Ecological impacts of non-native Pacific oysters (Crassostrea gigas) and management measures for protected areas in Europe

Pacific oysters are now one of the most ‘globalised’ marine invertebrates. They dominate bivalve aquaculture production in many regions and wild populations are increasingly becoming established, with potential to displace native species and modify habitats and ecosystems. While some fishing communities may benefit from wild populations, there is now a tension between the continued production of Pacific oysters and risk to biodiversity, which is of particular concern within protected sites. The issue of the Pacific oyster therefore locates at the intersection between two policy areas: one concerning the conservation of protected habitats, the other relating to livelihoods and the socio-economics of coastal aquaculture and fishing communities. To help provide an informed basis for management decisions, we first summarise evidence for ecological impacts of wild Pacific oysters in representative coastal habitats. At local scales, it is clear that establishment of Pacific oysters can significantly alter diversity, community structure and ecosystem processes, with effects varying among habitats and locations and with the density of oysters. Less evidence is available to evaluate regional-scale impacts. A range of management measures have been applied to mitigate negative impacts of wild Pacific oysters and we develop recommendations which are consistent with the scientific evidence and believe compatible with multiple interests. We conclude that all stakeholders must engage in regional decision making to help minimise negative environmental impacts, and promote sustainable industry development

The role of energy metabolism in amino acid stimulated insulin release in pancreatic β-HC9 cells

Fuel stimulation of insulin secretion from pancreatic p-cells is thought to be me-diated by metabolic coupling factors that are generated by energized mitochondria, including protons, adenine nucleotides and perhaps certain amino acids, as for instance aspartate, glutamate or glutamine. The goal of the present study was to evaluate the role of such factors when insulin release (IR) is stimulated by glucose or amino acids (AA), alone or combined, using 31P-, 23Na- and 1H-NMR-technology, respirometry and biochemical analysis to study the metabolic events that occur in continuously superfused mouse β-HC9 cells contained in agarose beads and enhanced by the phosphodiesterase inhibitor IBMX. Exposing β-HC9 cells to high glucose or 3.5 mM of a physiological mixture of 18 AA plus 2 mM glutamine (Q) caused a marked stimulation of insulin secretion associated with increased oxygen consumption (V02), c-AMP release and phosphorylation potential (P-potential) as evidenced by higher Phosphocreatine (PCr) and lower Pi peak areas of 31P NMR spectra. Diazoxide blocked stimulation of IR completely suggesting involvement of KATP channels in this process. However, levels of [MgATP] and [MgADP] which regulate channel activity changed only slowly and little while the rate of insulin release increased fast and very markedly. The involvement of other candidate coupling factors was therefore considered. High glucose or AAM + Q increased intracellular pH. The availability of temporal pH profiles allowed the precise computation of the phosphate potential (ATP/P × ADP) in fuel stimulated IR. Intracellular Na+ levels were greatly elevated by AAM + Q. However, glutamine alone or together with 2-amino-2-norbornane-carboxylic acid (BCH, which activates glutamate dehydrogenase) decreased β-cell Na levels. Stimulation of β-cells by glucose in the presence of AAM + Q (0.5 mM) was associated with rising cellular concentrations of glutamate, glutamine and strikingly lower aspartate levels. Methionine sulfoximine (MSO), an inhibitor of glutamine synthetase, blocked the glucose enhancement of AMM + Q induced IR and associated changes in glutamine and aspartate but did not prevent the accumulation of glutamate. The results of this study demonstrate again that an increased phosphate potential and a functional KATP channel are essential for metabolic coupling during fuel stimulated insulin release but illustrate that determining the identity and relative importance of all participating coupling factors and second messengers remains a challenge largely unmet

The second activating glucokinase mutation (A456V): Implications for glucose homeostasis and diabetes therapy

In this study, a second case of hyperinsulinemic hypoglycemia due to activation of glucokinase is reported. The 14-year-old proband had a history of neonatal hypoglycemia, treated with diazoxide. He was admitted with coma and convulsions due to nonketotic hypoglycemia. His BMI was 34 kg/m(2), and his fasting blood glucose ranged from 2.1 to 2.7 mmol/l, associated with inappropriately high serum levels of insulin, C-peptide, and proinsulin. An oral glucose tolerance test (OGTT) showed exaggerated responses of these peptides followed by profound hypoglycemia. Treatment with diazoxide and chlorothiazide was effective. His mother never had clinical hypoglycemic symptoms, even though her fasting blood glucose ranged from 2.9 to 3.5 mmol/l. Increases in serum insulin, C-peptide, and proinsulin in response to an OGTT suggested a lower threshold for glucose-stimulated insulin release (GSIR). Screening for mutations in candidate genes revealed a heterozygous glucokinase mutation in exon 10, substituting valine for alanine at codon 456 (A456V) in the proband and his mother. The purified recombinant glutathionyl S-transferase fusion protein of the A456V glucokinase revealed a decreased glucose S-0.5 (the concentration of glucose needed to achieve the half-maximal rate of phosphorylation) from 8.04 (wild-type) to 2.53 mmol/l. The mutant's Hill coefficient was decreased, and its maximal specific activity k(cat) was increased. Mathematical modeling predicted a markedly lowered GSIR threshold of 1.5 mmol/l. The theoretical and practical implications are manifold and significant