Factors influencing submerged macrophyte presence in fresh and brackish eutrophic waters and their impact on carbon emissions

In agricultural landscapes of North-Western Europe, the majority of water bodies do not meet the targets set by the European Water Framework Directive due to a lack of submerged macrophytes and associated biodiversity. These eutrophic waters can also be a substantial source of methane (CH4) and carbon dioxide (CO2) to the atmosphere. Here we present a two-year field experiment on the island of Goeree-Overflakkee (southwest Netherlands), conducted in six drainage ditches varying in salinity, where we monitored four permanent plots per ditch and varied the presence of both fish and macrophytes. We aimed to: 1) investigate factors limiting submerged macrophyte growth, focussing on exclusion of grazing pressure and bioturbation by fish; and 2) quantify the CO2 and CH4 emission under these conditions. Even in highly eutrophic, semi turbid ditches with fluctuating salinity levels and sulphide presence in the root zone, submerged macrophytes established successfully after introduction when the influence of grazing and bioturbation by fish was excluded. In the exclosures, diffusive CH4 and CO2 emissions, but not ebullitive CH4 emissions were significantly reduced. The spontaneous development of submerged macrophytes in the exclosures without macrophyte introduction underlined the effect of grazing and bioturbation by fish and suggest that abiotic conditions did not hamper submerged macrophyte development. Our results provide important insights into the influential factors for submerged macrophyte development and potential for future management practices. Large-scale fish removal may stimulate submerged macrophyte growth and reduce methane emissions, albeit that the macrophyte diversity will likely stay low in our study region due to fluctuating salinity and eutrophic conditions.</p

Rol del productor primario dominante y de la estructuratrófica asociada, sobre los flujos de carbono (CO2 y CH4) en lagos someros

ANII: POS_NAC_2017_1_14013

Primer registro de Cheloniidae (Testudines, Sauropsida) en el Mioceno tardío de Uruguay

La Formación Camacho de Edad Mamífero Huayqueriense (Mioceno tardío) es una unidad esencialmente de origen marginal marino (fluvio marino o estuarino). Aflora principalmente en las barrancas y plataformas costeras de los departamentos de San José y Colonia en el litoral oeste del territorio uruguayo y su fauna presenta un conjunto muy diverso de vertebrados, tanto continentales como marinos. El registro de vertebrados de origen marino consiste en diversos peces cartilaginosos, peces óseos y cetáceos. Entre la fauna de vertebrados de origen continental se encuentran especímenes bien preservados y de importancia bioestratigráfica correspondientes a los órdenes Rodentia, Litopterna, Notoungulata y Xenarthra, entre otros. El registro de Testudines ha sido pobremente estudiado en Uruguay, aunque son frecuentes los hallazgos en algunas unidades fosilíferas, principalmente cenozoicas y también mesozoicas. En la Formación Camacho sólo se ha registrado Phrynops (P. complex geofranus). Recientemente, un nuevo material fue hallado en las barrancas costeras de la localidad de San Pedro en el Departamento de Colonia, consistente en dos costillas costales, dos neurales y sus correspondientes vértebras, además de numerosos elementos indeterminados. Estos restos constituyen el primer hallazgo documentado de tortugas marinas (Cheloniidae) para el registro fósil de Uruguay y se asigna tentativamente a la Tribu Carettini debido a la evidente robustez de las placas y las costillas.Sesiones libresFacultad de Ciencias Naturales y Muse

Trophic and non-trophic effects of fish and macroinvertebrates on carbon emissions

Shallow aquatic systems exchange large amounts of carbon dioxide (CO2) and methane (CH4) with the atmosphere. The production and consumption of both gases is determined by the interplay between abiotic (such as oxygen availability) and biotic (such as community structure and trophic interactions) factors. Fish communities play a key role in driving carbon fluxes in benthic and pelagic habitats. Previous studies indicate that trophic interactions in the water column, as well as in the benthic zone can strongly affect aquatic CO2 and CH4 net emissions. However, the overall effect of fish on both pelagic and benthic processes remains largely unresolved, representing the main focus of our experimental study. We evaluated the effects of benthic and pelagic fish on zooplankton and macroinvertebrates; on CO2 and CH4 diffusion and ebullition, as well as on CH4 production and oxidation, using a full-factorial aquarium experiment. We compared five treatments: absence of fish (control); permanent presence of benthivorous fish (common carps, benthic) or zooplanktivorous fish (sticklebacks, pelagic); and intermittent presence of carps or sticklebacks. We found trophic and non-trophic effects of fish on CO2 and CH4 emissions. Intermittent presence of benthivorous fish promoted a short-term increase in CH4 ebullition, probably due to the physical disturbance of the sediment. As CH4 ebullition was the major contributor to the total greenhouse gas (GHG) emissions, incidental bioturbation by benthivorous fish was a key factor triggering total carbon emissions from our aquariums. Trophic effects impacted GHG dynamics in different ways in the water column and the sediment. Fish predation on zooplankton led to a top-down trophic cascade effect on methane-oxidising bacteria. This effect was, however, not strong enough as to substantially alter CH4 diffusion rates. Top-down trophic effects of zooplanktivorous and benthivorous fish on benthic macroinvertebrates, however, were more pronounced. Continuous fish predation reduced benthic macroinvertebrates biomass decreasing the oxygen penetration depth, which in turn strongly reduced water–atmosphere CO2 fluxes while it increased CH4 emission. Our work shows that fish can strongly impact GHG production and consumption processes as well as emission pathways, through trophic and non-trophic effects. Furthermore, our findings suggest their impact on benthic organisms is an important factor regulating carbon (CO2 and CH4) emissions

Uroguanylin prevents hepatic steatosis, mitochondrial dysfunction and fibrosis in obesity-associated NAFLD

Background: The biological mediators supporting the resolution of liver steatosis, inflammation and fibrosis after bariatric surgery in patients with obesity and NAFLD remain unclear. We sought to analyze whether uroguanylin and guanylin, two gut hormones involved in the regulation of satiety, food preference and adiposity, are involved in the amelioration of obesity-associated NAFLD after bariatric surgery. Methods: Proguanylin (GUCA2A) and prouroguanylin (GUCA2B) were measured in 214 participants undergoing bariatric surgery with biopsy-proven NAFLD diagnosis. Pathways involved in lipid metabolism, mitochondrial network and fibrogenesis were evaluated in liver biopsies (n = 137). The effect of guanylin and uroguanylin on these metabolic functions was assessed in HepG2 hepatocytes and LX-2 hepatic stellate cells (HSC) under lipotoxic and profibrogenic conditions. Results: Plasma and hepatic expression of GUCA2B were decreased in obesity-associated NAFLD. Both GUCA2A and GUCA2B levels were increased after sleeve gastrectomy and Roux-en-Y gastric bypass in parallel to the improved liver function. The liver of patients with type 2 diabetes showed impaired mitochondrial β-oxidation, biogenesis, dynamics as well as increased fibrosis. Uroguanylin diminished the lipotoxicity in palmitate-treated HepG2 hepatocytes, evidenced by decresased steatosis and lipogenic factors, as well as increased mitochondrial network expression, AMPK-induced β-oxidation and oxygen consumption rate. Additionally, uroguanylin, but not guanylin, reversed HSC myofibroblast transdifferentiation as well as fibrogenesis after TGF-β1 stimulation. Conclusions: Uroguanylin constitutes a protective factor against lipotoxicity, mitochondrial dysfunction and fibrosis. Increased GUCA2B levels might contribute to improve liver injury in patients with obesity-associated NAFLD after bariatric surgery

Uroguanylin prevents hepatic steatosis, mitochondrial dysfunction and fibrosis in obesity-associated NAFLD

Background: The biological mediators supporting the resolution of liver steatosis, inflammation and fibrosis after bariatric surgery in patients with obesity and NAFLD remain unclear. We sought to analyze whether uroguanylin and guanylin, two gut hormones involved in the regulation of satiety, food preference and adiposity, are involved in the amelioration of obesity-associated NAFLD after bariatric surgery. Methods: Proguanylin (GUCA2A) and prouroguanylin (GUCA2B) were measured in 214 participants undergoing bariatric surgery with biopsy-proven NAFLD diagnosis. Pathways involved in lipid metabolism, mitochondrial network and fibrogenesis were evaluated in liver biopsies (n = 137). The effect of guanylin and uroguanylin on these metabolic functions was assessed in HepG2 hepatocytes and LX-2 hepatic stellate cells (HSC) under lipotoxic and profibrogenic conditions. Results: Plasma and hepatic expression of GUCA2B were decreased in obesity-associated NAFLD. Both GUCA2A and GUCA2B levels were increased after sleeve gastrectomy and Roux-en-Y gastric bypass in parallel to the improved liver function. The liver of patients with type 2 diabetes showed impaired mitochondrial β-oxidation, biogenesis, dynamics as well as increased fibrosis. Uroguanylin diminished the lipotoxicity in palmitate-treated HepG2 hepatocytes, evidenced by decresased steatosis and lipogenic factors, as well as increased mitochondrial network expression, AMPK-induced β-oxidation and oxygen consumption rate. Additionally, uroguanylin, but not guanylin, reversed HSC myofibroblast transdifferentiation as well as fibrogenesis after TGF-β1 stimulation. Conclusions: Uroguanylin constitutes a protective factor against lipotoxicity, mitochondrial dysfunction and fibrosis. Increased GUCA2B levels might contribute to improve liver injury in patients with obesity-associated NAFLD after bariatric surgery