RESUMO
Non-lethal biomonitoring should provide an innovative approach to establish bioethical protocols for the management of both aquaculture and wild fisheries resources. We aimed to assess non-lethal biomarkers in Piaractus mesopotamicus caged in a rice field during a bifenthrin (BF) application. We analyzed parameters related to the immune system, energy metabolism and oxidative stress in fish skin mucus and blood plasma. Fish exposed to BF showed a significant increase in skin mucus glucose levels and the enzymatic activities of protease, alkaline phosphatase and superoxide dismutase. Regarding plasmatic parameters, BF increased the levels of glucose, total protein and albumin, but decreased triglycerides. In addition, increased activities of lysozyme and alkaline phosphatase were found in the blood plasma of exposed fish. Our results indicated an increased energy demand, altered immune function and a mild oxidative stress response in fish exposed in situ to BF. We have shown that skin mucus and blood plasma are very promising matrices for the development of non-lethal biomarkers to assess fish health in a stressed environment.
RESUMO
This study aimed to analyze the cold stress effects (in terms of hematology, energy reserves, and oxidative stress) in Piaractus mesopotamicus (pacú) and their mitigation by a Pyropia columbina red seaweed-supplemented diet. For this purpose, juvenile fish were fed with a control (CD) or a red seaweed-supplemented diet (RD) for 60 days, and then, the animals were exposed to a low temperature (14 °C) and a control temperature (24 °C) for 24 h. The cold shock generated an increase of hemoglobin levels in fish fed with both diets. In CD-fed fish, plasmatic triglycerides, cholesterol, and hepatic glycogen decreased after the thermal shock; meanwhile, the animals fed with RD showed decreased hepatic proteins, but increased cholesterol and hepatic glycogen. Regarding oxidative stress, antioxidant enzymes augmented their activity in the liver, intestine, and gills; meanwhile, lipid oxidative damage was observed in the liver and intestine of fish exposed to 14 °C and fed with both diets. Pacú was sensitive to cold shock, but no mitigation effects were observed in fish fed with the supplemented diet. Further research should target higher concentrations of P. columbina in supplemented diets to take advantage of this valuable resource.
Assuntos
Caraciformes , Resposta ao Choque Frio , Suplementos Nutricionais , Rodófitas , Alga Marinha , Animais , Caraciformes/sangue , Caraciformes/metabolismo , Dieta , Proteínas de Peixes/metabolismo , Brânquias/metabolismo , Glutationa Redutase/metabolismo , Glutationa Transferase/metabolismo , Glicogênio/metabolismo , Mucosa Intestinal/metabolismo , Metabolismo dos Lipídeos , Fígado/metabolismo , Músculos/metabolismo , Estresse Oxidativo , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
The present study analyses the effect of dietary chia seed rich in n-3 α-linolenic acid on the mechanisms underlying dyslipidaemia and liver steatosis developed in rats fed a sucrose-rich diet (SRD) for either 3 weeks or 5 months. The key hepatic enzyme activities such as fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), glucose-6-phosphate dehydrogenase (G-6-PDH), carnitine palmitoyltransferase-1 (CPT-1) and fatty acid oxidase (FAO) involved in lipid metabolism and the protein mass levels of sterol regulatory element-binding protein-1 (SREBP-1) and PPARα were studied. (1) For 3 weeks, Wistar rats were fed either a SRD with 11 % of maize oil (MO) as dietary fat or a SRD in which chia seed replaced MO (SRD+Chia). (2) A second group of rats were fed a SRD for 3 months. Afterwards, half the rats continued with the SRD while for the other half, MO was replaced by chia for 2 months (SRD+Chia). In a control group, maize starch replaced sucrose. Liver TAG and the aforementioned parameters were analysed in all groups. The replacement of MO by chia in the SRD prevented (3 weeks) or improved/normalised (5 months) increases in dyslipidaemia, liver TAG, FAS, ACC and G-6-PDH activities, and increased FAO and CPT-1 activities. Protein levels of PPARα increased, and the increased mature form of SREBP-1 protein levels in the SRD was normalised by chia in both protocols (1 and 2). The present study provides new data regarding some key mechanisms related to the fate of hepatic fatty acid metabolism that seem to be involved in the effect of dietary chia seed in preventing and normalising/improving dyslipidaemia and liver steatosis in an insulin-resistant rat model.
Assuntos
Dieta , Lipólise , Fígado/metabolismo , Estresse Oxidativo , Sementes , Fatores de Transcrição/metabolismo , Animais , Western Blotting , Metabolismo Energético , Masculino , Ratos , Ratos Wistar , Triglicerídeos/metabolismo , Aumento de PesoRESUMO
OBJECTIVE: The purposes of the present work were twofold: (1) investigate same mechanisms involved in the development of fat cell hypertrophy in the experimental model of dyslipidemia and whole-body insulin resistance induced in rats chronically fed a sucrose-rich diet (SRD); and (2) analyze the possible beneficial effect of fish oil on these mechanisms. METHODS: For 6 mo, male Wistar rats received a sucrose-rich diet (62.5% w/w sucrose, 8% corn oil) or a control diet in which sucrose was replaced by starch. After this period, the sucrose-fed animals were divided randomly into two groups: the first one continued with the same diet up to 8 mo and the second one received the same diet, but with corn oil replaced by 7% fish oil+1 % corn oil. Rats were fed with this diet for the next 2 mo. RESULTS: Although an enlarged fat cell lipolysis and an impaired insulin-stimulated glucose uptake were present in the fat cells of SRD-fed rats, an increase of several key enzymes of the novo lipogenesis could be one of the possible mechanisms involved in visceral adiposity. The addition of dietary fish oil restored or improved the above abnormalities. CONCLUSION: This study shows possible mechanisms conditioning the influence of nutrients on the development and management of dyslipidemia, insulin sensitivity, and fat cell accretion, all abnormalities present in the metabolic syndrome.
Assuntos
Adiposidade/efeitos dos fármacos , Glicemia/metabolismo , Dislipidemias/metabolismo , Enzimas/metabolismo , Óleos de Peixe/farmacologia , Resistência à Insulina , Gordura Intra-Abdominal/metabolismo , Lipogênese/efeitos dos fármacos , Adipócitos/efeitos dos fármacos , Adipócitos/enzimologia , Adipócitos/patologia , Animais , Óleo de Milho , Dieta , Gorduras na Dieta/administração & dosagem , Sacarose Alimentar/efeitos adversos , Modelos Animais de Doenças , Dislipidemias/tratamento farmacológico , Dislipidemias/enzimologia , Óleos de Peixe/uso terapêutico , Hipertrofia , Insulina/metabolismo , Secreção de Insulina , Gordura Intra-Abdominal/efeitos dos fármacos , Gordura Intra-Abdominal/enzimologia , Lipogênese/fisiologia , Masculino , Síndrome Metabólica/tratamento farmacológico , Síndrome Metabólica/enzimologia , Síndrome Metabólica/etiologia , Distribuição Aleatória , Ratos , Ratos Wistar , Sacarose/efeitos adversosRESUMO
Insulin resistance and adiposity induced by a long-term sucrose-rich diet (SRD) in rats could be reversed by fish oil (FO). Regulation of plasma leptin and adiponectin levels, as well as their gene expression, by FO might be implicated in these findings. This study was designed to evaluate the long-term regulation of leptin and adiponectin by dietary FO in a dietary model of insulin resistance induced by long-term SRD in rats and to determine their impact on adiposity and insulin sensitivity. Rats were randomized to consume a control diet (CD; n = 25) or an SRD (n = 50) for 7 mo. Subsequently, the SRD-fed rats were randomized to consume SRD+FO or to continue on SRD for an additional 2 mo. Long-term SRD induced overweight and decreased both plasma leptin and adiponectin levels without change in gene expression. Dyslipidemia, adiposity, and insulin resistance accompanied these modifications. Shifting the source of fat to FO for 2 mo increased plasma levels of both adipokines, reversed insulin resistance and dyslipidemia, and improved adiposity. These results were not associated with modifications in gene expression. These results suggest that increasing both adipokines by dietary FO might play an essential role in the normalization of insulin resistance and adiposity in dietary-induced, insulin-resistant models.