP-specific PDE inhibitor, sildenafil (SIL;10mg/kg ip/d) or the NFkb antagonist, pyrollidine dithiocarbamate (PDTC;70mg/kg ip/d). The latter inhibits the nuclear transcription factor, NFkb, responsible for inducing the expression of iNOS, while it also appears to mediate the glutamatergic actions on NOS expression, Stress significantly increased hippocampal NOS activity, as well as significantly increased hippocampal cGMP and NO, levels. These increases were blocked by pretreatment with either PDTC or 7-NINA, while memantine was without effect. Sildenafil significantly augmented stress induced NO, accumulation, as well as cGMP. although the latter failed to reach significance. 7-NINA and memantine significantly blocked the increase in cGMP evoked by time-dependent sensitisation (TDS)-stress, with PDTC attenuating this response, but not significantly. Additionally, administration of each drug separately for seven days without exposure to stress, did not evoke significant changes in NOx levels, compared to the control group. However, significant increases in cGMP levels, compared to the control group, were found with all four drugs. Repeated trauma therefore activates the NO-cGMP pathway, possibly involving actions on both nNOS and iNOS. The NMDA receptor appears less involved after chronic repeated stress, and may have limited therapeutic implications. Sub-cellular NO-modulation, however, may represent an important therapeutic strategy in preventing the effects of severe stress and in treating PTSD. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.

Posttraumatic stress disorder (PTSD) is a severe anxiety disorder characterised by hypothalamic-pituitary-adrenal (HPA)-axis abnormalities, hyperarousal, anxiety, flashbacks of trauma memories and avoidance. Increasing evidence is now accumulating that the disorder is also associated with shrinkage of the hippocampus and cognitive dysfunction that may have its origin in stress-induced excitotoxicity. Animal studies have indeed highlighted a potential role of the excitotoxic glutamatenitric oxide (NO) pathway in the stress response. Since PTSD appears to be an illness that progresses and worsens over time after an initial severe traumatic event, this study has used an animal model that emphasises repeated trauma to investigate the effect of stress on hippocampal NO synthase (NOS) activity, the release of the nitrogen oxide metabolites of NO (NOx), and also the evoked release of cGMP. Furthermore, the modulation and dependency of these responses on glutamate, NO and cGMP activity using drugs selective for these targets, will also be investigated. Rats (n=10/group) were exposed to repeated stress together with saline or drug administration immediately after the stress procedure and continuing for one week post-stress. The animals were then sacrificed for assay of hippocampal NOS activity, NO, and cGMP accumulation. Animals received either the glutamate-NMDA receptor antagonist, memantine (MEM;5mg/kg ip/d), the neuronal NOS selective inhibitor, 7- nitroindazole monosodium salt (7-NINA;20mg/kg ip/d), the cGMP-specific PDE inhibitor, sildenafil (SIL;10mg/kg ip/d) or the NFkb antagonist, pyrollidine dithiocarbamate (PDTC;70mg/kg ip/d). The latter inhibits the nuclear transcription factor, NFkb, responsible for inducing the expression of iNOS, while it also appears to mediate the glutamatergic actions on NOS expression, Stress significantly increased hippocampal NOS activity, as well as significantly increased hippocampal cGMP and NO, levels. These increases were blocked by pretreatment with either PDTC or 7-NINA, while memantine was without effect. Sildenafil significantly augmented stress induced NO, accumulation, as well as cGMP. although the latter failed to reach significance. 7-NINA and memantine significantly blocked the increase in cGMP evoked by time-dependent sensitisation (TDS)-stress, with PDTC attenuating this response, but not significantly. Additionally, administration of each drug separately for seven days without exposure to stress, did not evoke significant changes in NOx levels, compared to the control group. However, significant increases in cGMP levels, compared to the control group, were found with all four drugs. Repeated trauma therefore activates the NO-cGMP pathway, possibly involving actions on both nNOS and iNOS. The NMDA receptor appears less involved after chronic repeated stress, and may have limited therapeutic implications. Sub-cellular NO-modulation, however, may represent an important therapeutic strategy in preventing the effects of severe stress and in treating PTSD. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.

Introdução: Obesidade é uma questão de saúde pública em muitos países, inclusive no Brasil. O excesso de peso atinge 1 bilhão de adultos no mundo e, no Brasil, já é um problema maior que a desnutrição. O glutamato monossódico (GMS) é um agente flavorizante utilizado em níveis crescentes nos alimentos industrializados. O GMS administrado em ratos ocasiona obesidade e diminuição do hormônio do crescimento (GH). Objetivo: Avaliar o efeito do GMS nos fetos de ratas prenhas através da comparação do peso, comprimento nasal-anal (CNA) e índice de Lee (IL) ao nascimento e com 21 dias de vida. Métodos: Utilizamos ratas prenhas da linhagem Wistar divididas em três grupos: grupo controle (GC), G10 e G20. Estes, respectivamente, foram alimentados com ração contendo 0, 10 e 20% de GMS desde o período de acasalamento até o final da amamentação. Resultados: O peso e o CNA não foram diferentes entre os grupos ao nascimento. O grupo G20, ao nascimento, teve IL menor que o grupo GC (p < 0,05) e, aos 21 dias de vida, apresentou peso e CNA menores que o grupo G10, o qual foi menor que o GC (p < 0,01). O grupo G20, aos 21 dias de vida, teve IL semelhante aos outros dois grupos. O percentual de ganho de peso do nascimento ao 21º dia de vida foi menor no G20 em relação aos outros dois grupos (p < 0,01). O grupo G20 teve percentual de aumento de CNA do nascimento ao 21º dia de vida menor que o grupo G10, e este menor que o grupo GC (p < 0,01). Conclusões: O GMS nas concentrações de 10 e 20% na ração de ratas prenhas Wistar apresentou uma relação dose-dependente nas variáveis peso e CNA. Houve diminuição no padrão de ganho de peso e de aumento de CNA do nascimento ao 21º dia de vida com uso de GMS. O IL na prole do grupo G20 aumentou em relação ao do grupo GC após 3 semanas de acompanhamento. / Objective: Determine the effects of the MSG (monosodium glutamate) in the offspring of pregnant rats through the comparison of the weight, NAL (nasal-anal length) and IL (Index of Lee) at birth and with 21 days of life. Research Methods & Procedures: We have investigated pregnant Wistar rats and their offspring and divided them into 3 groups: GC, G10 and G20. Each of the groups received 0%, 10% and 20% of MSG, respectively from coupling until the end of the weaning period. Results: Neither weight nor NAL were different among the groups at birth. The group G20 at birth had an IL lower than the group GC (p<0,05) and with 21 days of life presented weight and NAL lower than the groups G10 and this lower than the GC (p<0,01). Otherwise the G20 at 21 days of life had the IL similar to the other two groups. The weight profit percentage from birth to the 21st day of life was lower in the G20 regarding the other two groups (p<0,01). The G20 had a NAL increase percentage from birth to the 21st day of life lower than the G10 and this lower than the GC (p<0,01). Conclusions: MSG presented a dose-dependent relation in the variables weight and NAL. It caused a decrease in the growth pattern as well as in the weight gain pattern until the 21st day of life. The IL of the group 20% had an increased in relation to the control group after 3 weeks of follow up.