Percorrer por autor "Rodrigues, Tiago"
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- Effect of enriched substrate on the growth of the sea cucumber Holothuria arguinensis Koehler and Vaney, 1906 juvenilesPublication . Rodrigues, Tiago; Silva, Francisco Azevedo e; Sousa, João; Félix, Pedro M.; Pombo, AnaThe sea cucumber Holothuria arguinensis (Koehler and Vaney, 1906) presents an increasing commercial value in Asian markets and its exportation depends exclusively on wild stock harvesting. Production through aquaculture has been acknowledged as an alternative to supply demand and reduce pressure on natural stocks, but there are still bottlenecks to overcome, such as low growth rate and survival. This study focuses on the evaluation of the growth of juveniles of H. arguinensis through substrate enrichment—direct mixing of Sargassum vulgare with sediment—in recirculating aquaculture systems (RAS), for 4 months, with a baseline diet of Saccorhiza polyschides. Compared to the control (no enrichment), sea cucumbers fed with enriched sediment showed the highest specific growth rate (SGR), the highest growth rate (GR) and the lowest size heterogeneity. The results obtained in this study showed a favorable growth of sea cucumbers when in the presence of a substrate enriched with Sargassum vulgare, representing an important step towards the viability of large-scale sea cucumber rearing in Europe.
- Evaluating the Impact of Different Hypercaloric Diets on Weight Gain, Insulin Resistance, Glucose Intolerance, and its Comorbidities in RatsPublication . Melo, Bernardete F.; Sacramento, Joana F.; Ribeiro, Maria J.; Prego, Claudia S.; Correia, Miguel C.; Coelho, Joana C.; Cunha-Guimaraes, Joao P.; Rodrigues, Tiago; Martins, Ines B.; Seiça, Raquel M.; Matafome, Paulo; Conde, Silvia V.; Guarino, Maria PedroAnimal experimentation has a long history in the study of metabolic syndrome-related disorders. However, no consensus exists on the best models to study these syndromes. Knowing that different diets can precipitate different metabolic disease phenotypes, herein we characterized several hypercaloric rat models of obesity and type 2 diabetes, comparing each with a genetic model, with the aim of identifying the most appropriate model of metabolic disease. The effect of hypercaloric diets (high fat (HF), high sucrose (HSu), high fat plus high sucrose (HFHSu) and high fat plus streptozotocin (HF+STZ) during different exposure times (HF 3 weeks, HF 19 weeks, HSu 4 weeks, HSu 16 weeks, HFHSu 25 weeks, HF3 weeks + STZ) were compared with the Zucker fatty rat. Each model was evaluated for weight gain, fat mass, fasting plasma glucose, insulin and C-peptide, insulin sensitivity, glucose tolerance, lipid profile and liver lipid deposition, blood pressure, and autonomic nervous system function. All animal models presented with insulin resistance and dyslipidemia except the HF+STZ and HSu 4 weeks, which argues against the use of these models as metabolic syndrome models. Of the remaining animal models, a higher weight gain was exhibited by the Zucker fatty rat and wild type rats submitted to a HF diet for 19 weeks. We conclude that the latter model presents a phenotype most consistent with that observed in humans with metabolic disease, exhibiting the majority of the phenotypic features and comorbidities associated with type 2 diabetes in humans.
- Functional abolition of carotid body activity restores insulin action and glucose homeostasis in rats: key roles for visceral adipose tissue and the liverPublication . Sacramento, Joana F.; Ribeiro, Maria J.; Rodrigues, Tiago; Olea, Elena; Melo, Bernardete F.; Guarino, Maria P.; Fonseca-Pinto, Rui; Ferreira, Cristiana R.; Coelho, Joana; Obeso, Ana; Seiça, Raquel; Matafome, Paulo; Conde, Silvia V.Aims/hypothesis: We recently described that carotid body (CB) over-activation is involved in the aetiology of insulin resistance and arterial hypertension in animal models of the metabolic syndrome. Additionally, we have demonstrated that CB activity is increased in animal models of insulin resistance, and that carotid sinus nerve (CSN) resection prevents the development of insulin resistance and arterial hypertension induced by high-energy diets. Here, we tested whether the functional abolition of CB by CSN transection would reverse pre-established insulin resistance, dyslipidaemia, obesity, autonomic dysfunction and hypertension in animal models of the metabolic syndrome. The effect of CSN resection on insulin signalling pathways and tissue-specific glucose uptake was evaluated in skeletal muscle, adipose tissue and liver. Methods: Experiments were performed in male Wistar rats submitted to two high-energy diets: a high-fat diet, representing a model of insulin resistance, hypertension and obesity, and a high-sucrose diet, representing a lean model of insulin resistance and hypertension. Half of each group was submitted to chronic bilateral resection of the CSN. Age-matched control rats were also used. Results: CSN resection normalised systemic sympathetic nervous system activity and reversed weight gain induced by high-energy diets. It also normalised plasma glucose and insulin levels, insulin sensitivity lipid profile, arterial pressure and endothelial function by improving glucose uptake by the liver and perienteric adipose tissue. Conclusions/interpretation: We concluded that functional abolition of CB activity restores insulin sensitivity and glucose homeostasis by positively affecting insulin signalling pathways in visceral adipose tissue and liver.