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1.
Int J Obes (Lond) ; 40(3): 479-86, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26443339

RESUMO

BACKGROUND/OBJECTIVES: The association between gluten and body weight is inconsistent. Previously, we showed that a gluten-free diet reduces weight gain without changing food intake in mice fed high-fat diets. In the present study, we investigated the effects of gluten intake on fat metabolism, thermogenesis and energy expenditure in mice fed a standard or high-fat diet. METHODS: Mice were fed four different experimental diets during 8 weeks: a control-standard diet (CD), a CD added with 4.5% of wheat gluten (CD-G), a high-fat diet (HFD) and a HFD added with 4.5% of wheat gluten (HFD-G). After 8 weeks, the mice received (99m)Tc-radiolabeled gluten orally to study gluten absorption and biodistribution or they underwent indirect calorimetry. After killing, subcutaneous and brown adipose tissues (SAT and BAT) were collected to assess thermogenesis-related protein expression. Lipid metabolism was studied in adipocyte cultures from the four groups. RESULTS: Despite having had the same energy intake, CD-G and HFD-G mice exhibited increased body weight and fat deposits compared with their respective controls. (99m)Tc-GLU or its peptides were detected in the blood, liver and visceral adipose tissue, suggesting that gluten can even reach extraintestinal organs. Uncoupling protein-1 expression was reduced in the BAT of HFD-G and in the SAT of CD-G and HFD-G mice. Indirect calorimetry showed lower oxygen volume consumption in CD-G and HFD-G groups compared with their controls. In HFD mice, daily energy expenditure was reduced with gluten intake. Gluten also reduced adiponectin, peroxisome proliferator-activated receptor (PPAR)-α and PPARγ and hormone-sensitive lipase in cultures of isolated adipocytes from HFD mice, whereas in the CD-G group, gluten intake increased interleukin-6 expression and tended to increase that of tumor necrosis factor. CONCLUSIONS: Wheat gluten promotes weight gain in animals on both HFD and CD, partly by reducing the thermogenic capacity of adipose tissues.


Assuntos
Metabolismo Energético/fisiologia , Glutens , Obesidade/metabolismo , Aumento de Peso/fisiologia , Adipogenia , Adiposidade , Animais , Modelos Animais de Doenças , Ingestão de Energia , Comportamento Alimentar , Regulação da Expressão Gênica , Metabolismo dos Lipídeos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Termogênese
2.
Nutr Metab Cardiovasc Dis ; 24(6): 606-13, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24602606

RESUMO

BACKGROUND & AIMS: Butyrate is a four-carbon fatty acid that presents anti-inflammatory, anti-oxidative and apoptotic properties in colon and several cell lines. Because atherosclerosis has important oxidative and inflammatory components, butyrate could reduce oxidation and inflammation, impairing atherogenesis. We evaluated the effects of butyrate supplementation of butyrate on atherosclerosis and its mechanisms of action. METHODS AND RESULTS: ApoE knockout mice were fed on chow diet or 1% butyrate-supplemented chow diet (Butyrate) for 10 weeks to assess atherosclerosis lesions area and inflammatory status. Macrophage and endothelial cells were also pretreated with butyrate (0.5 mM) for 2 h before oxLDL stimulation to study oxLDL uptake and pro and anti-inflammatory cytokine production. Butyrate reduced atherosclerosis in the aorta by 50%. In the aortic valve, butyrate reduced CCL2, VCAM1 and MMP2 productions in the lesion site, resulting in a lower migration of macrophage and increased collagen depositions in the lesion and plaque stability. When EA.hy926 cells were pretreated with butyrate, oxLDL uptake, CD36, VCAM1, CCL2 TNF, IL1ß and IL6 productions were reduced, whereas IL10 production was increased. These effects were accompanied by a lower activation of NFκB due to a lower nuclear translocation of the p65 subunit. CONCLUSION: Oral butyrate is able to slow the progression of atherosclerosis by reducing adhesion and migration of macrophages and increasing plaque stability. These actions are linked to the reduction of CD36 in macrophages and endothelial cells, decreased pro-inflammatory cytokines and lower activation of NFκB all of these data support a possible role for butyrate as an atheroprotective agent.


Assuntos
Anti-Inflamatórios não Esteroides/uso terapêutico , Antioxidantes/uso terapêutico , Aterosclerose/dietoterapia , Ácido Butírico/uso terapêutico , Suplementos Nutricionais , Placa Aterosclerótica/prevenção & controle , Fator de Transcrição RelA/antagonistas & inibidores , Animais , Anti-Inflamatórios não Esteroides/metabolismo , Antioxidantes/metabolismo , Aorta/imunologia , Aorta/metabolismo , Aorta/patologia , Valva Aórtica/imunologia , Valva Aórtica/metabolismo , Valva Aórtica/patologia , Aterosclerose/imunologia , Aterosclerose/metabolismo , Aterosclerose/fisiopatologia , Ácido Butírico/metabolismo , Antígenos CD36/antagonistas & inibidores , Antígenos CD36/metabolismo , Adesão Celular , Linhagem Celular , Movimento Celular , Núcleo Celular , Células Cultivadas , Endotélio Vascular/imunologia , Endotélio Vascular/metabolismo , Endotélio Vascular/patologia , Humanos , Macrófagos Peritoneais/imunologia , Macrófagos Peritoneais/metabolismo , Macrófagos Peritoneais/patologia , Masculino , Camundongos Knockout , Placa Aterosclerótica/etiologia , Transporte Proteico , Fator de Transcrição RelA/metabolismo
3.
J Sports Med Phys Fitness ; 54(6): 828-34, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25289709

RESUMO

AIM: Physical exercise and soybean intake reduced oxidative stress and atherosclerosis. However, the associated effects of both interventions have not been yet investigated. Thus, we aimed to evaluate the combined effects of swimming and soybean intake on lipid profile, oxidative stress and atherogenesis. METHODS: Ten-week-old male Low-Density Lipoprotein Receptor Knockout mice were divided into 4 groups (N.=8 for each group): control diet without swimming; control diet with swimming; soybean rich diet without swimming and soybean rich diet with swimming. Diets were based on American Institute of Nutrition 93 Growth. The diet of soybean groups was made by soybean extract contained isoflavones. The animals in the exercise groups underwent a 6-week swimming program five times per week. Plasma lipid profile was determined using enzymatic kits. Oxidative stress was measured by thiobarbituric acid reactive substances, hydroperoxide and the lipid oxidation resistance determinations. Atherosclerotic lesions were calculated by morphometry. RESULTS: Soybean intake increased high density lipoprotein cholesterol. Moreover, soybean and exercise individually reduced hepatic oxidative stress and atherogenesis in aortic valve. No additional effect was seen in soybean+exercise group. However, the association of soybean and exercise reduced the percentage of lesion area in arch, thoracic and abdominal aorta and increased serum antioxidant potential. CONCLUSION: Soybean intake and swimming are beneficial in reducing atherosclerosis besides improving lipid profile and reducing lipid peroxidation. The association of soybean and swimming aggregates beneficial effects in serum antioxidant potential and in aorta lesion.


Assuntos
Aterosclerose/dietoterapia , Terapia por Exercício , Glycine max/metabolismo , Estresse Oxidativo , Animais , Aterosclerose/metabolismo , Aterosclerose/patologia , Aterosclerose/terapia , Terapia Combinada , Humanos , Masculino , Camundongos , Camundongos Knockout , Glycine max/química , Natação
4.
Arch Oral Biol ; 98: 204-212, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30503976

RESUMO

The association between cardiovascular and periodontal diseases is characterized by chronic inflammatory processes, with a high prevalence worldwide and complex genetic-environment interactions. Although apolipoprotein E4 (ApoE4), one of the isoforms coded by a polymorphic APOE gene, has been widely recognized as a risk factor for cardiovascular diseases and as an immunoinflammatory factor, less is known regarding how ApoE4 affects atherosclerosis in periodontitis patients. The aim of this review was to investigate the potential underlying mechanisms related to APOE4 that could increase the risk of periodontal disease and, ultimately, of atherosclerosis. There have only been a few studies addressing apoE polymorphisms in patients with chronic periodontitis. To date, no studies have been performed that have assessed how ApoE4 affects atherosclerotic disease in chronic periodontitis patients. Although clinical studies are warranted, experimental studies have consistently documented the presence of periodontal pathogens, which are usually found in the oral cavity and saliva, in the atherosclerotic plaques of ApoE-deficient mice. In addition, in this review, the potential role of the APOE4 allele as an example of antagonistic pleiotropy during human evolution and its relation to oral health is discussed.


Assuntos
Apolipoproteínas E/metabolismo , Aterosclerose/etiologia , Doenças Periodontais/complicações , Animais , Apolipoproteína E3/metabolismo , Apolipoproteína E4 , Apolipoproteínas E/genética , Doenças Cardiovasculares/etiologia , Pleiotropia Genética , Humanos , Inflamação/etiologia , Camundongos , Microbiota , Boca , Polimorfismo Genético , Isoformas de Proteínas , Fatores de Risco
5.
Braz J Med Biol Res ; 39(5): 629-35, 2006 May.
Artigo em Inglês | MEDLINE | ID: mdl-16648901

RESUMO

Elevated blood cholesterol is an important risk factor associated with atherosclerosis and coronary heart disease. Several studies have reported a decrease in serum cholesterol during the consumption of large doses of fermented dairy products or lactobacillus strains. The proposed mechanism for this effect is the removal or assimilation of intestinal cholesterol by the bacteria, reducing cholesterol absorption. Although this effect was demonstrated in vitro, its relevance in vivo is still controversial. Furthermore, few studies have investigated the role of lactobacilli in atherogenesis. The aim of the present study was to determine the effect of Lactobacillus delbrueckii on cholesterol metabolism in germ-free mice and the possible hypocholesterolemic and antiatherogenic action of these bacteria using atherosclerosis-prone apolipoprotein E (apo E) knock-out (KO) mice. For this purpose, Swiss/NIH germ-free mice were monoassociated with L. delbrueckii and fed a hypercholesterolemic diet for four weeks. In addition, apo E KO mice were fed a normal chow diet and treated with L. delbrueckii for 6 weeks. There was a reduction in cholesterol excretion in germ-free mice, which was not associated with changes in blood or liver cholesterol concentration. In apo E KO mice, no effect of L. delbrueckii was detected in blood, liver or fecal cholesterol. The atherosclerotic lesion in the aorta was also similar in mice receiving or not these bacteria. In conclusion, these results suggest that, although L. delbrueckii treatment was able to reduce cholesterol excretion in germ-free mice, no hypocholesterolemic or antiatherogenic effect was observed in apo E KO mice.


Assuntos
Apolipoproteínas E/metabolismo , Aterosclerose/metabolismo , Colesterol/metabolismo , Hipercolesterolemia/metabolismo , Lactobacillus delbrueckii/fisiologia , Animais , Colesterol/análise , Cromatografia Líquida , Dieta Aterogênica , Modelos Animais de Doenças , Fezes/química , Vida Livre de Germes , Metabolismo dos Lipídeos/fisiologia , Fígado/química , Camundongos , Camundongos Knockout
6.
J Med Microbiol ; 54(Pt 4): 413-416, 2005 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15770029

RESUMO

Apoptosis is critical in the pathogenesis of several infectious diseases. The induction of apoptosis was assessed in mouse lymph node cells by four bacteria recovered from infected human dental pulp: Gemella morbillorum, Clostridium butyricum, Fusobacterium nucleatum and Bifidobacterium adolescentis. Smaller lymph nodes and smaller numbers of cells were observed after experimental dental pulp infection with C. butyricum, suggesting that this bacterium induces cell death. Apoptosis was evaluated by determination of cell ploidy and detection of DNA degradation in cells cultured with killed bacteria. Paraformaldehyde-killed C. butyricum and heat-killed G. morbillorum induced substantial cell death, while F. nucleatum and B. adolescentis induced cell death at lower levels. No bacterial preparations induced apoptosis in cells from mice genetically deficient for tumour necrosis factor receptor p55 (TNFRp55), implicating this receptor directly or indirectly as a mediator in the process. It was concluded that apoptosis may be induced during periapical lesions of pulpal origin.


Assuntos
Apoptose/fisiologia , Bactérias/classificação , Bactérias/isolamento & purificação , Polpa Dentária/microbiologia , Linfonodos/citologia , Linfonodos/fisiologia , Animais , Fenômenos Fisiológicos Bacterianos , DNA Bacteriano/genética , DNA Bacteriano/isolamento & purificação , Cavidade Pulpar/microbiologia , Camundongos , Camundongos Endogâmicos
7.
Atherosclerosis ; 154(1): 71-7, 2001 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-11137084

RESUMO

The effect of gelatin ingestion on cholesterol metabolism and on atheroma formation was evaluated in both wild type (n=14) and apoprotein E (apoE) knock out (apoE(-/-)) (n=20) C57BL/6 7-week-old mice. Animals were fed a cholesterol-free isoproteic semi-purified diet containing 20% of casein (control diet) or 10% of casein plus 10% of gelatin (gel diet) for 8 weeks. In wild type mice, dietary gelatin caused a reduction in the serum triacylglycerols levels associated with an increase in the fecal excretion. No difference in blood cholesterol was seen at the sixth week of experiment. At the eighth week of experiment, there was a modest but significant reduction of serum total and high density lipoprotein (HDL) cholesterol in apoE(-/-) mice fed on gel diet compared to the control. Total cholesterol/HDL cholesterol ratio was 2-fold higher in the gel group than that seen in the control group (14.39 and 7.84, respectively). Histological analyzes showed a 2.2-fold increase in the dimension of the atherosclerotic plaques in the proximal aorta in apoE(-/-) mice fed on a gel diet compared to those fed on a control diet. The gel diet also promoted a reduction in the fecal excretion of bile acids. Hepatic cholesterol was similar in both groups. In conclusion, although gelatin reduced total serum cholesterol, this reduction was associated to a decrease of HDL cholesterol and consequent increase of total cholesterol/HDL cholesterol ratio, resulting in an acceleration of atherogenesis.


Assuntos
Apolipoproteínas E/deficiência , Arteriosclerose/etiologia , Gelatina/administração & dosagem , Animais , Aorta/efeitos dos fármacos , Aorta/patologia , Apolipoproteínas E/genética , Arteriosclerose/patologia , Caseínas/administração & dosagem , Caseínas/farmacologia , Colesterol/sangue , HDL-Colesterol/antagonistas & inibidores , HDL-Colesterol/sangue , Dieta , Feminino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout/genética , Farmacologia
8.
Braz J Med Biol Res ; 35(2): 161-73, 2002 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-11847519

RESUMO

We demonstrated that 4 mM butyrate induces apoptosis in murine peritoneal macrophages in a dose- and time-dependent manner as indicated by studies of cell viability, flow cytometric analysis of annexin-V binding, DNA ladder pattern and the determination of hypodiploid DNA content. The activity of caspase-3 was enhanced during macrophage apoptosis induced by butyrate and the caspase inhibitor z-VAD-FMK (100 microM) inhibited the butyrate effect, indicating the major role of the caspase cascade in the process. The levels of butyrate-induced apoptosis in macrophages were enhanced by co-treatment with 1 microg/ml bacterial lipopolysaccharide (LPS). However, our data indicate that apoptosis induced by butyrate and LPS involves different mechanisms. Thus, LPS-induced apoptosis was only observed when macrophages were primed with IFN-gamma and was partially dependent on iNOS, TNFR1 and IRF-1 functions as determined in experiments employing macrophages from various knockout mice. In contrast, butyrate-induced macrophage apoptosis was highly independent of IFN-gamma priming and of iNOS, TNFR1 and IRF-1 functions.


Assuntos
Apoptose , Butiratos/farmacologia , Caspases/metabolismo , Macrófagos/efeitos dos fármacos , Óxido Nítrico/biossíntese , Fator de Necrose Tumoral alfa/biossíntese , Clorometilcetonas de Aminoácidos/farmacologia , Animais , Caspase 3 , Inibidores de Caspase , Sobrevivência Celular , Lipopolissacarídeos/farmacologia , Macrófagos/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Óxido Nítrico/análise , Peritônio/citologia , Fator de Necrose Tumoral alfa/análise
9.
Braz J Med Biol Res ; 27(3): 677-89, 1994 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-8081293

RESUMO

1. Twenty-two axenic (germfree) or thirty heteroxenic (axenic colonized with human flora) 2.5-3.5 months old female Fisher rats were fed for four weeks either a hypercholesterolemic (HYPER) diet or a HYPER diet containing 5% guar gum (GG) sterilized by heat or by gamma irradiation. 2. Axenic rats fed the irradiated GG diet had higher cholesterolemia than their counterparts fed an autoclaved diet (4.50 vs 2.29 mmol/l), whereas the method of sterilization had no effect on plasma cholesterol in axenic HYPER or heteroxenic animals (7.35 vs 6.51 mg/dl). 3. The levels of hepatic esterified cholesterol were higher in heteroxenic animals fed the irradiated GG diet than in their counterparts fed the autoclaved GG diet (5.65 vs 3.57 mmol/g tissue). 4. The composition of volatile fatty acids in the cecal content of heteroxenic rats was dependent on the method of sterilization regardless of the presence of fiber: the levels of butyrate were 2.88 and 0.85 mumol/g for rats fed the autoclaved and irradiated diets, respectively. 5. Gamma irradiation abolished the cholesterol-lowering effect of guar gum, whereas sterilization by heat preserved this effect. 6. The hypocholesterolemic effect of guar was reduced by gamma irradiation sterilization and was probably mediated by qualitative changes in the intestinal microflora which interfered with bile acid absorption.


Assuntos
Colesterol/sangue , Fibras na Dieta , Galactanos/administração & dosagem , Mananas/administração & dosagem , Esterilização , Animais , Ceco/metabolismo , Fibras na Dieta/efeitos da radiação , Ácidos Graxos Voláteis/metabolismo , Feminino , Galactanos/efeitos da radiação , Raios gama , Vida Livre de Germes , Temperatura Alta , Fígado/metabolismo , Mananas/efeitos da radiação , Gomas Vegetais , Ratos , Aumento de Peso
10.
Braz J Med Biol Res ; 37(6): 809-16, 2004 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-15264023

RESUMO

Food allergy is most frequently the result of IgE-mediated hypersensitivity reactions. Here, we describe a chronic model in which some of the intestinal and systemic consequences of continuous egg white solution ingestion by ovalbumin-sensitized eight-week-old BALB/c mice, 6 animals per group, of both sexes, were investigated. There was a 20% loss of body weight that began one week after antigen exposure and persisted throughout the experiment (3 weeks). The sensitization procedure induced the production of anti-ovalbumin IgG1 and IgE, which were enhanced by oral antigen exposure (129% for IgG1 and 164% for IgE, compared to sensitization values). Intestinal changes were determined by jejunum edema at 6 h (45% Evans blue extravasation) and by a significant eosinophil infiltration with a peak at 48 h. By day 21 of continuous antigen exposure, histological findings were mild, with mast cell hyperplasia (100%) and increased mucus production (483%). Altogether, our data clearly demonstrate that, although immune stimulation was persistently occurring in response to continuous oral antigen exposure, regulatory mechanisms were occurring in the intestinal mucosa, preventing overt pathology. The experimental model described here reproduces the clinical and pathological changes of mild chronic food allergy and may be useful for mechanistic studies of this common clinical condition.


Assuntos
Modelos Animais de Doenças , Hipersensibilidade Alimentar/imunologia , Imunoglobulina E/imunologia , Intestino Delgado/imunologia , Ovalbumina/imunologia , Animais , Doença Crônica , Feminino , Hipersensibilidade Alimentar/patologia , Intestino Delgado/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Testes de Neutralização
11.
Braz J Med Biol Res ; 33(9): 1027-36, 2000 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-10973133

RESUMO

Eggplant (Solanum melongena) is consumed extensively in Brazil. It has been believed that infusion of a powdered preparation of the fruit may reduce serum cholesterol. However, there are few documented reports on its effects on cholesterol metabolism and its possible hypocholesterolemic effect has not been proved by well-controlled studies. The aim of the present study was to observe the effects of S. melongena on the serum cholesterol and triglycerides of 38 hypercholesterolemic human volunteers ingesting S. melongena infusion for five weeks. Thirty-eight hypercholesterolemic subjects receiving either S. melongena infusion (N = 19) or placebo (N = 19) participated in two clinical experiments in which the effect of S. melongena infusion was studied with (N = 16) or without (N = 38) dietary orientation. Total cholesterol and its fractions, triglycerides, and apolipoproteins A and B were measured in blood at the beginning of the experiment and three and five weeks thereafter. No differences were observed compared to control. Intraindividual analysis showed that S. melongena infusion significantly reduced the blood levels of total and LDL cholesterol and of apolipoprotein B. After dietary orientation, no intra- or intergroup differences were seen for any of the parameters analyzed. The results suggest that S. melongena infusion had a modest and transitory effect, which was not different from that obtained with standard orientation for dyslipidemia patients (diet and physical activities).


Assuntos
Colesterol/sangue , Hipercolesterolemia/terapia , Fitoterapia , Extratos Vegetais/uso terapêutico , Triglicerídeos/sangue , Verduras/uso terapêutico , Adulto , Estudos de Casos e Controles , HDL-Colesterol/sangue , LDL-Colesterol/sangue , VLDL-Colesterol/sangue , Método Duplo-Cego , Feminino , Humanos , Hipercolesterolemia/sangue , Masculino , Pessoa de Meia-Idade , Extratos Vegetais/química , Verduras/química
12.
ISRN Allergy ; 2013: 545184, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23840965

RESUMO

Background. Food allergies have been shown to reduce serum triacylglycerol, glucose, cholesterol, and free fatty acid levels in mice. In turn, dyslipidemias, especially dyslipidemias presenting with low levels of HDL cholesterol, are important risk factors for the development of atherosclerosis. However, the consequences of food allergies on dyslipidemia and atherosclerosis have not been fully investigated. Methods. Food allergy was induced using an egg white solution (EWS) in ovalbumin- (OVA-) sensitized C57BL/6 and low-density lipoprotein receptor knockout mice (LDLr(-/-)) for 5 weeks and was confirmed by the high production of anti-OVA IgE and IgG1 antibodies in both mouse strains. Results. The allergic C57BL/6 mice exhibited EWS aversion that was associated with less visceral fat and high levels of anti-Ova IgE antibodies after 5 weeks of EWS intake compared to controls. However, LDLr(-/-) allergic mice showed reduced anti-Ova IgE levels that were similar to the nonsensitized group. The LDLr(-/-) allergic mice also demonstrated a reversal of food aversion and sustained visceral fat after 5 weeks of allergy. Although HDL cholesterol levels were reduced in both sensitized mouse strains, lipid deposition in thoracic and abdominal aorta as well as area and composition of atherosclerotic plaques as unaffected by chronic ingestion of EWS. Conclusion. LDLr(-/-) mice develop an attenuated food allergy, as they showed a reversal of food aversion and lower IgE production after 5 weeks of induced allergy. The development of atherosclerosis, in turn, was not accelerated in the allergic LDLr(-/-) group despite the more atherogenic lipid profile.

13.
Braz J Med Biol Res ; 45(7): 601-9, 2012 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-22570088

RESUMO

Pequi is the fruit of Caryocar brasiliense and its oil has a high concentration of monounsaturated and saturated fatty acids, which are anti- and pro-atherogenic agents, respectively, and of carotenoids, which give it antioxidant properties. Our objective was to study the effect of the intake of a cholesterol-rich diet supplemented with pequi oil, compared to the same diet containing soybean oil, on atherosclerosis development, and oxidative stress in atherosclerosis-susceptible LDL receptor-deficient mice (LDLr(-/-), C57BL/6-background). Female mice were fed a cholesterol-rich diet containing 7% soybean oil (Soybean group, N = 12) or 7% pequi oil (Pequi group, N = 12) for 6 weeks. The Pequi group presented a more atherogenic lipid profile and more advanced atherosclerotic lesions in the aortic root compared to the Soybean group. However, the Pequi group presented a less advanced lesion in the aorta than the Soybean group and showed lower lipid peroxidation (Soybean group: 50.2 ± 7.1; Pequi group: 30.0 ± 4.8 µmol MDA/mg protein) and anti-oxidized LDL autoantibodies (Soybean group: 35.7 ± 9.4; Pequi group: 15.6 ± 3.7 arbitrary units). Peritoneal macrophages from the Pequi group stimulated with zymosan showed a reduction in the release of reactive oxygen species compared to the Soybean group. Our data suggest that a pequi oil-rich diet slows atherogenesis in the initial stages, possibly due to its antioxidant activity. However, the increase of serum cholesterol induces a more prominent LDL migration toward the intimae of arteries, increasing the advanced atherosclerotic plaque. In conclusion, pequi oil associated with an atherogenic diet worsens the lipid profile and accelerates the formation of advanced atherosclerotic lesions despite its antioxidant action.


Assuntos
Antioxidantes/farmacologia , Aterosclerose/etiologia , Colesterol na Dieta/efeitos adversos , Dieta Aterogênica/efeitos adversos , Gorduras Insaturadas na Dieta/farmacologia , Ericales/química , Óleo de Soja/farmacologia , Animais , Gorduras Insaturadas na Dieta/efeitos adversos , Suplementos Nutricionais , Feminino , Peroxidação de Lipídeos , Camundongos , Camundongos Endogâmicos C57BL , Óleo de Soja/efeitos adversos
14.
Br J Pharmacol ; 164(6): 1738-48, 2011 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21615722

RESUMO

BACKGROUND AND PURPOSE: Reduced NO availability has been described as a key mechanism responsible for endothelial dysfunction in atherosclerosis. We previously reported that neuronal NOS (nNOS)-derived H(2)O(2) is an important endothelium-derived relaxant factor in the mouse aorta. The role of H(2)O(2) and nNOS in endothelial dysfunction in atherosclerosis remains undetermined. We hypothesized that a decrease in nNOS-derived H(2)O(2) contributes to the impaired vasodilatation in apolipoprotein E-deficient mice (ApoE(-/-)). EXPERIMENTAL APPROACH: Changes in isometric tension were recorded on a myograph; simultaneously, NO and H(2)O(2) were measured using carbon microsensors. Antisense oligodeoxynucleotides were used to knockdown eNOS and nNOS in vivo. Western blot and confocal microscopy were used to analyse the expression and localization of NOS isoforms. KEY RESULTS: Aortas from ApoE(-/-) mice showed impaired vasodilatation paralleled by decreased NO and H(2)O(2) production. Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice. Confocal microscopy showed increased nNOS immunostaining in endothelial cells of ApoE(-/-) mice. However, ACh stimulation of vessels resulted in less phosphorylation on Ser852 in ApoE(-/-) mice. CONCLUSIONS AND IMPLICATIONS: Our data show that endothelial nNOS-derived H(2)O(2) production is impaired and contributes to endothelial dysfunction in ApoE(-/-) aorta. The present study provides a new mechanism for endothelial dysfunction in atherosclerosis and may represent a novel target to elaborate the therapeutic strategy for vascular atherosclerosis.


Assuntos
Aterosclerose/fisiopatologia , Endotélio Vascular/fisiopatologia , Peróxido de Hidrogênio/metabolismo , Óxido Nítrico Sintase Tipo I/fisiologia , Acetilcolina/farmacologia , Animais , Aorta Torácica/efeitos dos fármacos , Aorta Torácica/fisiopatologia , Apolipoproteínas E/deficiência , Apolipoproteínas E/genética , Aterosclerose/metabolismo , Catalase/farmacologia , Modelos Animais de Doenças , Endotélio Vascular/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Óxido Nítrico Sintase Tipo I/deficiência , Óxido Nítrico Sintase Tipo I/genética , Óxido Nítrico Sintase Tipo III/deficiência , Óxido Nítrico Sintase Tipo III/genética , Óxido Nítrico Sintase Tipo III/fisiologia , Vasodilatação/efeitos dos fármacos
15.
Clin Chim Acta ; 412(17-18): 1559-62, 2011 Aug 17.
Artigo em Inglês | MEDLINE | ID: mdl-21570960

RESUMO

BACKGROUND: Obesity has been linked to metabolic syndrome (MS), which increases the risk of cardiovascular disease (CVD). Polymorphisms of Apolipoprotein E have also been associated with increased CVD risk. Therefore, this study investigated the association between MS and Apo E polymorphisms. METHODS: We measured anthropometric and biochemical variables and determined the Apo E genotype of 147 grade III obese patients. RESULTS: The percentage of female subjects was 86.4%. The mean age and BMI of the subjects were 41 years and 53.5 kg/m(2), respectively. MS had been diagnosed in 79% of the subjects. The proportions of those exhibiting MS risk factors were as follows: 100% had a high BMI, 80% had hypertension, 65% had low levels of high-density lipoprotein (HDL), 38% had diabetes, and 39% had hypertriglyceridemia. We found five genotypes for which the allelic distribution was different in the MS group compared to the general population. The ε4 allele was more frequent in the group with neither MS nor hypertension. CONCLUSIONS: The morbidly obese patients exhibited a higher incidence of MS and a different allelic distribution when compared with other populations. The ε4 allele was associated with the absence of MS and hypertension.


Assuntos
Apolipoproteínas E/genética , Síndrome Metabólica/genética , Obesidade/genética , Polimorfismo Genético , Adulto , Índice de Massa Corporal , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
16.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;45(7): 601-609, July 2012. ilus, tab
Artigo em Inglês | LILACS | ID: lil-639459

RESUMO

Pequi is the fruit of Caryocar brasiliense and its oil has a high concentration of monounsaturated and saturated fatty acids, which are anti- and pro-atherogenic agents, respectively, and of carotenoids, which give it antioxidant properties. Our objective was to study the effect of the intake of a cholesterol-rich diet supplemented with pequi oil, compared to the same diet containing soybean oil, on atherosclerosis development, and oxidative stress in atherosclerosis-susceptible LDL receptor-deficient mice (LDLr-/-, C57BL/6-background). Female mice were fed a cholesterol-rich diet containing 7% soybean oil (Soybean group, N = 12) or 7% pequi oil (Pequi group, N = 12) for 6 weeks. The Pequi group presented a more atherogenic lipid profile and more advanced atherosclerotic lesions in the aortic root compared to the Soybean group. However, the Pequi group presented a less advanced lesion in the aorta than the Soybean group and showed lower lipid peroxidation (Soybean group: 50.2 ± 7.1; Pequi group: 30.0 ± 4.8 µmol MDA/mg protein) and anti-oxidized LDL autoantibodies (Soybean group: 35.7 ± 9.4; Pequi group: 15.6 ± 3.7 arbitrary units). Peritoneal macrophages from the Pequi group stimulated with zymosan showed a reduction in the release of reactive oxygen species compared to the Soybean group. Our data suggest that a pequi oil-rich diet slows atherogenesis in the initial stages, possibly due to its antioxidant activity. However, the increase of serum cholesterol induces a more prominent LDL migration toward the intimae of arteries, increasing the advanced atherosclerotic plaque. In conclusion, pequi oil associated with an atherogenic diet worsens the lipid profile and accelerates the formation of advanced atherosclerotic lesions despite its antioxidant action.


Assuntos
Animais , Feminino , Camundongos , Antioxidantes/farmacologia , Aterosclerose/etiologia , Colesterol na Dieta/efeitos adversos , Dieta Aterogênica/efeitos adversos , Gorduras Insaturadas na Dieta/farmacologia , Óleo de Soja/farmacologia , Ericales/química , Suplementos Nutricionais , Gorduras Insaturadas na Dieta/efeitos adversos , Peroxidação de Lipídeos , Óleo de Soja/efeitos adversos
17.
Comp Biochem Physiol Physiol ; 109(2): 503-10, 1994 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-7956125

RESUMO

Germ-free (GF) and heteroxenic (Hx) rats were given a hypocholesterolemic diet (Hyper) with or without 5% guar gum (GG) for 4 weeks. The GF and Hx rats fed GG diets showed a lower hepatic and plasmatic cholesterol level when compared with Hyper groups. This reduction of cholesterolemia was due to a decrease in the chylomicron + very low density lipoprotein (VLDL) fraction. The caecal and portal concentrations of propionate were 30% higher in Hx rats fed the GG diet than in Hx rats fed the Hyper diet. These results exclude the participation of the intestinal microflora in the hypocholesterolemic effect of GG, and show that guar gum nullifies the effect of the hypocholesterolemic diet in the GF rats.


Assuntos
Fibras na Dieta , Galactanos/uso terapêutico , Hipercolesterolemia/dietoterapia , Intestinos/microbiologia , Mananas/uso terapêutico , Animais , Colesterol/sangue , Colesterol/metabolismo , Feminino , Fígado/metabolismo , Gomas Vegetais , Ratos , Ratos Endogâmicos F344
18.
Nutr Cancer ; 28(2): 212-7, 1997.
Artigo em Inglês | MEDLINE | ID: mdl-9290130

RESUMO

Swiss mice fed commercial or elemental diets and an oral short-chain fatty acid (SCFA) solution or saline were treated with the cytostatic drug Ara-C (cytarabine, 3.6 mg/mouse/day) for two or four days. Histopathological examination revealed less damage (atrophy, inflammation, or necrosis) to the small intestine and colon caused by Ara-C when SCFA was administered. Accordingly, protein and nucleotide concentrations in the intestinal mucosa were higher in the group receiving SCFA than in the group receiving a placebo of the same pH and osmolarity. Improvement by SCFA treatment was correlated with an increase in the height of the intestinal villi, with no alterations of the crypts. Furthermore, the number of intraepithelial lymphocytes was similar to normal values in animals receiving SCFA and Ara-C. When large doses of SCFA were administered, xanthomized enterocytes appeared, suggesting an accumulation of fatty acids in these cells. We conclude that oral administration of SCFA at close to physiological proportions reduces the inflammation and necrosis caused by Ara-C administration, thus representing a potential factor for the improvement of patients with mucositis caused by cancer treatment.


Assuntos
Antimetabólitos Antineoplásicos/toxicidade , Citarabina/toxicidade , Ácidos Graxos Voláteis/uso terapêutico , Enteropatias/tratamento farmacológico , Mucosa Intestinal/patologia , Administração Oral , Animais , Antimetabólitos Antineoplásicos/administração & dosagem , Estudos de Coortes , Citarabina/administração & dosagem , Dieta , Ácidos Graxos Voláteis/administração & dosagem , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Inflamação/patologia , Enteropatias/induzido quimicamente , Enteropatias/patologia , Mucosa Intestinal/efeitos dos fármacos , Intestino Delgado/química , Intestino Delgado/efeitos dos fármacos , Camundongos , Nucleotídeos/análise
19.
Chemotherapy ; 50(5): 221-8, 2004 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-15528887

RESUMO

BACKGROUND: Apoptosis is an essential form of cell death, the failure of which can lead to cancer development. Cancer including leukemia is usually treated with chemotherapeutic drugs that can be effective, but frequently problems are encountered that impair the success of the treatment. Butyrate is a short-chain fatty acid that can have many effects on different cells, including apoptosis. METHODS: The effect of a combination treatment with butyrate and antineoplastic agents Ara-C, etoposide and vincristine is evaluate on the leukemic cell line THP-1. RESULTS: We show that butyrate increased apoptosis induced by the three agents as seen by measurement of DNA content, annexin exposure and morphological characteristics. We also demonstrate that the process of apoptosis induced by butyrate and chemotherapeutic drugs involves the participation of caspases and induced activation of caspase-3, -8 and -9. CONCLUSIONS: We believe that butyrate could be a promising therapeutic agent for the treatment of leukemia in combination with other antineoplastic drugs.


Assuntos
Antineoplásicos/farmacologia , Butiratos/farmacologia , Sinergismo Farmacológico , Leucemia Monocítica Aguda/tratamento farmacológico , Leucemia Monocítica Aguda/patologia , Clorometilcetonas de Aminoácidos/farmacologia , Clorometilcetonas de Aminoácidos/uso terapêutico , Antineoplásicos/classificação , Antineoplásicos/uso terapêutico , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Western Blotting , Butiratos/química , Butiratos/uso terapêutico , Inibidores de Caspase , Caspases/metabolismo , Caspases/uso terapêutico , Linhagem Celular Tumoral , Citarabina/farmacologia , Citarabina/uso terapêutico , Replicação do DNA/efeitos dos fármacos , Relação Dose-Resposta a Droga , Ensaios de Seleção de Medicamentos Antitumorais/métodos , Quimioterapia Combinada , Etoposídeo/farmacologia , Etoposídeo/uso terapêutico , Humanos , Leucemia Monocítica Aguda/metabolismo , Vincristina/farmacologia , Vincristina/uso terapêutico
20.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;39(5): 629-635, May 2006. ilus, tab, graf
Artigo em Inglês | LILACS | ID: lil-425786

RESUMO

Elevated blood cholesterol is an important risk factor associated with atherosclerosis and coronary heart disease. Several studies have reported a decrease in serum cholesterol during the consumption of large doses of fermented dairy products or lactobacillus strains. The proposed mechanism for this effect is the removal or assimilation of intestinal cholesterol by the bacteria, reducing cholesterol absorption. Although this effect was demonstrated in vitro, its relevance in vivo is still controversial. Furthermore, few studies have investigated the role of lactobacilli in atherogenesis. The aim of the present study was to determine the effect of Lactobacillus delbrueckii on cholesterol metabolism in germ-free mice and the possible hypocholesterolemic and antiatherogenic action of these bacteria using atherosclerosis-prone apolipoprotein E (apo E) knock-out (KO) mice. For this purpose, Swiss/NIH germ-free mice were monoassociated with L. delbrueckii and fed a hypercholesterolemic diet for four weeks. In addition, apo E KO mice were fed a normal chow diet and treated with L. delbrueckii for 6 weeks. There was a reduction in cholesterol excretion in germ-free mice, which was not associated with changes in blood or liver cholesterol concentration. In apo E KO mice, no effect of L. delbrueckii was detected in blood, liver or fecal cholesterol. The atherosclerotic lesion in the aorta was also similar in mice receiving or not these bacteria. In conclusion, these results suggest that, although L. delbrueckii treatment was able to reduce cholesterol excretion in germ-free mice, no hypocholesterolemic or antiatherogenic effect was observed in apo E KO mice.


Assuntos
Animais , Camundongos , Apolipoproteínas E/metabolismo , Aterosclerose/metabolismo , Colesterol/metabolismo , Hipercolesterolemia/metabolismo , Lactobacillus delbrueckii/fisiologia , Cromatografia Líquida , Colesterol/análise , Dieta Aterogênica , Modelos Animais de Doenças , Fezes/química , Vida Livre de Germes , Metabolismo dos Lipídeos/fisiologia , Fígado/química , Camundongos Knockout
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