Óleos insaturados – o mais prestigiado dos venenos do nosso cotidiano
Nosso metabolismo é mantido baixo pela presença desses óleos tóxicos de sementes
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Os óleos insaturados foram naturalizados na nossa alimentação, nos restaurantes e, basicamente, a nenhum cozinheiro ocorre se perguntar sobre tais óleos. Será que são tão bons para a saúde como parecem [já que não se fala sobre seus males]Ɂ
E não se perguntam por uma razão: não fazem a mais longínqua ideia do estrago que causam na nossa saúde e da enorme dificuldade de tirá-los do nosso organismo uma vez que eles sejam incorporados aos nossos tecidos adiposos a partir da alimentação.
Na medicina, por sua vez, também reina o mais profundo silêncio e cumplicidade com a indústria dos óleos tóxicos, óleos vegetais de sementes. No mundo chamado alternativo, idem, as sementinhas são uma dádiva da natureza, são algo que passa inocência, saúde, mas se enxerga o o perigo da lenta destruição da saúde por tais óleos tóxicos e do inevitável comprometimento da tireoide.
Sim os óleos insaturados das sementes são tóxicos. Também os óleos insaturados das nozes e castanhas. Também o óleo de peixe [P]. Nenhum deles aporta qualidade à nossa saúde, tudo na contramão da propaganda incessante e bem lubrificada. Todos eles nos intoxicam inexoravelmente. Já examinamos esse problema aqui, aqui e também aqui. E aqui.
Nas sementes, in natura, tais óleos são parte do seu sistema de defesa contra predadores e também do processo de germinação. Uma vez no corpo de animais do sangue quente e oxigenado, como nós, eles se degradam, se peroxidam e minam nossa saúde lentamente.
Todos eles são agressores endócrinos, disrruptores hormonais, uma palavra que até é bem utilizada em relação aos plásticos e seus derivados, mas não é lembrada quando se trata do óleo de cozinha. Ou dos ômegas em geral.
A propaganda vem sendo aperfeiçoada a cada década, embora, na direção oposta, acumulem-se trabalhos científicos mostrando que o mais prestigiado veneno do nosso cotidiano – mais prestigiado que o álcool – não passa de um insidioso antinutriente que mina nossos hormônios, promove inflamação e está na raiz na condição de parte das causas fundamentais de cada doença crônico-degenerativa.
Não é essa a tendência da produção chamada científica e nem a perspectiva que a pesquisa em geral se coloca. Prevalece a lenda de que são “essenciais” e as pesquisas são formatadas e escritas com esse molde.
Mas fatos são o que são.
Óleos insaturados bloqueiam a liberação do hormônio na tireoide, bloqueiam a conversão do hormônio tireoidiano [de T4 a T3] seja localmente, seja sistemicamente [N]. Também bloqueiam o transporte do mesmo hormônio; em experiência a respeito, os cientistas concluíram que “óleos insaturados de cadeia longa são potentes inibidores da ligação tiroxina na globulina-ligadora-de-tiroxina, ao passo que os saturados possuem pequeno ou nenhum efeito na ligação-tiroxina” [O]. E inibem a entrada na célula do T3 e sua ação endócrina, pró-respiração celular oxidativa.
Óleo insaturado suprime a ação do T3 [J]. Óleos insaturados inibem a enzima detox do fígado, a glucoronosiltransferase [I] Oleos insaturados inibem a enzima proteolítica [H]. Os óleos insaturados possuem atividade endócrina nefasta, mais especificamente seus metabólitos, que podem cumprir o papel de sinalizadores que alteram funções celulares [G]. Determinadas enzimas [lipooxigenases e peroxidases] produzem eicosanoides a partir do óleo insaturado, muitos dos quais são inflamatórios e promovem aterosclerose [F].
Óleos insaturados podem ser oxidados em peróxidos um provável fator na placa de aterosclerose [C]. E também da chamada mancha senil.
Os óleos insaturados são parte do processo de adaptação ao baixo metabolismo em animais que vivem em baixas temperaturas, como foi dito; o óleo soma com o rebaixamento do metabolismo necessário àquela situação de menor taxa metabólica [L]. E o próprio metabolismo aumenta quando o organismo não possui óleos insaturados, a taxa metabólica basal sobe [M].
O sistema imune é francamente inibido pelos óleos insaturados. Não é uma prática desconhecida a de que quem vai receber um transplante de órgão também seja alvo de uma transfusão de óleos insaturados para suprimir a resposta imune ao corpo estranho que está chegando.
Quem possui mais óleos insaturados nos seus sistemas, terá pior prognóstico quando apresente um agravamento de qualquer doença – por conta do estresse e liberação desses ácidos graxos no plasma e da inibição metabólica que promovem – e, em caso de uma estação gripal, será o mais forte candidato a adoecer pelo ataque viral.
Os metabólitos dos óleos insaturados alimentam processos inflamatórios. A cascata inflamatória é nutrida pelos ácidos graxos insaturados e seus derivados [pela via das citadas ciclooxigenases].
Em poucas palavras, os óleos insaturados tornam o metabolismo mais lento, inibem a respiração celular mais eficiente, se somam à amplificação de qualquer processo de estresse. São inibidores metabólicos, moléculas inflamatórias, imunossupressoras e disrruptores endócrinos.
No entanto, no mundo como ele é, bugado pelo mercado, é possível, sim, que alguém defenda – seguindo obviamente o pensamento médico mainstream – que os óleos insaturados são necessários para a saúde humana. Os ômega 6 e também os ômega 3 [P]. Há, inclusive, materiais nas revistas chamadas científicas [que não chegam perto da neutralidade científica] para todos os gostos. E há quem os chame de “óleos essenciais”.
O problema é que, para fazer tal defesa, quem a faça terá que cancelar, suprimir ou simplesmente não permitir que o interlocutor apresente o farto material científico acumulado mostrando que óleos insaturados não passam – para os humanos – de óleos tóxicos.
GM Fontes, Brasília, 15-12-23
As informações aqui presentes não pretendem servir para uso diagnóstico, prescrição médica, tratamento, prevenção ou mitigação de qualquer doença humana. Não pretendem substituir a consulta ao profissional médico ou servir como recomendação para qualquer plano de tratamento. Trata-se de informações com fins estritamente educativos.
Referências ____________________
[A] WIERSINGA W M CHOPRA I J 1998. Inhibition of nuclear T3 binding by fatty acids. Metabolism. 1988 Oct;37(10):996-1002. doi: 10.1016/0026-0495(88)90159-x. PMID: 3173114 DOI: 10.1016/0026-0495(88)90159-x “Studies were performed to evaluate a possible modulatory role of lipids on the binding of T3 to rat liver nuclear receptors in vitro. Unsaturated fatty acids were potent inhibitors of the binding of [125I] T3 to isolated rat liver nuclei. Doses (in mumol/L) causing a 50% inhibition of nuclear T3 binding were 10 for palmitoleic acid, 11 for linoleic acid, 22 for oleic acid, 24 for arachidonic acid, and 37 for linolenic acid. Other lipids had less or no inhibitory activity. Unsaturated fatty acids reduced the affinity constant (Ka) of the binding of T3 to nuclear receptors to 57.4% +/- 11.0% that of controls (mean +/- SE 1.04 +/- 0.14 v 1.97 +/- 0.23 10(9) L/M, n = 5; P less than .02) but did not affect the maximal binding capacity (MBC) (1.47 +/- 0.20 v 1.55 +/- 0.10 10(-10) M/L; NS). Evaporated ether extracts of rat liver homogenate pretreated with phospholipase A2 for five to 20 minutes (that liberates unsaturated fatty acids from phospholipids) demonstrated a progressive inhibition of nuclear T3 binding with time when compared with ether extracts of untreated rat liver homogenate (F = 16.1; P less than .01). Evaporated, fatty-acid-rich ether extracts of human sera caused a dose-dependent inhibition in the binding of [125I] T3 to nuclear T3 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)”
[B] POWER G W YAQOOB, P, 1994. The effect of dietary lipid manipulation on hepatic mitochondrial phospholipid fatty acid composition and carnitine palmitoyltransferase I activity. Biochem Mol Biol Int. 1994 Oct;34(4):671-84. PMID: 7866292 “The maximal activity of the overt from of carnitine palmitoyltransferase I (CPT I; EC 2.3.1.21) and its sensitivity to inhibition by malonyl CoA were measured in mitochondria prepared from the livers of rats which had been fed for 10 weeks on either a low fat diet (LF; 2.4% fat by weight) or on one of four high fat diets which contained 20% by weight of either hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO) or menhaden (fish) oil (MO). CPT I activity (i.e. activity per g of liver tissue), was elevated in animals fed the OO, SO or MO diets compared with those fed the LF or HCO diets. Feeding the HCO diet did not result in elevation of CPT I activity compared with feeding the LF diet. CPT I specific activity (i.e. activity per mg mitochondrial protein) was elevated in animals fed SO diet, but not in animals fed any of the other high fat diets. These observations suggest that an elevated fat load is not solely responsible for increasing CPT I activity, but that the fatty acid composition of the diet also plays a role. Hepatic CPT I activity of rats fed the LF diet was most sensitive to inhibition by malonyl CoA ([I50] = 0.53 microM). Each of the high fat diets decreased the sensitivity of CPT I to inhibition by malonyl CoA; CPT I activity in the livers from animals fed the MO diet was the least sensitive to malonyl CoA inhibition ([I50] = 1.8 microM). The fatty acid compositions of the major mitochondrial membrane phospholipids, phosphatidylcholine, phosphatidylethanolamine and cardiolipin were modified according to the fatty acid composition of the diet. Each of these phospholipids had a distinct fatty acid composition and similar effects of dietary lipid manipulation on the fatty acid compositions were observed. Feeding the SO diet resulted in fatty acid compositions which were most similar to those found after feeding the LF diet. Feeding the HCO and OO diets increased the proportions of stearic and oleic acids, respectively, while decreasing the proportion of linoeic acid. Feeding the MO diet resulted in increased proportions of palmitic, palmitoleic, eicosapentaenoic and docosahexaenoic acids and decreased proportions of linoleic and arachidonic acids in each of the phospholipids. It is proposed that the effects of dietary lipid manipulation upon CTP I activity and sensitivity to inhibition by malonyl CoA are due to alterations in the fatty acid composition of the phospholipids in the mitochondrial membrane where CPT I resides”. Se é certo que lipólise tende a engendrar resistência insulínica [via Randle], também é verdade que a inibição do metabolismo da glicose pelos ácidos graxos é maior com o maior tamanho da cadeia e o grau de instauração dos ácidos graxos.
[C] STEINBRECHER U P PARTHASARATHY Sm 1984. Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids. Proc Natl Acad Sci U S A. 1984 Jun;81(12):3883-7. doi: 10.1073/pnas.81.12.3883. PMID: 6587396 PMCID: PMC345326 DOI: 10.1073/pnas.81.12.3883 “Low density lipoprotein (LDL) incubated with cultured endothelial cells from rabbit aorta or human umbilical vein is altered in several ways (EC-modified): (i) It is degraded by macrophages much faster than LDL similarly incubated in the absence of cells or incubated with fibroblasts. (ii) Its electrophoretic mobility is increased. (iii) Its density is increased. We report here that antioxidants completely prevent these changes. We also report that these changes do not take place if transition metals in the medium are chelated with EDTA. During EC-modification as much as 40% of the LDL phosphatidylcholine is degraded to lysophosphatidylcholine by a phospholipase A2-like activity. When incubation conditions in the absence of cells were selected to favor oxidation--for example, by extending the time of incubation of LDL at low concentrations, or by increasing the Cu2+ concentration--LDL underwent changes very similar to those occurring in the presence of cells, including degradation of phosphatidylcholine. Hence, some phospholipase activity appears to be associated with the isolated LDL used in these studies. The results suggest a complex process in which endothelial cells modify LDL by mechanisms involving generation of free radicals and action of phospholipase (s)”. Óleos insaturados podem ser oxidados em peróxidos um provável fator na placa de aterosclerose.
[D] YOUNG I S McENENY J, 2001. Lipoprotein oxidation and atherosclerosis. Biochem Soc Trans. 2001 May;29(Pt 2):358-62. doi: 10.1042/0300-5127:0290358. PMID: 11356183
DOI: 10.1042/0300-5127:0290358 “Lipoprotein oxidation is a key early stage in the development of atherosclerosis. Oxidation of low-density lipoprotein (LDL) is initiated by both enzyme-mediated and non-enzymic mechanisms in vivo, and oxidized LDL has many atherogenic properties. Oxidation of LDL in vivo is likely to be influenced by local environmental factors, such as pH. The composition of LDL is also important, including such factors as antioxidant content, fatty acid composition and particle size”. Existe um papel para os óleos insaturados na gênese da placa aterosclerótica.
[E] YIN H XU L, 2011. Free Radical Lipid Peroxidation: Mechanisms and Analysis. August 2011 Chemical Reviews 111(10):5944-72 DOI:10.1021/cr200084z PubMed “The free radical chain oxidation of organic compounds has historically been referred to by organic and physical chemists as autoxidation. The peroxide products of the reaction can serve as initiators of the process under certain conditions, and under those circumstances, the rate of oxygen consumption increases over time as peroxide products are formed. Tyrosyl radicals in myoglobin and hemoglobin also initiate peroxidation reactions that play a potentially significant role in rhabdomyolysis, subarachnoid hemorrhage, malaria, and sickle cell disease. The pentadienyl carbon radicals derived from linoleate and the other fatty acid esters have the odd electron spin distributed principally on the two terminal carbons and one central carbon of the five-carbon framework. Cholesterol, a monounsaturated sterol lipid, is an order of magnitude more reactive than oleate, a monounsaturated fatty acid”. Derivados de óleo insaturado atacam membranas celulares via peroxidação e também o colesterol.
[F] RICCIOTTI, E FITZGERALD G A, 2011. Prostaglandins and Inflammation. Arterioscler Thromb Vasc Biol. 2011 May; 31(5): 986–1000. doi: 10.1161/ATVBAHA.110.207449 PMCID: PMC3081099 NIHMSID: NIHMS271399 PMID: 21508345 “Prostaglandins are lipid autacoids derived from arachidonic acid. They both sustain homeostatic functions and mediate pathogenic mechanisms, including the inflammatory response. They are generated from arachidonate by the action of cyclooxygenase (COX) isoenzymes and their biosynthesis is blocked by nonsteroidal anti-inflammatory drugs (NSAIDs), including those selective for inhibition of COX-2. Despite the clinical efficacy of NSAIDs, prostaglandins may function in both the promotion and resolution of inflammation. This review summarizes insights into the mechanisms of prostaglandin generation and the roles of individual mediators and their receptors in modulating the inflammatory response. Prostaglandin biology has potential clinical relevance for atherosclerosis, the response to vascular injury and aortic aneurysm”. Disponível em: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081099/
[G] GEORGIADI A KERSTEN S, 2012. Mechanisms of gene regulation by fatty acids. Adv Nutr. 2012 Mar 1;3(2):127-34. doi: 10.3945/an.111.001602. PMID: 22516720 PMCID: PMC3648713 DOI: 10.3945/an.111.001602 “Consumption of specific dietary fatty acids has been shown to influence risk and progression of several chronic diseases, such as cardiovascular disease, obesity, cancer, and arthritis. In recent years, insights into the mechanisms underlying the biological effects of fatty acids have improved considerably and have provided the foundation for the emerging concept of fatty acid sensing, which can be interpreted as the property of fatty acids to influence biological processes by serving as signaling molecules. An important mechanism of fatty acid sensing is via stimulation or inhibition of DNA transcription. Here, we focus on fatty acid sensing via regulation of gene transcription and address the role of peroxisome proliferator-activated receptors, sterol regulatory element binding protein 1, Toll-like receptor 4, G protein-coupled receptors, and other putative mediators”.
[H] JOBLING J W, PETERSEN W, 1914. Jobling JW, Petersen W. Ferment-inhibiting substances in tubercle bacilli. J Exp Med 1914;19:251–8. J Exp Med. 1914 Mar 1; 19(3): 251–258. doi: 10.1084/jem.19.3.251 PMCID: PMC2125157 PMID: 19867765 1. Tubercle bacilli contain unsaturated fatty acids which, when saponified, have the property of inhibiting the action of trypsin and leucoprotease. 2. In proportion to their iodin value these soaps are more active as inhibiting agents than the soaps prepared from linseed, olive, and cod-liver oils. 3. The activity of the soaps is dependent on the presence of unsaturated carbon bonds. 4. Saturation of the soaps with iodin destroys their inhibiting action. 5. Soaps probably play an important part in the production of the condition known as caseation in tuberculosis. Disponível em: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2125157/
[I] ROWLAND A GAGANIS P, 2007. Binding of inhibitory fatty acids is responsible for the enhancement of UDP-glucuronosyltransferase 2B7 activity by albumin: implications for in vitro-in vivo extrapolation. J Pharmacol Exp Ther. 2007 Apr;321(1):137-47. doi: 10.1124/jpet.106.118216. Epub 2007 Jan 19. PMID: 17237258 DOI: 10.1124/jpet.106.118216 “Studies were performed to elucidate the mechanism responsible for the reduction in Km values of UDP-glucuronosyltransferase 2B7 (UGT2B7) substrates observed for incubations conducted in the presence of albumin. Addition of bovine serum albumin (BSA) and fatty acid-free human serum albumin (HSA-FAF), but not "crude" HSA, resulted in an approximate 90% reduction in the Km values for the glucuronidation of zidovudine (AZT) by human liver microsomes (HLM) and UGT2B7 and a 50 to 75% reduction in the S50 for 4-methylumbelliferone (4MU) glucuronidation by UGT2B7, without affecting Vmax. Oleic, linoleic, and arachidonic acids were shown to be the most abundant unsaturated long-chain fatty acids present in crude HSA and in the membranes of HLM and human embryonic kidney (HEK)293 cells, and it was demonstrated that these and other unsaturated long-chain fatty acids were UGT2B7 substrates. Glucuronides with Rf (retention factor) values corresponding to the glucuronides of linoleic and arachidonic acid were detected when HLM and HEK293 cell lysates were incubated with radiolabeled cofactor, and the intensity of the bands was modulated by the presence of crude HSA (increased) and BSA or HSA-FAF (decreased). Oleic, linoleic, and arachidonic acid inhibited AZT and 4MU glucuronidation by HLM and/or UGT2B7, due to an increase in Km/S50 without a change in Vmax. Addition of BSA and HSA-FAF reversed the inhibition. Likewise, coexpression of UGT2B7 and HSA in HEK293 cells reduced the Km/S50 values of these substrates. It is postulated that BSA and HSA-FAF sequester inhibitory fatty acids released during incubations, and the apparent high Km values observed for UGT2B7 substrates arise from the presence of these endogenous inhibitors.
[J] CLARKE S D HEMBREE J, 1990. Inhibition of triiodothyronine's induction of rat liver lipogenic enzymes by dietary fat. J Nutr. 1990 Jun;120(6):625-30. doi: 10.1093/jn/120.6.625. PMID: 2352037 DOI: 10.1093/jn/120.6.625 “The objective of these studies was to demonstrate that the reduction in lipogenic enzymes caused by ingestion of dietary polyunsaturated fat can in part be attributed to an inhibition of triiodothyronine's induction of hepatic lipogenic enzymes. A 3 x 4 factorial design was employed to examine the effect of diets containing no fat, beef tallow or safflower oil on the triiodothyronine-mediated (0, 2, 4 or 8 micrograms/100 g injected daily intraperitoneally) induction of rat liver lipogenic enzymes. Triiodothyronine (T3) administration induced (p less than 0.05) the activity of malic enzyme, fatty acid synthase and glucose-6-phosphate dehydrogenase in a dose-dependent manner. Malic enzyme activity was increased five- to sevenfold by 8 micrograms T3/100 g daily. Fatty acid synthase activity at the 8 micrograms dose had increased two- to threefold whereas glucose-6-phosphate dehydrogenase activity was elevated only 15-35%. Beef tallow and safflower oil supplementation of the high glucose, fat-free diet significantly reduced the T3 induction of all the enzymes. Safflower oil was more effective than tallow as a repressor of T3 action. The effect of dietary fat, particularly safflower oil, was to increase the amount of T3 required to induce the activity of lipogenic enzymes. In a second study, with a 2 x 2 factorial design, daily injection of 15 micrograms T3/100 g was found to overcome the safflower oil inhibition of lipogenic enzymes. These data support the hypothesis that polyunsaturated fats uniquely suppress the gene expression of lipogenic enzymes by functioning as competitive inhibitors of T3 action, possibly at the nuclear receptor level”.
[K] WOJTYLA L LECHOWSKA K, 2016. Different Modes of Hydrogen Peroxide Action during Seed Germination. Front Plant Sci. 2016; 7: 66. Published online 2016 Feb doi: 10.3389/fpls.2016.00066 PMCID: PMC4740362 PMID: 26870076 “Hydrogen peroxide was initially recognized as a toxic molecule that causes damage at different levels of cell organization and thus losses in cell viability. From the 1990s, the role of hydrogen peroxide as a signaling molecule in plants has also been discussed. The beneficial role of H2O2 as a central hub integrating signaling network in response to biotic and abiotic stress and during developmental processes is now well established. Seed germination is the most pivotal phase of the plant life cycle, affecting plant growth and productivity. The function of hydrogen peroxide in seed germination and seed aging has been illustrated in numerous studies; however, the exact role of this molecule remains unknown. This review evaluates evidence that shows that H2O2 functions as a signaling molecule in seed physiology in accordance with the known biology and biochemistry of H2O2. The importance of crosstalk between hydrogen peroxide and a number of signaling molecules, including plant phytohormones such as abscisic acid, gibberellins, and ethylene, and reactive molecules such as nitric oxide and hydrogen sulfide acting on cell communication and signaling during seed germination, is highlighted. The current study also focuses on the detrimental effects of H2O2 on seed biology, i.e., seed aging that leads to a loss of germination efficiency. The dual nature of hydrogen peroxide as a toxic molecule on one hand and as a signal molecule on the other is made possible through the precise spatial and temporal control of its production and degradation. Levels of hydrogen peroxide in germinating seeds and young seedlings can be modulated via pre-sowing seed priming/conditioning. This rather simple method is shown to be a valuable tool for improving seed quality and for enhancing seed stress tolerance during post-priming germination. In this review, we outline how seed priming/conditioning affects the integrative role of hydrogen peroxide in seed germination and aging. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740362/ A água ativa a germinação de sementes em parte pelo descolamento dos óleos insaturados das suas enzimas. O H2O2 é central nesse processo.
[L] JOHNSTON I A DUNN J, 1987. Temperature acclimation and metabolism in ectotherms with particular reference to teleost fish. Symp Soc Exp Biol. 1987:41:67-93. PMID: 3332497 “As body temperature decreases, changes in the physical chemistry of the cell produce a reduction in metabolic activity. In temperate fish, cold water temperatures either lead to dormancy or else trigger a range of homeostatic responses which serve to offset the passive effects of reduced temperature. Compensatory adjustments to temperature occur with time courses ranging from less than a second to more than a month. Although swimming performance may increase with cold-acclimation, active metabolic rate remains significantly below that for warm-acclimated fish. Compensatory and dormancy responses are not mutually exclusive and sometimes occur in the same species depending on the temperature. Cold-acclimation results in significant increases in the density of mitochondria and capillaries in skeletal muscle. This serves to reduce diffusion distances and increase the capacity for aerobic ATP production relative to fish acutely exposed to low temperature. There is evidence that cold acclimation has differential effects on the synthesis and degradation rates of mitochondrial proteins leading to a net increase in their concentration. In contrast, the activities of enzymes associated with glycolysis and phosphocreatine hydrolysis show no consistent changes with thermal acclimation suggesting that flux through these pathways is modulated by factors other than enzyme concentration. Higher mitochondrial densities have also been reported for the liver, brain and gill tissue of cold compared with warm acclimated fish. In spite of their increased concentration, the activities of aerobic enzymes remain much lower at cold than warm temperatures. Acclimation temperature affects hepatosomatic index, the concentration of energy reserves, and the relative importance of glucose and fatty acid catabolism in liver. The fraction of glucose oxidized by the hexose monophosphate shunt (HMPS) pathway also increases with cold acclimation in some species. It is likely that many of the changes in liver metabolism with temperature acclimation reflect associated changes in feeding behaviour and/or diet, and other energetic demands (e.g. gametogenesis). Possible mechanisms underlying alterations in pathway utilization with temperature acclimation are discussed. They include changes in factors influencing enzyme structure and activity (e.g. pH, substrate/modulator concentrations, phosphorylation state, membrane composition), and effects of temperature on gene expression.”.
[M] RAFAEL J PATZELT J, 1984. The effect of essential fatty acid deficiency on basal respiration and function of liver mitochondria in rats. J Nutr. 1984 Feb;114(2):255-62. doi: 10.1093/jn/114.2.255. PMID: 6693988 DOI: 10.1093/jn/114.2.255 “Rats were fed a diet poor (0.05%) in essential fatty acids (EFA) with hydrogenated coconut oil as fat component, or a control diet containing 4% of the total energy intake in the form of linoleic acid. Effects of dietary EFA deficiency were investigated during a period of 2-30 weeks. Growth retardation becomes significant after 4 weeks of deficiency and attains about 25% when the deficiency is maintained for longer than 12 weeks. Respiration, body weight and age of EFA-deficient rats and controls are in a nonlinear relationship. Basal respiration in relation to the body weight is significantly increased by EFA deficiency; it is unchanged when related to total animals under the employed experimental conditions. Oxidative phosphorylation in isolated liver mitochondria is unaffected by EFA deficiency, i.e., the increased metabolic rate of EFA-deficient rats, related to the body weight, cannot be explained from impaired functional integrity of the inner mitochondrial membrane. Respiratory chain enzyme activities in mitochondria from heart and skeletal muscle and specific amounts of mitochondria in these tissues are unchanged by EFA deficiency”.
[N] CHOPRA I J HUANG T S, 1985. Evidence for an inhibitor of extrathyroidal conversion of thyroxine to 3,5,3'-triiodothyronine in sera of patients with nonthyroidal illnesses. J Clin Endocrinol Metab. 1985 Apr;60(4):666-72. doi: 10.1210/jcem-60-4-666. PMID: 2857729 DOI: 10.1210/jcem-60-4-666 “To determine whether an inhibitor of extrathyroidal conversion (IEC) of T4 to T3 is present in sera of patients with nonthyroidal illness (NTI), we incubated rat liver homogenate (approximately 4 mg protein) with T4 (2.5 microM) and dithiothreitol (5 mM) in the presence of evaporated diethyl ether extracts of normal or NTI sera. The T3 produced was quantified by RIA. Extracts of NTI sera caused dose-dependent inhibition in the conversion of T4 to T3. T3 produced in the presence of 20 NTI sera (1.0 mleq aliquots) was 76 +/- 5.5% (mean +/- SE; range, 18-116) that of normal sera (100 +/- 4.1% n = 10; P less than 0.01); it was more than 2 SD below the normal mean in eight patients. Inhibition of T3 production by NTI sera was correlated highly significantly with the activity of a thyroid hormone-binding inhibitor (THBI) also present in ether extracts of these sera (r = 0.82; n = 20; P less than 0.001). Since THBI may be a lipid, we studied the effect of lipids on hepatic conversion of T4 to T3. Several fatty acids were potent inhibitors of the conversion in vitro. Doses (in micromoles) causing 50% inhibition in different experiments varied between 0.2-0.52 for arachidonic acid, 0.3-0.56 for linolenic acid, 0.38-0.40 for linoleic acid, and 0.8-0.9 for oleic acid. Other lipids had less or no inhibitory activity. The inhibition of hepatic T4 5'-monodeiodination by arachidonic acid was competitive in nature (Ki, approximately 0.11 mM). Pretreatment of rat liver with phospholipase A2 for 10-60 min led to a progressive reduction in the conversion of T4 to T3. Moreover, the evaporated ether extract of phospholipase A2-treated rat liver homogenate reduced T4 to T3 conversion by untreated rat liver homogenate. There was a significant correlation between serum concentrations of free fatty acids and IEC activity in NTI sera (r = 0.74; n = 10; P less than 0.02). The various data suggest that 1) many NTI sera contain a potent IEC; 2) some fatty acids are potent IECs; 3) like THBI, IEC may be a lipid moiety; and 4) activation of tissue phospholipases may contribute importantly to reduced extrathyroidal T3 production in NTI, presumably by releasing inhibitory fatty acids that act locally first and more generally after their release into the circulation”.
[O] TABACHNICK M KORCEK L, 1986. Effect of long-chain fatty acids on the binding of thyroxine and triiodothyronine to human thyroxine-binding globulin. Biochim Biophys Acta. 1986 Apr 11;881(2):292-6. doi: 10.1016/0304-4165(86)90016-4. PMID: 2869786
DOI: 10.1016/0304-4165(86)90016-4 “The effect of long-chain fatty acids on the binding of thyroxine to highly purified human thyroxine-binding globulin has been studied by equilibrium dialysis performed at pH 7.4 and 37 degrees C. At a fixed molar ratio of 2000:1 of fatty acid to thyroxine-binding globulin, the degree of binding inhibition based on the percent change in nK value relative to the control as determined from Scatchard plots was: palmitic, 0%; stearic, 0%; oleic, 76%; linoleic, 69%; and linolenic, 61%. At a 500:1 molar ratio of oleic acid to thyroxine-binding globulin, equivalent to 0.125 mM free fatty acid in serum, thyroxine binding was inhibited by 18%, increasing to 93% at a 4500:1 molar ratio. At molar ratios of oleic acid to thyroxine-binding globulin of 1000:1, 2000:1 and 4000:1, the degree of inhibition of triiodothyronine binding was 24%, 41% and 76%, respectively. The results indicate that the unsaturated long-chain fatty acids are potent inhibitors of thyroxine binding to thyroxine-binding globulin, whereas the saturated fatty acids have little or no effect on thyroxine binding”.
[P] STONEY R M WOODS R K HOSKING C S, 2004. Maternal breast milk long-chain n-3 fatty acids are associated with increased risk of atopy in breastfed infants. First published: 27 February 2004. https://doi.org/10.1111/j.1365-2222.2004.01852.x “Background Australia has one of the highest prevalence rates internationally of allergic conditions, such as asthma and eczema. Atopy is one hallmark for the development of allergic disease and predisposes to allergic inflammation in the target organs. ω-3 (n-3) fatty acids (FAs) are thought to act as precursors to the formation of less active inflammatory mediators, with the potential to reduce inflammation. Objective To investigate whether increased n-3 FA levels in maternal breast milk are associated with a lower risk of developing atopy in infancy. Methods Subjects were part of the prospective Melbourne atopy cohort study, which involved 620 children born into families where at least one first-degree relative had an atopic disease. Some 224 women (mean age 31.4±4.2 (SD) years, with 73.2% (n=164) having self-reported atopy) provided either a colostrum (n=194) or 3-month expressed breast milk (EBM) sample (n=118). Maternal colostrum and 3-month EBM samples were analysed for FA content by gas chromatography. Skin prick tests (SPTs) to six common allergens were performed on infants at 6, 12 and 24 months of age and on mothers who agreed at study entry. Results For infants sensitized to foods at 6 months (n=29), the total n-3 FA level in the colostrum was significantly higher (P=0.004) as were levels of individual long-chain n-3 FAs, docosoapentaenoic acid (DPA, C22:5, P=0.001) and docosahexaenoic acid (DHA, C22:6, P=0.002) than in non-sensitized infants. Infants with aero-allergen sensitization at 24 months (n=30) had higher levels of the n-3 FA, DPA (P=0.002) and DHA (P=0.007), and similarly higher total n-3 FA (P=0.009) in maternal colostrum than those infants who were not sensitized. Conclusion Higher n-3 FA levels in the colostrum do not appear to confer protection against, but may be a risk factor for, the eventual development of atopy in high-risk breastfed infants”. Disponível em: https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2222.2004.01852.x
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