Bioaccumulation Trends of Ten Metals in a Pelagic Food Web of Lake Champlain

Many metals have serious toxic effects when ingested by aquatic organisms, and the process of bioaccumulation intensifies this problem. A better understanding of bioaccumulation trends of anthropogenically introduced metals in freshwater food webs is necessary for the development of effective management strategies to protect aquatic organisms, as well as organisms (including humans) that consume top-predator fish in these food webs. Various fish species representing different trophic levels of a pelagic food chain were sampled from Lake Champlain (VT/NY). Atomic absorption spectrometry (AAS) was used to determine levels of chromium, copper, cobalt, cadmium, lead, zinc, nickel, rubidium, cesium and potassium in the fish samples. Metal concentrations for chromium, cobalt, nickel, cesium, cadmium (<5.0 ppm) and lead (<10.0 ppm) were found to be all below detection limits. Carbon and nitrogen isotopic ratios were analyzed to determine the trophic relationship of each fish species. Stable isotope and AAS metal data were used in tandem to produce linear regressions for each metal against trophic level to assess biomagnification. Both potassium and zinc showed no biomagnification because they are homeostatically regulated essential trace metals. Copper was under the detection limits for all fish species with the exception of the sea lamprey; but showed a significant biodiminution among the invertebrates and lamprey. Rubidium, a rarely studied metal, was shown to increase with trophic level in a marginally significant linear relationship suggesting biomagnification is possible where more trophic levels are sampled.

The Function of Intestinal Afferent Neurons in Regulating Satiety During Health and Obesity

Background and aim: Within the gastrointestinal tract, vagal afferents regulate satiety and food intake via chemical and mechanical mechanisms. Cysteinyl Leukotrienes (CysLTs) are lipid mediators that are believed to regulate food intake and body weight. However, the involvement of vagal afferents in this effect remains to be established. Conversely, Glucagon like peptide-1 (GLP-1) is a satiety and incretin peptide hormone. The effect of obesity on GLP-1 mediated gut-brain signaling has yet to be investigated. Since intestinal vagal afferents’ activity is reduced during obesity, it is intriguing to investigate their responses to GLP-1 in such conditions. Methods: Extracellular recordings were performed on intestinal afferents from normal C57Bl6, low fat fed (LFF), and high fat fed (HFF) mice. To examine the effect on neuronal calcium signaling, calcium-imaging experiments were performed on isolated nodose ganglion neurons. Food intake experiments were conducted using LFF and HFF mice. Oral glucose tolerance tests (OGTT) were carried out. Whole cell patch clamp recordings were performed on nodose ganglion neurons from A) normal C57Bl mice to test the effect of CysLTs on membrane excitability, B) LFF and HFF mice to examine GLP-1 effect on membrane excitability during obesity. c-Fos immunohistochemical techniques were performed to measure the level of neuronal activation in the brainstem of both LFF and HFF mice in response to Ex-4. Results: CysLTs increased intestinal afferent firing rate and mechanosensitivity. In single nodose neuron experiments, CysLTs increased excitability. The GLP-1 agonist Ex-4 significantly decreased food intake in LFF but not HFF mice. However, Ex-4 markedly attenuated the rise in blood glucose in both LFF and HFF mice. The observed increase in nerve firing and mechanosensitivity following the application of GLP-1 and Ex-4 was abolished in HFF mice. Cell membrane excitability was significantly increased by Ex-4 in nodose from LFF but not HFF mice. Ex-4 significantly increased the number of activated neurons in the NTS area of LFF mice but not in their HFF counterparts. Conclusion: The previous observations indicate that the role CysLTs play in regulating satiety is likely to be vagally mediated. Also that satiety, but not incretin, effects of GLP-1 are impaired during obesity.