Luisa Andrea Ketzer

Este trabalho tem como propósito descrever e analisar uma atividade disparadora fundamentada no Ensino de Ciências por Investigação. Essa atividade, chamada "Qual é a folha?", constituiu a primeira etapa de uma oficina científica que foi ofertada em três edições para 32 professores de ciências de escolas públicas municipais de Itaboraí (RJ). A partir de uma proposta bastante simples e acessível, buscou-se fomentar a discussão sobre aspectos relacionados à atividade científica e estimular a curiosidade sobre a metodologia científica. A atividade foi capaz de promover descontração e interação, além de ter envolvido os participantes em práticas científicas como observação, descrição, argumentação e utilização de materiais. Considerando que a investigação constitui um elemento central da Base Nacional Comum Curricular para o ensino de ciências, espera-se que a formação tenha contribuído para que os docentes compreendam a abordagem investigativa, de maneira a incluí-la em seus planejamentos de ensino, visando a promoção da alfabetização científica.

Neste trabalho, buscamos entender a relação entre dois pilares do bem-estar subjetivo (afetação positiva e afetação negativa) e a aprendizagem significativa. Participaram do estudo 137 crianças do 5º ano do Ensino Fundamental de diferentes categorias escolares: privadas, públicas urbanas e públicas rurais. Como estratégia pedagógica, utilizamos o ensino de ciências por investigação para demonstrar as etapas da digestão e a importância do sistema digestório como parte de um organismo integrado. A coleta de dados foi realizada com questionários e desenhos. Duas metodologias qualitativas foram utilizadas: a Escala Panas, para organização dos dados sobre o bem-estar subjetivo e a Teoria dos Modelos Mentais para investigar indícios de aprendizagem significativa. Nossos resultados demonstraram que o ensino de ciências por investigação foi capaz de aumentar a afetação positiva dos alunos, diminuir a afetação negativa e trazer ganhos conceituais com indícios de aprendizagem significativa, especialmente com os alunos das escolas públicas rurais

New Findings: What is the central question of this study? Does glucocorticoid excess disrupt brown adipose tissue (BAT) phenotype and function? What is the main finding and its importance? Glucocorticoid excess induced an extensive remodelling of interscapular BAT, resulting in a white‐like phenotype in association with metabolic disturbances. Glucocorticoids might be an important modulator of BAT physiology and BAT may have a role in pathophysiology of metabolic disturbances induced by glucocorticoid excess. In mammals, brown adipose tissue (BAT) is centrally involved in energy metabolism. To test the hypothesis that glucocorticoid excess disrupts BAT phenotype and function, male Wistar rats were treated with corticosterone in drinking water for 21 days. To confirm induction of glucocorticoid excess and metabolic disturbances, adrenal weight, corticotrophin releasing hormone mRNA levels and corticosterone serum levels were measured and a glucose tolerance test and serum triacylglycerol analyses were performed. Adipose tissue deposits were excised, weighed and evaluated by a set of biochemical, histological and molecular procedures, including thin‐layer chromatography, histochemistry, immunohistochemistry, quantitative real‐time polymerase chain reaction, high‐resolution oxygraphy, ATP synthesis and enzymatic activity measurements. The approach was successful in induction of glucocorticoid excess and metabolic disturbances. Lower body weight and increased adiposity were observed in corticosterone‐treated rats. Interscapular brown adipose tissue (iBAT) showed higher sensitivity to glucocorticoids than other fat deposits. The treatment induced lipid accumulation, unilocular rearrangement, increased collagen content and decreased innervation in iBAT. Furthermore, expression of Prdm16 ( P < 0.05), Ucp1 ( P Slc7a10 ( P Fasn ( P Lep ( P P P P P <0.05) were observed in iBAT of glucocorticoid‐treated rats. Glucocorticoid excess induced an extensive remodelling of interscapular brown adipose tissue, resulting in a white‐like phenotype in association with metabolic disturbances.

Encontrar mecanismos para transferir o treinamento científico acumulado no Brasil para a educação oferecida nas escolas é um dos desafios enfrentados pelos cientistas brasileiros. Neste contexto, desenvolvemos um curso com o objetivo de proporcionar aos professores da Educação Básica ferramentas para o uso da metodologia científica em sua prática profissional. Este curso, denominado "Transformações de energia nos organismos vivos", trata dos três principais tópicos de Bioquímica que fazem parte do currículo do Ensino Médio (fermentação, fotossíntese e respiração celular) e compreende 5 encontros de dia inteiro. As principais descobertas que estabeleceram as bases conceituais em cada tópico são apresentadas no início dos três primeiros dias. Em seguida, os participantes são desafiados a formular questões sobre o tema e a desenhar e executar experimentos que as respondam. Uma aula contendo os conceitos fundamentais sobre os temas é dada após a discussão dos resultados obtidos nos experimentos. O quarto dia é dedicado à elaboração de uma proposta de aula investigativa no tema do curso. Finalmente, os participantes apresentam suas propostas e a forma como pretendem aplicá-las em sala de aula. Os depoimentos dos participantes mostram que eles se sentem confiantes de que adquiriram os conceitos necessários para desenvolver atividades em suas escolas.

Menopause is associated with increased visceral adiposity and disrupted glucose homeostasis, but the underlying molecular mechanisms related to these metabolic changes are still elusive. Brown adipose tissue (BAT) plays a key role in energy expenditure that may be regulated by sexual steroids, and alterations in glucose homeostasis could precede increased weight gain after ovariectomy. Thus, the aim of this work was to evaluate the metabolic pathways in both the BAT and the liver that may be disrupted early after ovariectomy. Ovariectomized (OVX) rats had increased food efficiency as early as 12 days after ovariectomy, which could not be explained by differences in feces content. Analysis of isolated BAT mitochondria function revealed no differences in citrate synthase activity, uncoupling protein 1 expression, oxygen consumption, ATP synthesis, or heat production in OVX rats. The addition of GDP and BSA to inhibit uncoupling protein 1 decreased oxygen consumption in BAT mitochondria equally in both groups. Liver analysis revealed increased triglyceride content accompanied by decreased levels of phosphorylated AMP-activated protein kinase and phosphorylated acetyl-CoA carboxylase in OVX animals. The elevated expression of gluconeogenic enzymes in OVX and OVX + estradiol rats was not associated with alterations in glucose tolerance test or in serum insulin but was coincident with higher glucose disposal during the pyruvate tolerance test. Although estradiol treatment prevented the ovariectomy-induced increase in body weight and hepatic triglyceride and cholesterol accumulation, it was not able to prevent increased gluconeogenesis. In conclusion, the disrupted liver glucose homeostasis after ovariectomy is neither caused by estradiol deficiency nor is related to increased body mass.

The UCP1 [first UCP (uncoupling protein)] that is found in the mitochondria of brown adipocytes [BAT (brown adipose tissue)] regulates the heat production, a process linked to non-shivering thermogenesis. The activity of UCP1 is modulated by GDP and fatty acids. In this report, we demonstrate that respiration and heat released by BAT mitochondria vary depending on the respiratory substrate utilized and the coupling state of the mitochondria. It has already been established that, in the presence of pyruvate/malate, BAT mitochondria are coupled by faf-BSA (fatty-acid-free BSA) and GDP, leading to an increase in ATP synthesis and mitochondrial membrane potential along with simultaneous decreases in both the rates of respiration and heat production. Oleate restores the uncoupled state, inhibiting ATP synthesis and increasing the rates of both respiration and heat production. We now show that in the presence of succinate: (i) the rates of uncoupled mitochondria respiration and heat production are five times slower than in the presence of pyruvate/malate; (ii) faf-BSA and GDP accelerate heat and respiration as a result and, in coupled mitochondria, these two rates are accelerated compared with pyruvate/malate; (iii) in spite of the differences in respiration and heat production noted with the two substrates, the membrane potential and the ATP synthesized were the same; and (iv) oleate promoted a decrease in heat production and respiration in coupled mitochondria, an effect different from that observed using pyruvate/malate. These effects are not related to the production of ROS (reactive oxygen species). We suggest that succinate could stimulate a new route to heat production in BAT mitochondria.

Brown adipose tissue (BAT) mitochondria thermogenesis is regulated by uncoupling protein 1 (UCP 1), GDP and fatty acids. In this report, we observed fusion of the endoplasmic reticulum (ER) membrane with the mitochondrial outer membrane of rats BAT. Ca²⁺-ATPase (SERCA 1) was identified by immunoelectron microscopy in both ER and mitochondria. This finding led us to test the Ca²⁺ effect in BAT mitochondria thermogenesis. We found that Ca²⁺ increased the rate of respiration and heat production measured with a microcalorimeter both in coupled and uncoupled mitochondria, but had no effect on the rate of ATP synthesis. The Ca²⁺ concentration needed for half-maximal activation varied between 0.08 and 0.11 µM. The activation of respiration was less pronounced than that of heat production. Heat production and ATP synthesis were inhibited by rotenone and KCN. Liver mitochondria have no UCP1 and during respiration synthesize a large amount of ATP, produce little heat, GDP had no effect on mitochondria coupling, Ca²⁺ strongly inhibited ATP synthesis and had little or no effect on the small amount of heat released. These finding indicate that Ca²⁺ activation of thermogenesis may be a specific feature of BAT mitochondria not found in other mitochondria such as liver.

Short-term response to cold promotes a small but significant rise in serum T3 in euthyroid rabbits, where the heart is an important target of T3 action. In this work, we measured changes in sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA2a) and phospholamban (PLB) in hearts of hypo- and hyperthyroid rabbits and compared them with modifications induced by short- and long-term cold exposure. Short-term cold exposure promotes a small increase in T3 and, similar to hyperthyroidism, induces an increase of heart SERCA2a expression. The total PLB content does not change in hyperthyroidism, but short-term cold exposure promotes a significant decrease in total PLB and an increase in the ratio between phosphorylated and total PLB. The temperature of a given tissue depends on the balance between the heat provided by blood circulation and the rate of heat production by the tissue. In an attempt to evaluate the heat contribution of cardiac tissue, we measured mitochondrial respiration in permeabilized cardiac muscle and heat produced by cardiac sarcoplasmic reticulum (SR) during Ca²⁺transport. We observed that there was an increase in oxygen consumption and heat production during Ca²⁺transport by cardiac SR in both hyperthyroidism and short-term cold exposure. In contrast, both the mitochondrial respiration rate and heat derived from Ca²⁺transport were decreased in hypothyroid rabbits. The heart changes in oxygen consumption, SERCA2a-PLB ratio, and Ca²⁺-ATPase activity detected during short-term cold exposure were abolished after cold adaptation. We hypothesize that the transient rise in serum T3 contributes to the short-term response to cold exposure.

Brown adipose tissue (BAT) is involved in rat and mice thermoregulation, and heat produced by BAT depends on the concerted action of thyroid hormones and catecholamines. Little is known about cold-induced thermogenesis in mammals that have little or no BAT, such as rabbits. In these animals, thermogenesis primarily occurs in skeletal muscle. In this work, we have studied the effect of cold acclimation (4 C for 10 d) in normal and hypothyroid rabbits. It is known that hypothyroid rats die after a few hours of cold exposure. We now show that, different from rats, hypothyroid rabbits sustain their body temperature and survive after 10 d cold exposure. When compared with rabbits kept at room temperature, the muscles of cold-exposed rabbits showed a dark red color characteristic of oxidative muscle fibers. According to this pattern, we observed that in both normal and hypothyroid rabbits, cold exposure promotes an increase in oxygen consumption by skeletal muscle mitochondria. Moreover, in red muscle, cold acclimation induces an increase in the expression and activity of sarcoplasmic reticulum Ca2+ ATPase isoform 1 (SERCA1), one of the muscle enzymes involved in heat production. We conclude that rabbit cold tolerance is probably related to increased muscle oxidative metabolism and heat production by SERCA1 and that these changes are not completely dependent on normal thyroid function.