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Modifying Fatty Acid Composition of Bovine Milk by Abomasal Infusion or Dietary Supplementation of Seed Oils or Fish OilBandara, Aloka B. 26 January 1998 (has links)
The potential for enhancing oleic acid (cis-18:1) and linoleic acid (18:2) content and lowering medium chain fatty acid (MCFA) content of bovine milk was investigated by abomasal infusion or dietary supplementation of oils. In experiment 1, olive oil, sesame oil, sunflower oil, or fish oil was abomasally infused (155 to 219 g/d) into Jersey cows during the last 6 d of each of four 14-d periods. In experiment 2, canola oil, olive oil, high-oleic sunflower oil, or distilled water (control) was abomasally infused (342 to 371 g/d) into three Holsteins and three Jerseys during the last 5 d of each of four 10-d periods. The intestinal digestibility and concentration of cis-18:1 and 18:2 in milk were proportional to flow of these fatty acids to the duodenum. Also, greater concentration of cis-18:1 in milk was associated with lowered yield of MCFA. During olive oil or sesame oil infusion in experiment 1, for each 100 g of cis-18:1 infused into the abomasum, milk cis-18:1 yield was increased by an average of 47 g, and MCFA yield was reduced by 42 g. The yield of 18:2 in milk was increased by approximately 46 g for each 100 g of infused 18:2 during olive oil or sesame oil infusion. Milk produced during sesame oil infusion, however, had an off-flavor when evaluated by a taste panel. In experiment 2, each 100 g of cis-18:1 infused daily increased milk cis-18:1 yield in Holsteins and Jerseys by 41 and 39 g/d, respectively, whereas recovery of infused 18:2 was 34 g/d for Jerseys and 42 g/d for Holsteins. In experiment 3, 22 Jersey cows were fed a basal diet, or the basal diet supplemented with 3.5% high-oleic canola oil, 3.5% soybean oil, or 1.75% high-oleic canola oil plus 1.75% soybean oil for 5 wk. Dietary canola oil supplementation increased conjugated linoleic acid (CLA) percentage in milk to a moderate level without raising trans-18:1 percentage, whereas feeding either supplement containing soybean oil raised both CLA and trans-18:1 percentages. Concentrations of trans-18:1 and CLA in milk apparently reflected the extent of unsaturated fatty acid biohydrogenation in the rumen. Dietary supplementation with canola oil increased yield of cis-18:1 in milk by 21 g for each 100 g of supplemental cis-18:1 intake. Yield of 18:2 in milk was raised by 3 g for each 100 g of supplemental 18:2 intake by cows fed soybean oil. Using abomasal infusion as an indicator of the maximum potential for apparent recovery of cis-18:1 in milk (39 to 49%), cis-18:1 recovery in response to supplemental cis-18:1 in the diet was approximately half of the potential response due to partial biohydrogenation in the rumen. The apparent recovery of dietary 18:2 in milk was reduced to only one-tenth of the potential yield (31 to 47%) indicated by abomasal infusion of seed oils. Results indicated that the fatty acid profile of bovine milk was altered in a manner that would be beneficial to human health when cows were fed supplemental oleic acid, but further research should focus on safe and economical methods to protect dietary unsaturated fatty acids from biohydrogenation. / Ph. D.
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Impact of a feeding strategy and management practices on the health and welfare of pullets and laying hensSelf, Gerald Rodney 08 August 2023 (has links) (PDF)
The overall purpose of this thesis is to understand the impact of management on commercial egg layers, whether that be environmental-related, health-related, or other possible stressors within the pullet and post-peak phases. Furthermore, the study seeks to examine what effects to performance and production these impacts may induce within a commercial layer in differing phases, specifically the pullet and post-peak phases. Chapter two explores into coccidiosis within the pullet phase, which induced by a commercial vaccine, can provide stress to a pullet, lowering protection against infection, and seriously compromising its growth and development into peak lay. Chapter three explores into the post-peak phase, a transition from a caged system of production to cage-free system of production was selected. incorporating multiple differing environmental stimuli that can induce stress. If commercial layers prove to possess the capabilities to adapt to these impacts in multiple phases, the possibility of extended production is possible.
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Screening of fatty alcohol dehydrogenase and its application on alkane production / 脂肪族アルコール脱水素酵素の探索とそのアルカン生産への応用SUI, YU-AN 23 March 2023 (has links)
京都大学 / 新制・課程博士 / 博士(農学) / 甲第24671号 / 農博第2554号 / 新制||農||1099(附属図書館) / 学位論文||R5||N5452(農学部図書室) / 京都大学大学院農学研究科応用生命科学専攻 / (主査)教授 小川 順, 教授 阪井 康能, 教授 白井 理 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DFAM
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Branched-Chain Amino Acid Metabolism in the Neonatal PigYonke, Joseph Allan 29 June 2022 (has links)
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.
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Hepatic Lipid metabolism in Neonatal PigsGerrard, Samuel David 19 December 2024 (has links)
Medium chain-fatty acids (MCFA) are a group of fatty acids containing hydrocarbon chains between 6-12 carbons. They are rapidly absorbed and taken up by cells which has led to their incorporation into neonatal formulas as an alternative source of energy. While abundant literature is available on proposed beneficial effects of MCFA at low levels of incorporation, little is known about utilization of MCFAs in formulas and the effects on growth and liver health. Therefore, we set out to test the hypothesis that MCFAs are metabolized differently than long-chain fatty acids (LCFAs) when they are the main energy substrate of the formula. We sought to investigate the mechanism that differentiates MCFA from LCFA from a metabolic and physiologic standpoint. Feeding high-fat diets of MCFA and LCFA resulted in steatosis from both classes of fatty acids. However, MCFA fed group accumulated 4 more fat in their livers than the LCFA group. Steatosis was accompanied by decreased - oxidation and increased expression of fatty acid synthetic enzymes in MCFA pigs. Peripherally, skeletal muscle displayed an upregulation of cholesterol-related genes. Lowering the amount of MCFA in the formula relieved hepatic steatosis however, only removing the MCFA source entirely from the diet lowered the steatosis below 20% of liver weight. Isolated mitochondria from pigs fed high MCFA formula were unable to oxidize pyruvate and malate as effectively as pigs without MCFA in their formula. Mitochondria also oxidized laurate more effectively when attached to carnitine. Regardless, pigs fed higher amounts of MCFA, or MCFA at any level, had higher levels of fat in their livers than the LCFA counterparts. Taken together, these data suggest that MCFA and LCFA are handled differently from a cellular perspective and MCFA changed the hepatic phenotype of neonatal pigs however, several unanswered questions arose from the completed studies. / Doctor of Philosophy / Medium-chain fatty acids (MCFAs) are a group of molecules that contain between 6 to 12 carbon units. These fatty acids are readily available for cells to use for energy and because of this, MCFAs are commonly added to infant formulas to increase nutrient availability for infants. Using MCFAs at low levels in experimental diets has been heavily researched however, there is not much information related to feeding high amounts of MCFAs. So, we set out to determine whether MCFAs are handled the same as long-chain fatty acids (LCFAs) at higher levels in experimental formulas. Our goal was to understand how MCFA are different from LCFA in their utilization and circulation. Feeding high amounts of MCFA and LCFA resulted in fat accumulation in the liver of neonatal pigs however, pigs that were fed MCFA had higher fat content in their livers. Livers from these pigs also had a lower ability to use fatty acids for energy and had higher mRNA expression of enzymes to make more lipids. Feeding less MCFA helped to lower the amount of fat in the liver. The ability of the mitochondria to breakdown MCFA from these pigs was lower than pigs fed more LCFA. Overall, these studies highlight that high levels of MCFA lead to fat accumulation in the liver; more work needs to be done to understand the disease process.
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Élévation aigüe de la cétonémie : effets cétogènes de produits alimentaires dérivés de l’huile de noix de coco et influence d’une combinaison avec de l’exercice de type aérobie / Acute plasma ketone stimulation : ketogenic effects of products derived from coconut oil and influence of a combination with aerobic exerciseVandenberghe, Camille January 2017 (has links)
Depuis maintenant plus de 30 ans, il est reconnu qu’au début de la maladie
d’Alzheimer, le cerveau utilise moins bien le glucose, son principal carburant.
Cependant, ce problème énergétique précoce dans la maladie semblerait limité au
glucose et ne concernerait pas un autre carburant, celui-ci dérivé des gras, les cétones.
Ces dernières sont produites par le corps après un exercice physique d’intensité
modérée. Leur production est également stimulée avec la prise de suppléments
alimentaires à base d’huile de noix de coco, un aliment riche en triglycérides de
moyennes chaînes (MCT). La capture des cétones au cerveau augmente
proportionnellement à leur concentration plasmatique. Ainsi, des conditions élevant la
cétonémie augmentent aussi la capture cérébrale des cétones. Par conséquent,
l’élévation de l’apport en cétones pourrait constituer une approche novatrice qui
permettrait de potentiellement ralentir le développement de la maladie d’Alzheimer.
Notre objectif général était d’optimiser le type de supplément MCT à utiliser afin
d’élever la cétonémie de manière aigüe et, en second lieu, d’employer ce dernier en
combinaison avec une seconde stratégie cétogène, l’exercice physique de type aérobie
(EA). Lors de la première phase de ce projet, l’effet cétogène de différents produits
alimentaires dérivant de l’huile de noix de coco (acide caprylique [C8], acide caproïque
[C10], mélange de MCT typique [C8+C10]) était comparé chez 9 participants jeunes
sains. Des échantillons sanguins étaient récoltés toutes les 30 min pendant 8 h. Lors de
la seconde phase, le potentiel cétogène de la combinaison d’EA à une supplémentation
MCT était évalué chez 10 femmes âgées saines pendant 5 jours. Les cétones
plasmatiques sous ces différentes conditions étaient mesurées. Lors de cette étude, le
C8 était le produit le plus cétogène testé suivi du supplément C8+C10. L’huile de noix de
coco n’a pas induit une cétonémie plus élevée qu’un 8 h sans MCT. De plus, l’ajout de 5
jours d’EA a potentialisé la cétonémie observée suite à la prise de MCT C8+C10 seul.
Ainsi, la combinaison de stratégies cétogènes, tant au niveau de la diversité des
molécules utilisées ou des stratégies cétogènes employées, permet d’augmenter la
présence de cétones dans le sang. / Abstract : Brain glucose consumption deteriorates with age, a situation that worsens with the onset of Alzheimer's disease. However, this early energy problem in the disease is limited to glucose and does not affect brain ketone uptake. Ketones are the main alternative fuel for the brain when glucose concentrations are decreased. They are produced endogenously after moderate aerobic exercise (AE) or with a medium chain triglyceride (MCT) exogenous supplement. Ketone brain uptake increases in proportion to their plasma concentration. Thus, providing a daily ketogenic fuel could help support brain energy needs during aging. Our aim was to optimize the type of MCT to use in a ketogenic supplementation and to combine this supplement with another ketogenic strategy, AE. In the first phase of this project, the acute ketogenic effect of products derived from coconut oil was compared. Nine healthy adults took various MCT supplements (coconut oil, caprylic acid [C8], capric acid [C10], classic MCT mix [C8+C10]). Blood was sampled every 30 min over 8 h. In the second phase, we evaluated the acute ketogenic potential of the combination of AE and MCT supplementation. Ten healthy older women took C8+C10 MCT supplement for 5 days combined with a 5-days AE program. Automated spectrophotometric assays where used to measure plasma ketones under these different conditions. Our results show that in this 8 h experimental design, C8 was the most ketogenic MCT followed by C8+C10. Coconut oil alone did not induce more net ketosis than an 8 h visit with no added MCT. Furthermore, the combination of AE and MCT supplementation enhanced the ketogenic response over 4 h compared to the control day. Thus, the combination of ketogenic strategies, both in terms of the diversity of the molecules or the ketogenic strategy employed, makes it possible to increase the presence of ketones in the blood.
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Ácidos graxos de cadeia média como ligantes da proteína PPAR / Medium chain fatty acids like PPAR ligandLiberato, Marcelo Vizoná 06 February 2009 (has links)
Receptores ativados da proliferação de peroxissomos (PPAR) são receptores nucleares que regulam o metabolismo de gordura e glicose, adipogênese e polarização de macrófagos, e são os mediadores da ação de uma grande classe de fármacos usada no tratamento de diabetes tipo 2, as tiazolidinadionas (TZD). Enquanto as TZDs reduzem a glicose do sangue e aumentam efetivamente a sensibilidade à insulina, elas podem também apresentar efeitos colaterais como aumento do risco de complicações cardiovasculares, ganho de peso, retenção de fluido e toxicidade hepática. Por causa disso, novos fármacos que possuem respostas mais favoráveis devem ser desenvolvidos, e o mecanismo de ativação do PPAR por ligantes vem sendo intensamente examinado. Para entender a relação entre a ligação de agonistas ao PPAR e a ativação transcricional, pretendíamos primeiramente obter cristais de PPAR-LBD (domínio de ligação ao ligante) humano na forma apo. Porém, surpreendentemente, a análise do sítio de ligação ao ligante revelou a presença de três pequenas moléculas, identificadas como ácidos nonanoicos e octanoicos. Este trabalho reporta a análise da estrutura cristalográfica do PPAR LBD complexado simultaneamente com três ácidos graxos de cadeia média (AGCM), provindos de bactérias (organismo de expressão), localizados no sítio de ligação ao ligante. A análise estrutural e funcional sugere que os AGCM são agonistas parciais que estabilizam a conformação do LBD do PPAR por mecanismo independente da hélice 12. / PPARs (peroxisome proliferator activated receptors) are nuclear receptors that regulate glucose and fat metabolism, adipogenesis and macrophage polarization and mediate actions of a major class of drugs that are used to treat type 2 diabetes, the thiazolidinediones. While TZDs reduce blood glucose and improve insulin sensitivity effectively, they can also exhibit deleterious side effects such as increased cardiovascular risk, weight gain, fluid retention and liver toxicity. Because it is desirable to develop new PPAR drugs with more favorable spectrums of response, mechanisms of PPAR ligand activation have come under intense scrutiny. To understand relationships between PPAR ligand binding and transcriptional activation, we sought to obtain apo human PPAR-LBD (ligand binding domain) crystals that diffract to high resolution. More surprisingly, close analysis of the ligand binding pocket revealed the presence of three small molecules, identified as nonanoic acid and octanoic acid. Here, we report the X-ray structural analysis of the PPAR LBD complexed with three bacterial (expression organism) medium chain fatty acids (MCFAs) that simultaneously occupy the buried ligand binding pocket (LBP). Structural and functional analysis suggests that MCFAs are partial agonists that stabilize PPAR LBD conformation, through a helix 12 independent mechanism.
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Avaliação toxicológica subcrônica de dieta cetogênica à base de trienantina em ratos jovens. / Subchronic toxicologicalevaluation of a ketogenic diet based upon trienantin in rats.Lucena, Ana Luiza de Melo 20 December 2007 (has links)
The classic ketogenic diet, rich in long chain triacylglycerols (LCT), is characterised by a high
concentration of lipids and a low concentation of carbohydrates and proteins, promoting
ketonemia and ketonuria, a property used in the treatment of disorders that affect cerebral
metabolism and function, for example epilepsy resistant to medication. Medium chain
triacylglycerols (MCT) are considered alternative substrates to LCT in the production of this
diet, to promote a more rapid increase in the levels of the body´s blood ketones. Trienantin, a
medium chain triacyglycerol from enantic fatty acid (7:0), has been used with success with
children suffering hereditary metabolic syndromes, but has had few studies about its
toxicological effects. The objective of this dissertation was to evaluate the toxicity of a
subchronic consumption of a ketogenic diet with a trienantin base on young rats, and is
submitted in the form of two articles. The first, under the name of: Substitution of LCT with
MCT in nutritional therapy: an emphasis on ketogenic therapy presents a revision of the
ketogenic diet, comparing the data of LCT and MCT in animal and clinical studies. The
more rapid ketonemia promoted by MCT allows a lower quantity of lipids and a greater
proportion of proteins and carbohydrates, enhancing the palatability of the diet. The effect of
replacing LCT with MCT on physiological parameters, such as serum lipid profile, remains
controversial and requires additional studies to comprehend the repercussions of this class
of lipids on human health. The second article entitled: Toxicological evaluation of a
subchronic ketogenic diet based upon trienantin in young rats deals with an experimental
study of male Wistar rats in which 3 groups (n=10), named according to their received diet:
Control (diet pattern AIN-93) KetoTAGC7 (ketogenic based upon AIN-93G: modified to
contain 4% soy oil, 25.79% trienantin and 40% margarine) and Keto TAGsoy (ketogenic
based upon soya: AIN-93G modified to contain 29.79% soya oil and 40% margarine). The
proportion of lipid:carbohydrate+protein in the ketogenic diets was 3.5:1 (control diet, 1:11.8)
and the experimental duration was 6 weeks. Triacylglycerols, total cholesterol, HDLc, VLDLc
and LDLc, in addition tests for hepatic and renal function and injury, were performed from
serum obtained, and samples of liver,stomach, kidney and small intestine were collected for
histological analysis. It was verified that the energy value of the portions of rations ingested
did not differ amongst the three groups during the experimental period, however the animals
submitted to the ketogenic diets had ingested a similar quantity of rations within the group,
but less than (p=0.005) the control group. The ketogenic diet promoted similar weight gain
amongst the group and only the animals in group KetoTAGC7 exhibited weight gain less than
that of the control group (p=0.004) between the second and fifth weeks of the experiment. At
the end of the study, all groups presented equivalent weights. There were no significant
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differences between the three groups as to the lipid profile, serum glucose and of the
markers for hepatic function and injury. Histological analysis of samples from the small
intestine, stomach and kidney did not show any significant morphological alteration and the
presence of lipid infiltration within hepatocytes was detected in the same manner amongst
the three groups. A ketogenic diet with a trienantin base did not promote toxic effects, under
the conditions of this study, indicating the possibility that MCT could be administered to
patients suffering neurological and metabolic defects, as part of ketogenic diet. / Fundação de Amparo a Pesquisa do Estado de Alagoas / A dieta cetogênica clássica, rica em triacilgliceróis de cadeia longa (TCL), é caracterizada
por uma alta concentração de lipídeos e, ao mesmo tempo, por uma baixa concentração de
carboidratos e proteínas para promover cetonemia/cetonúria, propriedade utilizada no
tratamento de várias desordens que afetam o metabolismo e a função cerebral, a exemplo
da epilepsia resistente ao uso de medicamentos. Os triacilgliceróis de cadeia média (TCM)
são considerados um substrato alternativo aos TCL na elaboração desta dieta, por
promoverem um aumento mais rápido nos níveis dos corpos cetônicos sanguíneos. A
trienantina é um triacilglicerol de cadeia média do ácido graxo enântico (7:0), utilizada com
sucesso em crianças portadoras de síndromes metabólicas herdadas, havendo poucos
estudos sobre seus efeitos toxicológicos. A presente dissertação teve como objetivo avaliar
a toxicidade do consumo subcrônico da dieta cetogênica à base de trienantina em ratos
jovens, sendo desenvolvida na forma de dois artigos. No primeiro, denominado Substituição
de TCL por TCM na terapia nutricional: uma ênfase no tratamento cetogênico, apresenta-se
uma revisão sobre a dieta cetogênica, confrontando-se dados sobre os efeitos dos TCL e
dos TCM, em experimentos animais e ensaios clínicos. A mais rápida cetonemia promovida
pelos TCM permite utilizar uma menor quantidade de lipídios e maior de proteínas e de
carboidratos, aumentando a palatabilidade da dieta. O efeito da substituição de TCL por
TCM sobre parâmetros fisiológicos, como o perfil lipídico sérico, é controverso,
necessitando-se de pesquisas adicionais para entendimento da repercussão dessa classe
de lipídios sobre a saúde humana. O segundo artigo, intitulado Avaliação toxicológica
subcrônica de dieta cetogênica à base de trienantina em ratos jovens, trata do estudo
experimental realizado em ratos Wistar, em que foram estabelecidos 3 grupos (n=10),
denominados, segundo a dieta recebida, em Controle (dieta padrão AIN-93G), CetoTAGC7
(cetogênico à base de trienantina; AIN-93G modificada para conter 4% de óleo de soja,
25,79% de trienantina e 40% de margarina) e CetoTAGsoja (cetogênico à base de soja;
AIN-93G modificada para conter 29,79% de óleo de soja e 40% de margarina). A proporção
lipídeos:carboidratos+proteína das dietas cetogênicas foi de 3,5:1 (dieta controle, 1:11,8) e o
período experimental totalizou 6 semanas. Triacilgliceróis, colesterol total, HDLc, VLDLc e
LDLc, além de provas de função e lesão hepática e renal, foram medidos nas amostras de
soro obtidas e fragmentos de fígado, estômago, rim e intestino delgado foram coletados
para a análise histológica. Verificou-se que o valor energético da cota de ração ingerida
pelos três grupos, no período experimental, não foi diferente, embora os animais submetidos
às dietas cetogênicas tenham ingerido uma quantidade de ração semelhante entre si, mas
inferior (P<0,005) aos do grupo controle. As dietas cetogênicas promoveram ganho de peso
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semelhante entre si e apenas os animais do grupo CetoTAGC7 exibiram ganho de peso
inferior (P=0,004) em relação aos do grupo controle, entre a 2ª e a 5ª semana de
experimento. Ao final do estudo, todos os grupos apresentaram pesos equivalentes. Não
houve diferenças significativas entre os três grupos quanto ao perfil lipídico e glicose séricos
e aos marcadores de função e lesão hepática e renal. A análise histológica dos fragmentos
de intestino delgado, estômago e rim não evidenciou qualquer alteração morfológica
importante e a presença de infiltração lipídica nos hepatócitos foi detectada de maneira
semelhante para os três grupos. A dieta cetogênica à base de trienantina não promoveu
efeitos tóxicos, nas condições do presente estudo, indicando a possibilidade deste TCM ser
administrado em pacientes portadores de desordens neurológicas e defeitos metabólicos,
inclusive, em concentrações cetogênicas.
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Efeito de dieta cetogênica à base de óleo de coco sobre as crises convulsivas de ratos portadores de epilepsia induzida por pilocarpina / Effect of the ketogenic diet based on coconut oil upon seizures of rats with epilepsy induced by pilocarpineRêgo, Elisabete da Silva Mendonça 20 April 2011 (has links)
Epilepsy is a chronic disturbance of brain function characterized by the presence of recurrent and spontaneous seizures, making one of the most frequent and severe neurological diseases, affecting approximately 50 million people worldwide, mainly children. Among these, 40% had antiepileptic drug refractory seizures. Non-drug options as surgery, vagus nerve stimulation and the ketogenic diet are timely. This diet, used since 1921 in treatment of drug-resistant epilepsy is characterized by a high concentration of lipids and often by low concentration of carbohydrates and proteins. Traditionally, the ketogenic diet use long chain triacylglycerols (LCT), however, the medium chain triacylglycerols (MCT) are considered an alternative substrate for promoting faster ketonemia-ketonuria. The oil from coconut (Cocos nucifera L.) is a natural source of MCT, and is used for several purposes, including therapeutic. This dissertation aims to investigate the effects of the ketogenic diet based on coconut oil and soybean oil on epileptic seizures in rats, consists of a review chapter, entitled Drug-resistant epilepsies: an emphasis on treatment ketogenic, and an article from the results, entitled Effects of ketogenic diet based on coconut oil on the seizures of rats with epilepsy induced by pilocarpine. The article deals an experimental study conducted in Wistar rats, divided into three groups (n=10), named according to the diet received, in Control (standard diet AIN-93G), CetoTAGcoco (ketogenic diet based in coconut oil; AIN-93G diet modified to contain 7% soybean oil, 22.79% of extra virgin coconut oil and 40% margarine) and CetoTAGsoja (ketogenic diet based in soybean oil; AIN-93G diet modified to contain 29.79% of soybean oil and 40% margarine). The ratio lipid:carbohydrate+protein of ketogenic diets was 3.5:1 (control diet, 1:11.8). The experimental period lasted 19 days. The animals fed ketogenic diets showed food intake (g) below, however, dispend energetic and weight gain similar to Control group. The behavioral analysis showed that the experimental groups did not differ in frequency and duration of seizures, however, the animals in group CetoTAGcoco had shorter duration of seizures in the 19th day, that the Control group (0.00±0.00 against 22.78±2.95, respectively, P<0.05). Additionally, the CetoTAGcoco group presented lower variation of frequency and duration of seizures between the 19th and 1st day of treatment than the Control group (9.00±1.73 against 11.00±1.00, for frequency, and 20.80±12.61 against 49.14±21.15, for duration, respectively, P<0.05). The results of this study suggest a possible protective effect of ketogenic diet based on extra virgin coconut oil on seizures. That result, coupled with studies attesting to confidence and tolerance of the coconut oil, particularly in ketogenic ratios, indicating a potential benefit of this oil for control the seizures, especially for individuals with medically refractory epilepsy. / Fundação de Amparo a Pesquisa do Estado de Alagoas / A epilepsia é um disturbio crônico da função cerebral, caracterizado pela presença de crises convulsivas recorrentes e espontâneas. Trata-se de uma das mais frequentes e graves doenças neurológicas, que afeta cerca de 50 milhões de pessoas no mundo, principalmente crianças. Dentre estas, 40% apresentam crises refratárias às drogas antiepilépticas existentes. Opções não farmacológicas, como cirurgia, estimulação do nervo vago e dieta cetogênica, são oportunas. Esta dieta, utilizada desde 1921 no tratamento da epilepsia fármaco-resistente, caracteriza-se por alta concentração de lipídeos e, frequentemente, por baixa concentração de carboidratos e proteínas. Tradicionalmente, a dieta cetogênica utiliza como fonte lipídica os triacilgliceróis de cadeia longa (TCL); porém, os triacilgliceróis de cadeia média (TCM) são considerados um substrato alternativo, por promoverem cetonemia/cetonúria de forma mais rápida. O óleo proveniente do coco (Cocos nucifera L.) representa uma fonte natural de TCM, sendo utilizado para diversos fins, inclusive terapêuticos. A presente dissertação visa investigar os efeitos de dieta cetogênica à base de óleo de coco e óleo de soja sobre as crises convulsivas de ratos epilépticos. É constituída por um capítulo de revisão, intitulado Epilepsias fármaco-resistentes: uma ênfase no tratamento cetogênico, e um artigo de resultados, intitulado Efeito de dieta cetogênica à base de óleo de coco sobre as crises convulsivas de ratos portadores de epilepsia induzida por pilocarpina. O artigo trata de um estudo experimental realizado com ratos Wistar, alocados em três grupos (n=10), denominados, segundo a dieta recebida, em Controle (dieta padrão AIN-93G), CetoTAGcoco (dieta cetogênica à base de óleo de coco; AIN-93G modificada, com 7% de óleo de soja, 22,79% de óleo de coco extra-virgem e 40% de margarina) e CetoTAGsoja (dieta cetogênica à base de óleo de soja; AIN-93G modificada, com 29,79% de óleo de soja e 40% de margarina). A proporção lipídeos: carboidratos+proteína das dietas cetogênicas foi de 3,5:1 (dieta controle, 1:11,8). O período experimental totalizou 19 dias. Os animais submetidos aos tratamentos cetogênicos apresentaram consumo alimentar (g) inferior, porém, consumo energético (Kcal) e ganho de peso corporal (g) semelhantes ao grupo Controle. As análises comportamentais demonstraram que os animais dos grupos experimentais não diferiram entre si quanto à freqüência e à duração total das crises; entretanto, os animais do grupo CetoTAGCcoco tiveram menor duração média de crises no 19º dia, que o grupo Controle (0,00±0,00 contra 22,78±12,95, respectivamente; p<0,05). Adicionalmente, o grupo CetoTAGcoco apresentou valores inferiores de variação de frequência e de duração das crises entre o 19° e o 1° dia de tratamento, que o grupo Controle (9,00±1,73 contra 11,00±1,00, para freqüência, e 20,80±12,61 contra 49,14±21,15, para duração, respectivamente; p<0,05). Os resultados do presente estudo apontam para um possível efeito protetor da dieta cetogênica à base de óleo de coco extra-virgem sobre as crises convulsivas. Tais resultados, associados a estudos que atestem a confiabilidade e a tolerância do consumo de óleo de coco, particularmente em proporções cetogênicas, poderiam indicar um benefício potencial deste óleo no controle das crises convulsivas, especialmente para indivíduos portadores de epilepsia refratária a medicamentos.
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Ácidos graxos de cadeia média como ligantes da proteína PPAR / Medium chain fatty acids like PPAR ligandMarcelo Vizoná Liberato 06 February 2009 (has links)
Receptores ativados da proliferação de peroxissomos (PPAR) são receptores nucleares que regulam o metabolismo de gordura e glicose, adipogênese e polarização de macrófagos, e são os mediadores da ação de uma grande classe de fármacos usada no tratamento de diabetes tipo 2, as tiazolidinadionas (TZD). Enquanto as TZDs reduzem a glicose do sangue e aumentam efetivamente a sensibilidade à insulina, elas podem também apresentar efeitos colaterais como aumento do risco de complicações cardiovasculares, ganho de peso, retenção de fluido e toxicidade hepática. Por causa disso, novos fármacos que possuem respostas mais favoráveis devem ser desenvolvidos, e o mecanismo de ativação do PPAR por ligantes vem sendo intensamente examinado. Para entender a relação entre a ligação de agonistas ao PPAR e a ativação transcricional, pretendíamos primeiramente obter cristais de PPAR-LBD (domínio de ligação ao ligante) humano na forma apo. Porém, surpreendentemente, a análise do sítio de ligação ao ligante revelou a presença de três pequenas moléculas, identificadas como ácidos nonanoicos e octanoicos. Este trabalho reporta a análise da estrutura cristalográfica do PPAR LBD complexado simultaneamente com três ácidos graxos de cadeia média (AGCM), provindos de bactérias (organismo de expressão), localizados no sítio de ligação ao ligante. A análise estrutural e funcional sugere que os AGCM são agonistas parciais que estabilizam a conformação do LBD do PPAR por mecanismo independente da hélice 12. / PPARs (peroxisome proliferator activated receptors) are nuclear receptors that regulate glucose and fat metabolism, adipogenesis and macrophage polarization and mediate actions of a major class of drugs that are used to treat type 2 diabetes, the thiazolidinediones. While TZDs reduce blood glucose and improve insulin sensitivity effectively, they can also exhibit deleterious side effects such as increased cardiovascular risk, weight gain, fluid retention and liver toxicity. Because it is desirable to develop new PPAR drugs with more favorable spectrums of response, mechanisms of PPAR ligand activation have come under intense scrutiny. To understand relationships between PPAR ligand binding and transcriptional activation, we sought to obtain apo human PPAR-LBD (ligand binding domain) crystals that diffract to high resolution. More surprisingly, close analysis of the ligand binding pocket revealed the presence of three small molecules, identified as nonanoic acid and octanoic acid. Here, we report the X-ray structural analysis of the PPAR LBD complexed with three bacterial (expression organism) medium chain fatty acids (MCFAs) that simultaneously occupy the buried ligand binding pocket (LBP). Structural and functional analysis suggests that MCFAs are partial agonists that stabilize PPAR LBD conformation, through a helix 12 independent mechanism.
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