RESUMO
Aerobic training induces adaptive responses in skeletal muscles and white adipose tissues, thus facilitating lipid utilization as energy substrates during a physical exercise session. However, the effects of training on cytokines levels and on transcription factors involved in lipid metabolism in muscle and different white adipose depots are still unclear; therefore, these were the aims of the present study. Nineteen adult male Wistar rats were randomly assigned to a trained group or a control, non-trained group. The 10-week training protocol consisted of running on a treadmill, during 1 hour per day, 5 days per week, at 75% of maximum aerobic speed. As expected, trained rats improved their aerobic performance and had augmented citrate synthase activity in the soleus, while the control rats did not. Although body weight was not different between groups, the adiposity index and white adipose depots (ie, epididymal and retroperitoneal) were reduced in trained rats. Training reduced serum concentration of insulin, but failed to change serum concentrations of glucose, triacylglycerol, total cholesterol, and nonesterified fatty acids. Training increased sterol regulatory element-binding protein-1c expression in the gastrocnemius and epididymal adipose tissue, and reduced peroxisome proliferator-activated receptor γ (PPARγ) expression in most of the tissues analyzed. The expression of PPARα and carnitine palmitoyltransferase 1 increased in the gastrocnemius and mesenteric adipose tissue but reduced in epididymal adipose tissue. Triacylglycerol content and tribbles 3 expression reduced in the gastrocnemius of trained rats. Tumor necrosis factor-α and interleukin-6 were increased in all adipose depots evaluated. Collectively, our data indicate that the 10-week aerobic training changed gene expression to improve muscle oxidative metabolism and facilitate lipid degradation in adipose tissues. Our data also highlight the existence of adaptive responses that are distinct between the skeletal muscle and white adipose tissue and between different adipose depots.
Assuntos
Tecido Adiposo Branco/metabolismo , Regulação da Expressão Gênica/fisiologia , Metabolismo dos Lipídeos/fisiologia , Músculo Esquelético/metabolismo , Condicionamento Físico Animal , Tecido Adiposo Branco/citologia , Animais , Masculino , Músculo Esquelético/citologia , Ratos , Ratos WistarRESUMO
We have previously shown that the cafeteria diet increases body fat mass, plasma triacylglycerol (TAG) and insulin levels, glucose uptake by white and brown adipose tissues, as well as the sympathetic activity to both adipose tissues in Wistar rats. The metabolic pathways responsible for the development of non-alcoholic fatty liver disease (NAFLD) were examined in cafeteria diet-fed rats. After 3 weeks offering cafeteria diet, we evaluated: (i) activity of the sympathetic nervous system by norepinephrine turnover rates; (ii) de novo fatty acid synthesis in vivo using 3H2O; (iii) secretion of very low density lipoprotein (VLDL)-TAG secretion measuring serum TAG levels after administration of lipase lipoprotein inhibitor, (iv) liver cytosolic lipases activities and (v) liver mRNA expression of enzymes involved in lipids secretion and oxidation by RT-PCR. The cafeteria diet induced an increase in TAG (120%) and cholesterol (30%) liver contents. Cafeteria diet did not change the sympathetic nervous system activity to liver, but induced a marked increase in the lipogenesis (approximately four-fold) and significant increase in cytosolic lipases activities (46%) and VLDL-TAG secretion (22%) compared to control diet-fed rats. The cafeteria diet also increased the microsomal triglyceride transfer protein (30%) and carnitine palmitoyltransferase I (130%) mRNA expression but decreased the apolipoprotein B100 (26%) mRNA expression. Our findings demonstrate that the increase in the cytosolic lipases activities and VLDL-TAG secretion rates were not able to compensate for the increased lipogenesis rates induced by the cafeteria diet, resulting in NAFLD.
Assuntos
Peso Corporal/fisiologia , Citosol/enzimologia , Fígado/enzimologia , Animais , Glicemia/metabolismo , Carnitina O-Palmitoiltransferase/sangue , Proteínas de Transporte/sangue , Metabolismo dos Lipídeos/fisiologia , Lipogênese/fisiologia , Lipoproteínas VLDL/sangue , Masculino , Hepatopatia Gordurosa não Alcoólica/sangue , Ratos , Ratos Wistar , Triglicerídeos/sangueRESUMO
Several studies have demonstrated that fish oil consumption improves metabolic syndrome and comorbidities, as insulin resistance, nonalcoholic fatty liver disease, dyslipidaemia and hypertension induced by high-fat diet ingestion. Previously, we demonstrated that administration of a fructose-rich diet to rats induces liver lipid accumulation, accompanied by a decrease in liver cytosolic lipases activities. In this study, the effect of replacement of soybean oil by fish oil in a high-fructose diet (FRUC, 60% fructose) for 8 weeks on lipid metabolism in liver and epididymal adipose tissue from rats was investigated. The interaction between fish oil and FRUC diet increased glucose tolerance and decreased serum levels of triacylglycerol (TAG), VLDL-TAG secretion and lipid droplet volume of hepatocytes. In addition, the fish oil supplementation increased the liver cytosolic lipases activities, independently of the type of carbohydrate ingested. Our results firmly establish the physiological regulation of liver cytosolic lipases to maintain lipid homeostasis in hepatocytes. In epididymal adipose tissue, the replacement of soybean oil by fish oil in FRUC diet did not change the tissue weight and lipoprotein lipase activity; however, there was increased basal and insulin-stimulated de novo lipogenesis and glucose uptake. Increased cytosolic lipases activities were observed, despite the decreased basal and isoproterenol-stimulated glycerol release to the incubation medium. These findings suggest that fish oil increases the glycerokinase activity and glycerol phosphorylation from endogenous TAG hydrolysis. Our findings are the first to show that the fish oil ingestion increases cytosolic lipases activities in liver and adipose tissue from rats treated with high-carbohydrate diets.
Assuntos
Tecido Adiposo/enzimologia , Carboidratos da Dieta/administração & dosagem , Óleos de Peixe/administração & dosagem , Lipase/metabolismo , Fígado/enzimologia , Óleo de Soja/administração & dosagem , Adipócitos/enzimologia , Ração Animal , Animais , Citosol/enzimologia , Modelos Animais de Doenças , Epididimo/metabolismo , Frutose/efeitos adversos , Teste de Tolerância a Glucose , Hidrólise , Insulina/química , Metabolismo dos Lipídeos , Lipogênese , Lipase Lipoproteica/metabolismo , Lipoproteínas VLDL/metabolismo , Masculino , Hepatopatia Gordurosa não Alcoólica/metabolismo , Fosforilação , Ratos , Ratos Wistar , Triglicerídeos/química , Triglicerídeos/metabolismoRESUMO
The angiotensin (Ang) converting enzyme 2/Ang-(1-7)/Mas axis has been described to have a beneficial role on metabolic disorders. In the present study, the use of a transgenic rat model that chronically overexpresses Ang-(1-7) enabled us to investigate the chronic effects of this peptide on lipid accumulation in the liver and adipose tissue. The transgenic group showed a marked tendency toward increased expression of peroxisome proliferator-activated receptor-γ (PPARγ) and decreased lipoprotein lipase (LPL) expression and activity in epididymal adipose tissue. We also showed that Mas receptor-knockout mice had decreased PPARγ expression in adipose tissue, accompanied by an increase in LPL activity. These results confirm the regulation of adipose tissue LPL activity by Ang-(1-7) and suggest that this occurs independent of PPARγ expression. The reduced adiposity index of transgenic rats, due to the effect of Ang-(1-7), was accompanied by a decrease in lipogenesis. These findings suggest a direct effect of Ang-(1-7) on lipogenesis, independent of the stimulatory effect of insulin. Furthermore, the decreased concentration of triacylglycerol in the liver of transgenic rats may result from increased activity of cytosolic lipases and decreased fatty acid uptake from the adipose tissue, determined from fatty acid-binding protein expression, and hepatic de novo fatty acid synthesis, evaluated by fatty acid synthase expression. The data clearly show that Ang-(1-7) regulates lipid metabolism in the adipose tissue and liver.
Assuntos
Tecido Adiposo/metabolismo , Angiotensina I/fisiologia , Metabolismo dos Lipídeos , Fígado/metabolismo , Fragmentos de Peptídeos/fisiologia , Adiposidade , Angiotensina I/genética , Animais , Ácidos Graxos/metabolismo , Hipertensão/metabolismo , Insulina/metabolismo , Lipase Lipoproteica/genética , Lipase Lipoproteica/metabolismo , Masculino , Camundongos , Obesidade/metabolismo , PPAR gama/genética , PPAR gama/metabolismo , Fragmentos de Peptídeos/genética , RNA Mensageiro/genética , Ratos , Ratos Transgênicos , Fatores de Tempo , Triglicerídeos/metabolismoRESUMO
Several studies have demonstrated that a high-fructose (FRUC) diet induces metabolic and haemodynamic abnormalities, known as the metabolic syndrome, which are characterised by obesity, glucose intolerance, insulin resistance, dyslipidaemia and hypertension. In this study, the effect of a FRUC diet (60 % fructose) for 8 weeks on the metabolism of lipids in liver and epididymal adipose tissue from Wistar rats was compared with the AIN-93M diet and the effects of the AIN-93M diet were compared with a chow diet. The FRUC diet induced marked increases in both hepatocyte lipid droplet volume and postprandial serum levels of triacylglycerol (TAG), but reduced the postprandial serum levels of insulin. The AIN-93M diet induced marked increases in the hepatocyte lipid droplet volume and the serum levels of insulin, without affecting the serum levels of TAG. We found that isocaloric substitution of cornstarch, dextrinised cornstarch and sucrose (AIN-93M diet) for fructose did not affect the hepatic VLDL-TAG secretion and adipose tissue glucose uptake, lipolysis and cytosolic lipases activities in rats. However, the high-fructose diet induced a severe steatosis in liver accompanied by a decrease in cytosolic lipases activities. In adipose tissue, the FRUC diet induced a decrease in the lipoprotein lipase activity, and an increase in lipogenesis. FRUC and AIN-93M diets induced changes in lipid homeostasis in liver and adipose tissue by distinct biochemical mechanisms.
Assuntos
Tecido Adiposo/efeitos dos fármacos , Carboidratos da Dieta/administração & dosagem , Frutose/administração & dosagem , Lipase/metabolismo , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Tecido Adiposo/enzimologia , Animais , Glicemia/metabolismo , Citosol/metabolismo , Hepatócitos/efeitos dos fármacos , Hepatócitos/enzimologia , Insulina/sangue , Gotículas Lipídicas/efeitos dos fármacos , Gotículas Lipídicas/metabolismo , Fígado/enzimologia , Masculino , Ratos , Ratos Wistar , Triglicerídeos/metabolismoRESUMO
The aim of the present study was to evaluate the potential of calcium supplementation from Lithothamnium muelleri algae on metabolic and inflammatory parameters in mice with increased adiposity. Male mice were fed and divided during 8 weeks in: control (C), a high refined carbohydrate-containing diet (HC), HC diet supplemented with 1% of Lithothamnion muelleri algae (HC + A) and HC diet supplemented with 0.9% calcium carbonate (HC + C). Animals fed HC diet had increased body weight gain and adiposity, serum glucose and cholesterol, glucose intolerance and decreased insulin sensitivity, compared to control diet. However, the HC + A and HC + C groups did not prevent these aspects and were not able to change the CD14 + cells population in adipose tissue of animals fed HC diet. Calcium supplementation with Lithothamnium muelleri algae and calcium carbonate had no protective effect against the development of adiposity, metabolic and inflammatory alterations induced by HC diet.
Assuntos
Adiposidade , Fármacos Antiobesidade/uso terapêutico , Cálcio da Dieta/uso terapêutico , Misturas Complexas/uso terapêutico , Suplementos Nutricionais , Obesidade/prevenção & controle , Rodófitas/química , Tecido Adiposo Branco/irrigação sanguínea , Tecido Adiposo Branco/imunologia , Tecido Adiposo Branco/patologia , Animais , Anti-Inflamatórios não Esteroides/análise , Anti-Inflamatórios não Esteroides/química , Anti-Inflamatórios não Esteroides/isolamento & purificação , Anti-Inflamatórios não Esteroides/uso terapêutico , Fármacos Antiobesidade/análise , Fármacos Antiobesidade/química , Fármacos Antiobesidade/isolamento & purificação , Vasos Sanguíneos/imunologia , Vasos Sanguíneos/patologia , Carbonato de Cálcio/administração & dosagem , Carbonato de Cálcio/análise , Carbonato de Cálcio/isolamento & purificação , Cálcio da Dieta/análise , Cálcio da Dieta/isolamento & purificação , Células Cultivadas , Misturas Complexas/química , Carboidratos da Dieta/efeitos adversos , Suplementos Nutricionais/análise , Manipulação de Alimentos , Intolerância à Glucose/etiologia , Intolerância à Glucose/prevenção & controle , Resistência à Insulina , Macrófagos/imunologia , Macrófagos/patologia , Masculino , Camundongos , Obesidade/etiologia , Obesidade/imunologia , Obesidade/fisiopatologia , Células Estromais/imunologia , Células Estromais/patologia , Aumento de PesoRESUMO
A obesidade, doença multifatorial definida como excesso de gordura corporal, apresenta concomitância entre fatores de risco genéticos e ambientais. O diagnóstico precoce e as intervenções no período crítico do desenvolvimento da obesidade - infância e adolescência - têm sido recomendados, buscando-se evitar desfechos desfavoráveis na idade adulta. Este estudo transversal teve como objetivo caracterizar perfil lipídico, glicemia, adiponectina, leptina e grelina de escolares entre seis e nove anos, portadores de sobrepeso e obesidade, do município de Ouro Preto-MG. Os dados foram analisados a partir do teste de normalidade Shapiro Wilk; e nas comparações entre os grupos foi aplicado o teste paramétrico (Teste t) ou não paramétrico (Teste Mann Whitney), adotando-se intervalo de confiança de 95% e nível de significância para valores ≤ 0,05. A idade média da população escolar foi de 7,8 ± 1,1 anos, com prevalência de 8,9% de sobrepeso e 3% de obesidade. Foram identificados hipercolesterolemia em 5,5%, HDL alterado em 98,7%, taxa limítrofe de LDL em 32,4% e glicemia alterada em 46,6% das crianças. Na análise estratificada quanto ao gênero, foram observados valores maisaltos para leptina em meninas (p=0,032) e grelina nos meninos (p=0,033), não havendo diferença para as demais variáveis. Os resultados demonstram ser o excesso de peso entre escolares problema de saúde relevante no município, ressaltando-se a importância de implementação de programa de intervenção precoce por parte dos gestores. Elucidar os precursores da obesidade na infância pode levar a intervenções capazes de atenuar ou impedir suas consequências na juventude e fase adulta.
Obesity, defined as an excess in body fat, is a multifactorial disease involving both genetic and environmental risk factors. Early diagnosis and interventions during critical periods of development of obesity - childhood and adolescence - have been recommended, aiming at preventing unfavorable outcomes at a later age. This cross-sectional study sought tocharacterize the lipid profile, glucose, adiponectin, leptin and ghrelin in schoolchildren between six and nine years of age with overweight and obesity in the city of Ouro Preto (MG). The data was analyzed with the Shapiro Wilk normality test, groups comparisons were made with either a parametric (T test) or a nonparametric (Mann Whitney) test, adopting confidence intervals of 95% and a significance level of ≤ 0.05. The average age of the school population was 7.8 ± 1.1 years, with a prevalence of 8.9% of overweight and 3% of obesity. Hypercholesterolemia was found in 5.5%, HDL was abnormal in 98.7%, LDL levels were borderline in 32.4% and altered glucose levels were present in 46.6% of the children. In stratified analysis by gender, higher values of leptin in girls (p = 0.032) and ghrelin in boys (p = 0.033) were found, with no difference for the other variables. The results show that overweight/obesity among schoolchildren should be considered a significant health problem in this population, highlighting the importanceof implementing early intervention programs. Uncovering the precursors of childhood obesity could lead to interventions so as to prevent or mitigate its consequences in youth and adulthood.
Assuntos
Humanos , Masculino , Feminino , Criança , Adiposidade , Estudantes/estatística & dados numéricos , Obesidade/diagnóstico , Brasil , Estado Nutricional , SobrepesoRESUMO
Ovarian hormones modulate the metabolism of adipose cells and present a protective effect against hypertension. The aim of this study was to compare the effect of estradiol on adiposity markers in spontaneously hypertensive rats. Ovariectomized spontaneously hypertensive rats treated with estradiol (5 µg/100 g/day), three weeks after ovariectomy, presented decreased blood pressure and insulin levels and increased hepatic glycogen content. Periuterine or mesenteric adipocytes from treated animals were smaller as compared to vehicle treated group, whereas no differences were observed in relation to the number of cells. Basal rates of glycerol release were higher only in periuterine adipocytes of treated rats. The increment of glycerol release over basal values in response to isoproterenol was 400% and 440%, 283% and 330% for vehicle and estradiol treated periuterine and mesenteric adipocytes, respectively. The estradiol treated group was more sensitive to insulin inhibition of isoproterenol-stimulated lipolysis than the control animals. The lipoprotein lipase activity decreased after treatment, only in periuterine adipose tissue. Estradiol administration increased basal and insulin-stimulated rates of glucose transport in adipocytes of both sites, although the values obtained by periuterine were higher than those observed for mesenteric adipocytes. Both adipose tissues from treated animals exhibited a decreased expression of the peroxisome proliferator-activated receptor-γ, but an increased expression of peroxisome proliferator-activated receptor-α in liver. These findings suggest that estrogen administration attenuates adiposity markers of spontaneously hypertensive rats as a result of the decreased expression levels of peroxisome proliferator-activated receptor-γ in adipose tissue and increased expression of peroxisome proliferator-activated receptor-α in liver.
Assuntos
Adipócitos/efeitos dos fármacos , Adiposidade/efeitos dos fármacos , Estradiol/farmacologia , Estrogênios/farmacologia , Gordura Intra-Abdominal/efeitos dos fármacos , Gordura Intra-Abdominal/metabolismo , Lipólise/efeitos dos fármacos , PPAR alfa/metabolismo , PPAR gama/metabolismo , Adipócitos/metabolismo , Agonistas Adrenérgicos beta/farmacologia , Animais , Biomarcadores/metabolismo , Glicemia/efeitos dos fármacos , Glicemia/metabolismo , Regulação para Baixo/efeitos dos fármacos , Estradiol/administração & dosagem , Estradiol/metabolismo , Estrogênios/administração & dosagem , Estrogênios/metabolismo , Feminino , Isoproterenol/farmacologia , Lipase Lipoproteica/efeitos dos fármacos , Lipase Lipoproteica/metabolismo , Ovariectomia , PPAR alfa/efeitos dos fármacos , PPAR gama/efeitos dos fármacos , Ratos , Ratos Endogâmicos SHR , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Regulação para Cima/efeitos dos fármacosRESUMO
AIMS: As cardiac performance is closely related to its energy supply, our study investigated the effect of the orotic acid cardioprotective agent on the pathways of energy supply, in both conditions of normal flow and ischemia. MAIN METHODS: Male Wistar rats were fed during nine days with a balanced diet only or supplemented with 1% orotic acid. KEY FINDINGS: Dietary administration of orotic acid increased the cardiac utilization of fatty acids, activity of the lipoprotein lipase, expression of the gene of peroxisome proliferator-activated receptor α and its target enzymes. In addition, orotic acid increased the myocardial uptake and incorporation of glucose, glycogen content and level of GLUT4, concentration of glycolytic metabolites and lactate production in both experimental conditions, baseline and after regional ischemia. SIGNIFICANCE: Thus, in orotic acid hearts there was a simultaneous stimulus of fatty acid oxidation and glycolytic pathway, reflected in increased energetic content even in pre-ischemia. The analysis of the cardiac contractility index showed a positive inotropic effect of orotic acid due, at least in part, to the increased availability of energy. The result allows us to suggest that the metabolic changes induced by orotic acid result in appreciable alterations on myocardial contractile function.
Assuntos
Dieta , Metabolismo Energético/efeitos dos fármacos , Coração/efeitos dos fármacos , Coração/fisiologia , Contração Miocárdica/efeitos dos fármacos , Isquemia Miocárdica/fisiopatologia , Miocárdio/metabolismo , Ácido Orótico/farmacologia , Animais , Ácidos Graxos/metabolismo , Glicólise/efeitos dos fármacos , Humanos , Lipase Lipoproteica/metabolismo , Masculino , Ácido Orótico/administração & dosagem , Oxirredução , Ratos , Ratos WistarRESUMO
The renin-angiotensin system is an important link between metabolic syndrome and cardiovascular diseases. Besides angiotensin II, other angiotensin peptides such as angiotensin-(1-7), have important biological activities. It has been demonstrated that angiotensin-(1-7), acting through the G protein-coupled receptor encoded by the Mas protooncogene have important actions on the cardiovascular system. However, the role of angiotensin-(1-7)-Mas axis in lipidic profile is not well established. In the present study, the adipocyte metabolism was investigated in wild type and FVB/N Mas-deficient male mice. The gene expression of peroxisome proliferator-activated receptor gamma, acetyl-CoA carboxylase and the amount of fatty acid synthase protein were reduced in the Mas-knockout mice. Serum nonesterified fatty acids of Mas-knockout showed a 50% increase in relation to wild type group. Basal and isoproterenol-stimulated lipolysis was similar between the groups, however, a significant decrease of the glycerol release (lipolytic index) in response to insulin was observed in wild type animals, while no effect of the insulin action was observed in a Mas-knockout group. The data suggest that the lack of angiotensin-(1-7) action through Mas receptor alters the response of adipocytes to insulin action. These effects might be related to decreased expression of PPARγ.