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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
11

EFFECTS OF THE NA-CL CO-TRANSPORTER (NCC) IN WESTERN DIET INDUCED METABOLIC AND CARDIAC DYSFUNCTION

Cutter, Zachary S 01 January 2018 (has links)
Interleukin-18 (IL-18) is a pro-inflammatory cytokine known to be involved in maintaining metabolic homeostasis; however, also capable of inducing cardiac dysfunction. Additionally, IL-18, has been shown to bind to a novel receptor, the Na-Cl Co-transporter (NCC). We hypothesized that NCC mediates IL-18 metabolic and cardiac signaling in mice. Using male C57BL/6J mice, we compared the metabolic and cardiac function changes after at least 8 weeks of high-saturated fat high sugar diet (Western Diet) in NCC knockout (NCCKO), IL-18 knockout (IL-18KO), and wild-type mice. We show that NCCKO mice have significantly increased body weight gain from baseline, no difference in fasting blood glucose, and attenuated cardiac diastolic dysfunction after WD compared to wild-type mice. Collectively, the metabolic and cardiac phenotypes of NCCKO mice resembled that of the IL-18KO mice, indicating that NCC may mediate IL-18 signaling in a mouse model of diet-induced obesity and cardiac dysfunction.
12

Bioenergética mitocondrial do coração na obesidade induzida por dieta ocidental em camundongos Swiss / Mitochondrial bioenergetics in heart fat diet-induced obesity in mice swiss

Fabiana Alves Neves 25 January 2012 (has links)
Fundação Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro / A obesidade, doença resultante do acúmulo excessivo de gordura corporal, é importante fator de risco para diabetes mellitus tipo 2, dislipidemias e doenças cardiovasculares, doenças de alta prevalência em todo o mundo. O processo de transição nutricional decorrente da globalização contribuiu para o crescente número de indivíduos com obesidade, principalmente pela modificação nos hábitos alimentares da população, com ampla inclusão de produtos industrializados ricos em gordura saturada, sal e açúcar, denominada dieta ocidental. Os mecanismos pelos quais a obesidade induzida por dieta leva ao desenvolvimento de doenças cardiovasculares ainda não estão completamente esclarecidos na literatura, porém sabe-se que a obesidade leva ao comprometimento da função cardíaca e do metabolismo energético, aumentando a morbidade e mortalidade. Em grande parte dos estudos relacionados à obesidade, o metabolismo energético celular comprometido associa-se à disfunção mitocondrial. Neste contexto, torna-se importante avaliar a função mitocondrial na obesidade, visto que as mitocôndrias são organelas com funções-chave no metabolismo energético. No presente estudo, avaliamos inicialmente o efeito obesogênico da dieta ocidental em camundongos Swiss por 16 semanas a partir do desmame. Para tal, analisamos a ingestão alimentar, evolução da massa corporal, Índice de Lee, peso das gorduras epididimal e retroperitoneal, peso e morfologia do fígado, relação entre o peso do fígado/massa corporal, peso do ventrículo esquerdo (VE)/massa corporal, glicemia de jejum e teste intraperitoneal de tolerância à glicose. Avaliamos também o consumo de oxigênio das fibras cardíacas através da respirometria de alta resolução. Além disso, o conteúdo das proteínas envolvidas no metabolismo energético: Carnitina Palmitoil Transferase 1 (CPT1), proteína desacopladora 2 (UCP2), Transportadores de glicose 1 e 4 (GLUT1 e GLUT4), proteína quinase ativada por AMP (AMPK), proteína quinase ativada por AMP fosforilada (pAMPK), receptor de insulina &#946; (IR&#946;) e substrato do receptor de insulina 1 (IRS-1) foi determinado por western blotting. Nossos resultados confirmaram o caráter obesogênico da dieta ocidental, visto que os camundongos submetidos a esta dieta (GO), apresentaram-se hiperfágicos (P<0,001) e obesos (72,031,82, P<0,001), com aumento progressivo no ganho de massa corporal. Além do aumento significativo dos parâmetros: Índice de Lee (362,902,44, P<0,001), gorduras epididimal e retroperitonial (3,310,15 e 1,610,11, P<0,001), relação entre o peso do fígado/massa corporal (0,060,003, P<0,001) e peso de ventrículo esquerdo (VE)/massa corporal (0,080,002, P<0,01), hiperglicemia de jejum (192,1014,75, P<0,01), intolerância à glicose (P<0,05, P<0,01) e deposição ectópica de gordura no fígado. A respirometria de alta resolução evidenciou disfunção mitocondrial cardíaca no grupo GO, com reduzida capacidade de oxidação de carboidratos e ácidos graxos (P<0,001) e aumento do desacoplamento entre a fosforilação oxidativa e a síntese de ATP (P<0,001). Os resultados de western blotting evidenciaram aumento nos conteúdos de CPT1 (1,160,08, P<0,05) e UCP2 (1,080,06, P<0,05) e redução no conteúdo de IRS-1 (0,600,08, P<0,05). Não houve diferença significativa nos conteúdos de GLUT1, GLUT4, AMPK, pAMPK, pAMPK/AMPK e IR&#946;. Em conclusão, o consumo da dieta ocidental resultou no desenvolvimento de obesidade com disfunção mitocondrial associada a alterações no metabolismo energético. / Obesity, a disease resulting from excessive accumulation of body fat is a risk factor for type 2 diabetes, dyslipidemia and cardiovascular diseases, which are of high prevalence worldwide. Nutritional transition, a process associated with globalization, has contributed to growing obesity, mainly by changing eating habits of the population, with broad inclusion of industrial products high in saturated fat, salt and sugar, the called Western diet. The mechanisms by which diet-induced obesity leads to cardiovascular disease are not completely understood, but it is known that obesity leads to impairment of cardiac function and energy metabolism, increasing morbidity and mortality. In most obesity studies, the related cellular energy metabolism is compromised associated with mitochondrial dysfunction. In this context, it becomes important to asses mitochondrial function in obesity, since mitochondria are organelles with key roles in energy metabolism. In the present study, we evaluated the effect of the Western diet in Swiss mice for 16 weeks from weaning. We analyzed the food intake, changes in body weight, Lee index, weight of epididymal and retroperitoneal fat, weight and morphology of the liver, the ratio of liver weight /body weight, weight of the left ventricle (LV)/body weight , fasting plasma glucose and intraperitoneal glucose tolerance test. We also evaluated the oxygen consumption of cardiac fibers by high-resolution respirometry. Furthermore, proteins content involved in energy metabolism: carnitine palmitoyl transferase 1 (CPT1), uncoupling protein 2 (UCP2), glucose transporters 1 and 4 (GLUT1 and GLUT4), AMP-activated protein kinase (AMPK), AMP-activated protein kinase phosphorylated (pAMPK), insulin receptor &#946; (IR&#946;) and insulin receptor substrate 1 (IRS-1) was determined by western blotting. Our results confirmed the obesogenic role of the Western diet. Thus, mice subjected to Western diet (WG), presented hyperphagia (P<0.001) and obesity (72.031.82, P<0.001), with a progressive increase in body mass gain. Also, the WG group compared to control had statistically significant increase of the all parameters studied: Lee index (362.902.44, P<0.001), epididymal and retroperitoneal fat (3.310.15 and 1.610.11, P<0.001), ratio of liver weight/body weight (0.060.003, P<0.001) and weight of the left ventricle (LV)/body weight (0.080.002, P<0.01), fasting hyperglycemia (192.1014.75, P<0.01), glucose intolerance (P<0.05, P<0.01) and ectopic fat deposition in liver. High-resolution respirometry showed cardiac mitochondrial dysfunction in the WG group, with reduced capacity of oxidation of carbohydrates and fatty acids and increased uncoupling between oxidative phosphorylation and ATP synthesis. Western blotting results revealed an increase in CPT1 (1.160.08, P<0.05) and UCP2 (1.080.06, P<0.05) content and reduction in IRS-1 content (0.600.08, P<0.05). There was no statistically significant difference in the GLUT1, GLUT4, AMPK, pAMPK, pAMPK/AMPK and IR&#946; content. In conclusion, the Western diet consumption resulted in the development of obesity with mitochondrial dysfunction associated to alterations in energy metabolism.
13

Bioenergética mitocondrial do coração na obesidade induzida por dieta ocidental em camundongos Swiss / Mitochondrial bioenergetics in heart fat diet-induced obesity in mice swiss

Fabiana Alves Neves 25 January 2012 (has links)
Fundação Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro / A obesidade, doença resultante do acúmulo excessivo de gordura corporal, é importante fator de risco para diabetes mellitus tipo 2, dislipidemias e doenças cardiovasculares, doenças de alta prevalência em todo o mundo. O processo de transição nutricional decorrente da globalização contribuiu para o crescente número de indivíduos com obesidade, principalmente pela modificação nos hábitos alimentares da população, com ampla inclusão de produtos industrializados ricos em gordura saturada, sal e açúcar, denominada dieta ocidental. Os mecanismos pelos quais a obesidade induzida por dieta leva ao desenvolvimento de doenças cardiovasculares ainda não estão completamente esclarecidos na literatura, porém sabe-se que a obesidade leva ao comprometimento da função cardíaca e do metabolismo energético, aumentando a morbidade e mortalidade. Em grande parte dos estudos relacionados à obesidade, o metabolismo energético celular comprometido associa-se à disfunção mitocondrial. Neste contexto, torna-se importante avaliar a função mitocondrial na obesidade, visto que as mitocôndrias são organelas com funções-chave no metabolismo energético. No presente estudo, avaliamos inicialmente o efeito obesogênico da dieta ocidental em camundongos Swiss por 16 semanas a partir do desmame. Para tal, analisamos a ingestão alimentar, evolução da massa corporal, Índice de Lee, peso das gorduras epididimal e retroperitoneal, peso e morfologia do fígado, relação entre o peso do fígado/massa corporal, peso do ventrículo esquerdo (VE)/massa corporal, glicemia de jejum e teste intraperitoneal de tolerância à glicose. Avaliamos também o consumo de oxigênio das fibras cardíacas através da respirometria de alta resolução. Além disso, o conteúdo das proteínas envolvidas no metabolismo energético: Carnitina Palmitoil Transferase 1 (CPT1), proteína desacopladora 2 (UCP2), Transportadores de glicose 1 e 4 (GLUT1 e GLUT4), proteína quinase ativada por AMP (AMPK), proteína quinase ativada por AMP fosforilada (pAMPK), receptor de insulina &#946; (IR&#946;) e substrato do receptor de insulina 1 (IRS-1) foi determinado por western blotting. Nossos resultados confirmaram o caráter obesogênico da dieta ocidental, visto que os camundongos submetidos a esta dieta (GO), apresentaram-se hiperfágicos (P<0,001) e obesos (72,031,82, P<0,001), com aumento progressivo no ganho de massa corporal. Além do aumento significativo dos parâmetros: Índice de Lee (362,902,44, P<0,001), gorduras epididimal e retroperitonial (3,310,15 e 1,610,11, P<0,001), relação entre o peso do fígado/massa corporal (0,060,003, P<0,001) e peso de ventrículo esquerdo (VE)/massa corporal (0,080,002, P<0,01), hiperglicemia de jejum (192,1014,75, P<0,01), intolerância à glicose (P<0,05, P<0,01) e deposição ectópica de gordura no fígado. A respirometria de alta resolução evidenciou disfunção mitocondrial cardíaca no grupo GO, com reduzida capacidade de oxidação de carboidratos e ácidos graxos (P<0,001) e aumento do desacoplamento entre a fosforilação oxidativa e a síntese de ATP (P<0,001). Os resultados de western blotting evidenciaram aumento nos conteúdos de CPT1 (1,160,08, P<0,05) e UCP2 (1,080,06, P<0,05) e redução no conteúdo de IRS-1 (0,600,08, P<0,05). Não houve diferença significativa nos conteúdos de GLUT1, GLUT4, AMPK, pAMPK, pAMPK/AMPK e IR&#946;. Em conclusão, o consumo da dieta ocidental resultou no desenvolvimento de obesidade com disfunção mitocondrial associada a alterações no metabolismo energético. / Obesity, a disease resulting from excessive accumulation of body fat is a risk factor for type 2 diabetes, dyslipidemia and cardiovascular diseases, which are of high prevalence worldwide. Nutritional transition, a process associated with globalization, has contributed to growing obesity, mainly by changing eating habits of the population, with broad inclusion of industrial products high in saturated fat, salt and sugar, the called Western diet. The mechanisms by which diet-induced obesity leads to cardiovascular disease are not completely understood, but it is known that obesity leads to impairment of cardiac function and energy metabolism, increasing morbidity and mortality. In most obesity studies, the related cellular energy metabolism is compromised associated with mitochondrial dysfunction. In this context, it becomes important to asses mitochondrial function in obesity, since mitochondria are organelles with key roles in energy metabolism. In the present study, we evaluated the effect of the Western diet in Swiss mice for 16 weeks from weaning. We analyzed the food intake, changes in body weight, Lee index, weight of epididymal and retroperitoneal fat, weight and morphology of the liver, the ratio of liver weight /body weight, weight of the left ventricle (LV)/body weight , fasting plasma glucose and intraperitoneal glucose tolerance test. We also evaluated the oxygen consumption of cardiac fibers by high-resolution respirometry. Furthermore, proteins content involved in energy metabolism: carnitine palmitoyl transferase 1 (CPT1), uncoupling protein 2 (UCP2), glucose transporters 1 and 4 (GLUT1 and GLUT4), AMP-activated protein kinase (AMPK), AMP-activated protein kinase phosphorylated (pAMPK), insulin receptor &#946; (IR&#946;) and insulin receptor substrate 1 (IRS-1) was determined by western blotting. Our results confirmed the obesogenic role of the Western diet. Thus, mice subjected to Western diet (WG), presented hyperphagia (P<0.001) and obesity (72.031.82, P<0.001), with a progressive increase in body mass gain. Also, the WG group compared to control had statistically significant increase of the all parameters studied: Lee index (362.902.44, P<0.001), epididymal and retroperitoneal fat (3.310.15 and 1.610.11, P<0.001), ratio of liver weight/body weight (0.060.003, P<0.001) and weight of the left ventricle (LV)/body weight (0.080.002, P<0.01), fasting hyperglycemia (192.1014.75, P<0.01), glucose intolerance (P<0.05, P<0.01) and ectopic fat deposition in liver. High-resolution respirometry showed cardiac mitochondrial dysfunction in the WG group, with reduced capacity of oxidation of carbohydrates and fatty acids and increased uncoupling between oxidative phosphorylation and ATP synthesis. Western blotting results revealed an increase in CPT1 (1.160.08, P<0.05) and UCP2 (1.080.06, P<0.05) content and reduction in IRS-1 content (0.600.08, P<0.05). There was no statistically significant difference in the GLUT1, GLUT4, AMPK, pAMPK, pAMPK/AMPK and IR&#946; content. In conclusion, the Western diet consumption resulted in the development of obesity with mitochondrial dysfunction associated to alterations in energy metabolism.
14

Alterações vasculares na prole de ratos machos expostos a uma dieta ocidental no período perinatal / Vascular changes in male rats offspring exposed to a western diet in the perinatal period

Santos, Robervan Vidal dos 14 August 2017 (has links)
Introduction: The intrauterine environment is responsible for the development and health of the progeny. Thus, consumption of diets with the western pattern during the perinatal period can cause deleterious effects on the fetus with persistent pathological consequences of adolescence and adult life. Objective: To evaluate the supply of a western diet during gestation and lactation, promoting vascular and markers of oxidative stress in offspring of male rats at 60 days of age. Methods: Sixteen male rats and eight male Wistar rats were available for 2 to 3 months. From the determination of pregnancy, a western diet (O = 8, 31% lipids) or control (C = 8, 18% of lipids) was offered until the weaning of the pups. After 60 days of life, rats from the western offspring (PO, n = 34) or control (PC, n = 32) were euthanized, and the thoracic aorta bed (LAT) was removed for the vascular reactivity study. Concentration curves were performed on acetylcholine (ACh), sodium nitroprusside (NPS), phenylephrine (FEN), potassium chloride (KCl) and calcium chloride (CaCl2) in an isolated organ bath. In addition, the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) was measured. Also, intracellular levels of nitric oxide (NO) and superoxide anion were measured in the muscle cells of the thoracic aorta by probes that emit fluorescence in the presence of these substrates (NO and O.-). Values were expressed as the mean ± SEM. Unpaired t-test for the maximum response (Rmax) and sensitivity (Log EC50) values extracted from the vascular reactivity curves. The unpaired t-test for oxidative stress markers was also used, except for NO bioavailability, which was used with Bonferroni post-test Anova one-way. Results: At 60 days, an increase in efficacy (RMax) to phenylephrine in rings without endothelium (PC: 5.78 ± 0.3 vs. PO: 7.7 ± 0.5 * mN / mm) and with endothelium (PC: 4.6 ± 0.4 vs. PO: 6.43 ± 0.4 * mN / mm), to potassium chloride (KCl) in rings with endothelium (PC: 3.89 ± 0.28 vs. PO: 4 (PC: 3,78 ± 0,12 vs PO: 4,82 ± 0,09 mN / mm) and to CaCl2 in rings without endothelium (PC: 5, 7 ± 0.16 vs. PO: 6.75 ± 0.18 mN / mm) and a reduction in efficacy to ACh (PC: 93 ± 3.1 vs. PO: 86 ± 1.8 *% relax) as in Sensitivity (Log EC50) to NPS (PC: 8.5 ± 0.05 vs. PO: 8.2 ± 0.04 *% relax). In addition, the PO presented a lower bioavailability of NO in the basal condition (PC: 1.0 ± 0.03 vs. PO: 0.4 ± 0.01 ua) and stimulated with Ach (PC: 1.46 ± 0, 04 vs. PO: 0.88 ± 0.02 water). In addition, PO presented a higher production of superoxide anion (PC: 1.0 ± 0.06 vs. PO: 2.06 ± 0.13 water) associated with a higher SOD activity (PC: 0.026 ± 0.004 vs. PO : 0.27 ± 0.06 mg / ptn) and a reduction of CAT (PC: 0.021 ± 0.03 vs. PO: 0.08 ± 0.03 mg / ptn). Conclusion: The introduction of a western diet in the perinatal period reduced relaxation and increased contraction of the thoracic aortic bed associated with the reduction of NO bioavailability and elevation of intracellular levels of superoxide anion in the offspring of 60 - day - old male rats. / Introdução: O ambiente intrauterino é responsável pelo desenvolvimento e saúde da progênie. Assim, o consumo de dietas com o padrão ocidental durante o período perinatal pode causar efeitos deletérios no feto com consequências patológicas persistentes da adolescência e vida adulta. Objetivo: Avaliar se à oferta de uma dieta ocidental durante a gestação e a lactação, promove alterações vasculares e nos marcadores do estresse oxidativo da prole de ratos machos com 60 dias de vida. Métodos: Foram utilizadas 16 ratas virgens e 8 ratos machos da linhagem Wistar com 2 a 3 meses. A partir da determinação da prenhez foi oferecida uma dieta ocidental (O = 8, 31% lipídios) ou controle (C = 8, 18% de lipídios) até o desmame dos filhotes. Após 60 dias de vida, os ratos da prole ocidental (PO, n = 34) ou controle (PC, n = 32) foram eutanasiados, e o leito aorta torácico (LAT) foi removido para a realização do estudo de reatividade vascular. Foram realizadas curvas concentração respostas à acetilcolina (ACh), nitroprussiato de sódio (NPS), fenilefrina (FEN), cloreto de potássio (KCl) e cloreto de cálcio (CaCl2) em um banho isolado de órgãos. Além disso, foi mensurada a atividade das enzimas antioxidantes superóxido dismutase (SOD) e catalase (CAT). Também, foram mensurados nas células musculares da aorta torácica os níveis intracelulares do óxido nítrico (NO) e do ânion superóxido através de sondas que emitem fluorescência na presença destes substratos (NO e O.-). Os valores foram expressos como a média ± EPM. Teste t não pareado para os valores da resposta máxima (Rmax) e sensibilidade (Log EC50) extraídos das curvas de reatividade vascular. Foi utilizado também o teste t não pareado para os marcadores do estresse oxidativo com exceção da biodisponibilidade de NO que foi utilizado Anova one way com pós-teste de Bonferroni. Resultados: Aos 60 dias foi observou-se um aumento na eficácia (RMax) à fenilefrina em anéis sem endotélio (PC:5,78±0,3 vs. PO:7.7±0,5* mN/mm) e com endotélio (PC:4,6±0,4 vs. PO:6,43±0,4* mN/mm), ao cloreto de potássio (KCl) em anéis com endotélio (PC: 3,89±0,28 vs. PO:4,64±0,26 mN/mm) e sem endotélio (PC:3,78±0,12 vs. PO:4,82±0,09 mN/mm) e ao CaCl2 em anéis sem endotélio(PC: 5,7 ± 0,16 vs. PO: 6,75 ± 0,18 mN/mm) e uma redução da eficácia à ACh (PC:93±3,1 vs. PO:86±1,8* %relax) como na sensibilidade (Log EC50) ao NPS (PC:8,5±0,05 vs. PO:8,2±0,04* %relax). Além disso, a PO apresentou uma menor biodisponibilidade do NO em condição basal (PC: 1,0 ± 0,03 vs. PO: 0,4 ± 0,01 ua) e estimulados com Ach (PC: 1,46 ± 0,04 vs. PO: 0,88 ± 0,02 ua). Ademais, a PO apresentou uma maior produção do ânion superóxido (PC: 1,0 ± 0,06 vs. PO: 2,06 ± 0,13 ua) associado a uma maior atividade da SOD (PC: 0,026 ± 0,004 vs. PO: 0,27 ± 0,06 mg/ptn) e uma redução da CAT (PC: 0,021 ± 0,03 vs. PO: 0,08 ± 0,03 mg/ptn). Conclusão: A introdução de uma dieta ocidental no período perinatal reduziu o relaxamento e aumentou a contração do leito aórtico torácico associado a redução da biodisponibilidade do NO e elevação nos níveis intracelulares do ânion superóxido na prole de ratos machos com 60 dias de vida. / São Cristóvão, SE
15

SEX- AND AGE-DEPENDENT WESTERN-DIET INDUCED BLOOD-BRAIN BARRIER DYSREGULATION AND RELATIONSHIP TO BEHAVIOR, HYPERGLYCEMIA, BODY WEIGHT, AND MICROGLIA

Elizabeth Sahagun (5930825) 28 April 2022 (has links)
<p>There has been a rapid shift in food environment of Western cultures that has increased consumption of diets high in fat and sugar, which have imparted negative effects on metabolic and neurocognitive health. There is also building evidence that the adverse effects of Western diet</p> <p>(WD) are different in males and females, such that males are impacted more at an earlier age and females are impacted later in life. The underlying biological mechanisms linking WD and neurocognitive health are often associated with energy dysregulation or neuroinflammation. WD</p> <p>disrupts glucose homeostasis and causes low grade inflammation in the body, and these can impact</p> <p>the brain by disrupting the blood-brain barrier (BBB). The BBB is the microvasculature found throughout the entire brain that tightly regulates what compounds get into the brain to ensure optimal neuronal function. WD disrupts the BBB, however, the effects of WD on BBB integrity</p> <p>in females and younger individuals remain largely unknown. Based on the metabolic and behavioral effects of WD, we hypothesized that the effects are age- and sex- specific. To test this, we gave male and female rats access to a WD for 8-10 weeks starting in juvenile period (post-natal</p> <p>day 21) or in adulthood (post-natal day 75), then measured body weight, behavior, glucose tolerance, the density of two different markers of BBB integrity. We also measured density of resident immune cells (microglia) to assess the relationship between inflammation and BBB integrity. First, we focused on the impact of hyperglycemia on the BBB since elevated glucose alters glucose transporter 1 (GLUT1). We found sex- and age- specific decreases in GLUT1 density in the prefrontal cortex and hippocampus—two brain regions commonly associated with neurocognitive impairments associated with WD. Correlational comparisons between WD and chow (CH) animals also found that the typically relationship between glucose tolerance and</p> <p>GLUT1 in the PFC and hippocampus were overall disrupted in WD animals. Second, we measured the leakage of albumin, a blood protein, since WD depletes the tight junctions that would typically prevent albumin from entering the brain and triggering a neuroinflammatory response. We did not find an increase in albumin density in WD animals, however, we found a main effect of age which</p> <p>offers insight to differential susceptibilities to BBB leakage. Third, we focused on inflammation and found that WD did not impact microglia density in our experiments, nor did it correlate with GLUT1, albumin, or behavior. Collectively, our findings support the hypothesis that the impact of</p> <p>WD on the BBB is sex- and age- specific, suggest that WD does not increase leakage of compounds such as albumin, and highlights the nuanced relationships between WD, metabolic disruption, behavioral deficits, and neuroinflammation.  </p>
16

The Role of Inflammation in Diet-Induced Insulin Resistance

Alexander, Lindsey Ann January 2009 (has links)
No description available.
17

Dynamique saisonnière du microbiome intestinal en réponse à la diète traditionnelle inuite

Dubois, Geneviève 12 1900 (has links)
Le microbiome intestinal humain est une importante communauté de microorganismes, spécifique aux individus et aux populations, dont la composition est influencée par de nombreux facteurs, tels que la génétique et les habitudes de vie de son hôte. La diète est cependant un élément majeur façonnant sa structure. Les influences de plusieurs diètes humaines sur le microbiome ont été largement investiguées. Toutefois, l’impact des variations saisonnières inhérentes à certaines diètes est peu connu. La diète traditionnelle inuite est un exemple de régime alimentaire riche en graisses et protéines animales qui varie temporellement en fonction de la disponibilité saisonnière des ressources. Afin d’étudier les dynamiques temporelles du microbiome intestinal inuit en réponse à la diète traditionnelle, des échantillons de papier hygiénique contenant des selles ont été récoltés auprès d’un groupe de volontaire Inuits du Nunavut (Canada) durant huit mois. Un groupe contrôle de Montréalais (Québec, Canada) de descendance européenne, consommant une diète typiquement occidentale, a également été sollicité. La diversité et la composition du microbiome ont été caractérisées par le séquençage de la région V4 de l’ARNr 16s. Les microbiomes obtenus par un échantillonnage de papier hygiénique et de selles ont été comparés. Ces deux méthodes offrent des représentations similaires mais non-identiques du microbiome intestinal. À partir du séquençage d’échantillons de papier hygiénique, nous avons trouvé que les variations inter-individuelles du microbiome sont plus importantes que les variations intra-individuelles au sein de Montréal et du Nunavut. Des différences significatives de la composition du microbiome s’expliqueraient par la consommation différentielle de certains groupes alimentaires. Bien qu’aucune différence saisonnière marquée n’ait été observée, en termes de composition, le microbiome fluctue davantage à travers le temps chez les individus inuits. Ces résultats suggèrent que le microbiome inuit pourrait être façonné par une diète plus variable. Ensemble, nos résultats suggèrent que la diète traditionnelle a encore un impact important sur la composition, la diversité et la stabilité de microbiome inuit, malgré les transitions alimentaires vécues au Nunavut. / The human gut microbiome represents a diverse microbial community specific to individuals and populations, which is heavily influenced by factors such as genetics and lifestyle. Diet is a major force shaping the gut microbiome, and the effects of dietary choices on microbiome composition have been thoroughly investigated. It has been shown that a change in diet also changes the gut microbiome, but the effects of seasonal diets are poorly known. The traditional Inuit diet is primarily based on animal products, which vary seasonally based on prey availability. To investigate the dynamics of the Inuit diet over time, we collected gut microbiome samples from Inuit volunteers living in Resolute Bay (Nunavut, Canada), and compared them to samples collected from individuals of European descent living in Montréal (Québec, Canada) and consuming a typical Western diet. We sequenced the V4 region of the 16S rRNA gene to characterize the diversity and composition of the Inuit microbiome, and surveyed differences among samples collected with toilet paper or from stool. Our results show that these sampling methods provide similar, but non-identical portraits of the microbiome. Based on sequencing from toilet paper samples alone, we found that inter-individual variations of the microbiome community composition were greater than within-individual variations, both in Nunavut and Montreal, with significant differences in microbiome explained by dietary preferences. No defined seasonal shift of microbiome composition was detected in samples collected over time. However, within-individual microbial diversity fluctuated more with time in Nunavut than in Montreal. Together, these results underline that the traditional Inuit diet still has an important impact on the composition, diversity and stability of the Inuit gut microbiome, even if the traditional seasonality of the diet is less pronounced than expected, due to an increasingly westernized diet in Nunavut.
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Estudo do metabolismo energético hepático e da via de sinalização da grelina na obesidade induzida por dieta ocidental / Hepatic metabolism energy study and ghrelin signaling pathway in the Western diet-induced obesity

Patricia Soares Pacheco 10 June 2015 (has links)
Fundação Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro / A obesidade é um dos maiores problemas de saúde pública que cresce em todo o mundo, resultante de um desequilíbrio entre ingestão alimentar e gasto energético. Pode-se dizer que a obesidade é o principal fator de risco para o desenvolvimento de doenças crônicas de maior prevalência como dislipidemias, doenças cardiovasculares, diabetes do tipo 2 e esteatose hepática não alcóolica, acarretando na redução da qualidade e expectativa de vida. A Grelina é um hormônio sintetizado pelo estômago, que atua em diferentes tecidos através de um receptor específico (GHS-R1a), incluindo hipotálamo e tecidos periféricos, como o fígado. Esse hormônio está envolvido no comportamento alimentar e adiposidade, modulando o armazenamento ou utilização dos substratos energéticos no coração, músculo esquelético, adipócitos e fígado, além disso, revela-se de grande importância na manutenção do metabolismo energético hepático. Estes dados suportam a hipótese de que as vias de sinalização responsivas à grelina são um importante componente da regulação do metabolismo energético hepático e da homeostase glicêmica. O objetivo deste trabalho, foi estudar o metabolismo energético hepático e a sinalização da grelina em camundongos Swiss adultos obesos submetidos a dieta ocidental rica em gordura saturada e carboidratos simples. Avaliamos o efeito desta dieta a partir do 21 dia de idade (desmame) até o 133 dia destes animais, através de parâmetros biométricos e bioquímicos, avaliação histomorfológica, respirometria de alta resolução, conteúdo de glicogênio hepático e conteúdo de algumas proteínas envolvidas na sinalização de insulina e grelina, além do metabolismo energético hepático. Baseado em nossos resultados observamos que o consumo de dieta ocidental rica em gordura saturada e carboidrato simples durante 16 semanas causa hiperfagia, levando ao quadro de obesidade na idade adulta e prejuízo nas vias de sinalização dos hormônios insulina e grelina, que são importantes moduladores do metabolismo energético hepático, favorecendo o desenvolvimento de esteatose hepática não alcoólica. / Obesity is a major public health problem growing around the world, resulting from an imbalance between food intake and energy expenditure. Obesity is one of the main risk factor for developing the most prevalent chronic diseases as dyslipidemia, cardiovascular disease, type 2 diabetes and non-alcoholic fat liver disease, resulting in lower life expectancy and quality of life. Ghrelin is a hormone synthesized into the stomach, which has an important role in different tissues by a specific receptor (GHS-R1a), including the hypothalamus and peripheral tissues such as the liver. This hormone is involved in feeding behavior and adiposity by modulating storage or use of energy substrates in heart, skeletal muscle, adipocytes and liver. Moreover, Ghrelin is important in maintaining liver energy metabolism. These data support the hypothesis that ghrelin signaling pathways is a key component in the regulation of energy metabolism and hepatic glucose homeostasis. The aim of this study was to investigate the hepatic energy metabolism and signaling of ghrelin in obese adults Swiss mice fed the Western diet, rich in saturated fat and simple carboidrate. We analyzed the effect of this diet starting from 21 days of age (weaning) up to 133 days, using biometric and biochemical parameters, histomorphological assessment, high resolution respirometry, hepatic glycogen content and proteins content involved in insulin and ghrelin signaling besides the hepatic energy metabolism. Based on our results we found that the consumption of rich Western diet for 16 weeks promoves overeating leading to obesity in adulthood, metabolic desorders and impairment in signaling pathways of hormones insulin and ghrelin, which are important metabolic modulators of liver energy, contributing to the development of NAFLD.
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Efeito da cirurgia de derivação duodeno-jejunal sobre a doença hepática gordurosa não alcoólica em ratos obesos por dieta de cafeteria / Effect of bypass surgery duodenal-jejunal on nonalcoholic fatty liver disease in obese mice by cafeteria diet

Ebertz, Claudia Emanuelli 17 December 2013 (has links)
Made available in DSpace on 2017-07-10T14:17:07Z (GMT). No. of bitstreams: 1 Claudia Ebertz.pdf: 1969807 bytes, checksum: 61f18bbc24e26e53d1b8941d93aadc58 (MD5) Previous issue date: 2013-12-17 / Purpose: Bariatric surgeries reduce non-alcoholic fatty liver disease (NAFLD), which is associated with metabolic syndrome co-morbidities; however, the effects of duodenal-jejunal bypass (DJB) have not been investigated. This study aimed to evaluate the effects of DJB on serum and hepatic profiles of obese rats fed on a western diet (WD). Methods: Male Wistar rats were fed a standard rodent chow diet (CTL group) or WD ad libitum. After 10 weeks, WD rats were submitted to sham (WD SHAM) or duodenal-jejunal bypass (WD DJB). Body weight, fat pad depots, glycemia, insulinemia, HOMA-IR, TyG, lipids profile and hepatic analyses were evaluated two months after surgery. Results: The WD SHAM group presented greater obesity, hyperglycemia, hyperinsulinemia, insulin resistance, hypertriglyceridemia and hepatic steatosis than the CTL group. WD DJB rats presented decreased serum glucose and insulin resistance, when compared to WD SHAM animals, without changes in insulinemia. In addition, DJB surgery normalized serum TG and attenuated TG accumulation and steatosis in the liver of the WD DJB group. Hepatic ACC and FAS protein expressions were similar in all groups. Conclusions: DJB attenuates hepatic parameters of NAFLD in obese rats fed on a WD diet / Introdução: Cirurgias bariátricas reducem a doença hepática gordurosa não alcoólica (DHGNA), a qual está associada a comorbidades da síndrome metabólica, entretanto, os efeitos da derivação duodeno-jejunal (DDJ) não foram investigados. Este estudo tem por objetivo avaliar os efeitos da DDJ no perfil sérico e hepático de ratos obesos submetidos à dieta de cafeteria. Métodos: Ratos Wistar foram alimentados com ração padrão para roedores (grupo CTL) ou dieta de cafeteria (grupo CAF) ad libitum. Após 10 semanas de dieta, os animais do grupo CAF foram submetidos à falsa cirurgia (CAF FO) ou à derivação duodeno-jejunal (CAF DDJ). O peso corporal, peso dos depósitos de gorduras, glicemia, insulinemia, HOMA-IR, índice TyG, perfil lipídico e análises hepáticas foram avaliados dois meses após a cirurgia. Resultados: O grupo CAF FC apresentou obesidade, hiperglicemia, hiperinsulinemia, resistência à insulina, hipertrigliceridemia e esteatose hepática em relação ao grupo CTL. Os animais CAF DDJ apresentaram diminuição da glicose sérica e resistência à insulina, sem alterações na insulinemia, quando comparados aos animais CAF FC. Além disso, a DDJ normalizou a concentração sérica de triglicérides e atenuou o acúmulo hepático de triglicérides, bem como a esteatose hepática no grupo CAF DDJ. A expressão proteica de ACC e FAS hepáticas foram similares nos três grupos. Conclusões: A DDJ atenuou os parâmetros hepáticos da DHGNA em ratos obesos por dieta de cafeteria
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Efeito da derivação duodeno-jejunal sobre a secreção de insulina em ratos obesos pela dieta de cafeteria / Effect of duodenal-jejunal bypass on insulin secretion in obese rats bywestern diet

Mendes, Mariana Carla 02 February 2015 (has links)
Made available in DSpace on 2017-07-10T14:17:16Z (GMT). No. of bitstreams: 1 Mariana Carla Mendes.pdf: 1848607 bytes, checksum: 083213cf0c0ad5bc3014210dd258c5e6 (MD5) Previous issue date: 2015-02-02 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / This study was designed to evaluate whether DJB in western diet (WD)-obese rats could have effects on pancreatic &#946;-cell morphology and islet responsiveness to potentiating agents involved with the protein kinase A (PKA) and C (PKC) pathway. Male Wistar rats with 8 weeks of life were fed a standard rodent chow diet (CTL group) or WD ad libitum. After 10 weeks, WD rats were submitted to sham operation or DJB, forming WD SHAM and WD DJB group, respectively. After two months, the obesity parameters, insulin resistance (IR), pancreas morphology, insulin secretion stimulate by different secretagogues and islet protein expression were verified. WD SHAM rats displayed obesity, hyperglycemia, hyperinsulinemia, glucose intolerance and IR. In addition, they also presented an increase in islets and &#946;-cells area and mass. The glucose-induced insulin secretion stimulated by 11.1 mM glucose in the presence of carbachol (CCh), PMA, Forskolin or IBMX was higher in WD SHAM islets than CTL islets. DJB surgery did not alter body weight but normalized glucose, insulinemia, IR, and decreased islet and &#946;-cells mass. The insulin release stimulated by glucose in the presence of CCh, PMA, Forskolin or IBMX was too normalized in WD DJB group. The expression of glucokinase, PKC, PKA and sintaxin was not altered in WD SHAM rats, but the M3 receptor was down-regulated. DJB did not influence these protein expressions. DJB surgery normalized glicemia, insulinemia and IR, reduced islets and &#946;-cell mass and normalized insulin secretion by PKC and PKA pathway. / O presente estudo avaliou o efeito da derivação duodeno jejunal (DDJ) em ratos obesos pela dieta de cafeteria (CAF) sobre a morfofisiologia, com enfâse na ação de agentes potencializadores da secreção de insulina. Ratos Wistar com 8 semanas de vida receberam dieta padrão formando o crupo controle (CTL) ou CAF ad libitum. Após 10 semanas, os ratos CAF foram submetidos à falsa operação ou a DDJ, formando os grupos CAF SHAM e CAF DDJ, respectivamente. Após dois meses, foram avaliados os parâmetros de obesidade, resistência à insulina (RI), morfologia do pâncreas, secreção de insulina estimulada por glicose, carbacol (CCh), PMA, IBMX e Forscolina, e a expressão proteica de glicoquinase (GCK), receptor muscarínico M3, proteina quinase C e A (PKC e PKA) e Sintaxina-1, nas ilhotas. Os animais do grupo CAF SHAM tornaram-se obesos, hiperglicêmicos, hiperinsulinêmicos, intolerantes à glicose e resistentes à insulina. Além disso, apresentaram aumento na massa da ilhota e das células &#946;. A secreção de insulina estimulada por 11.1 mM de glicose na presença de CCh, PMA, Forskolin ou IBMX foi significativamente maior no grupo CAF SHAM em relação ao grupo CTL. A DDJ não alterou o peso corporal, mas normalizou a glicemia, insulinemia, a RI e diminuiu a massa das ilhotas e das células &#946;. A secreção de insulina estimulada pelos diferentes secretagogos também foi normalizada no grupo CAF DDJ. A expressão proteica da GCK, PKC, PKA e sintaxina não foi alterada no grupo CAF SHAM em relação ao CTL, todavia a expressão do receptor M3 foi reduzida. A DDJ não influenciou na expressão dessas proteínas. Em conclusão, a cirurgia de DDJ normalizou a glicemia, a insulinemia e a RI, reduziu a massa das ilhotas e das células &#946; bem como, normalizou a secreção de insulina via PKC e PKA.

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