No abstract

Dietary sodium intake for freshwater salmonids feeding in the wild (invertebrate diet) or in captivity (pellet diet) was calculated and compared with published branchial sodium influx values. Dietary sodium intake (mmol kg-' per month) increases from winter minimum values of 5 and 3C-40 to reach maximum values in summer of 175 and 240 for invertebrate and pellet diet, respectively. In summer, dietary sodium intake for fish feeding in the wild was of the same magnitude as branchial sodium influx. The implications of dietary sodium intake for sodium balance in freshwater fish are discussed.

AimTo investigate glucose and insulin metabolism in participants with ataxia telangiectasia in the absence of a diagnosis of diabetes.MethodsA standard oral glucose tolerance test was performed in participants with ataxia telangiectasia (n = 10) and in a control cohort (n = 10). Serial glucose and insulin measurements were taken to permit cohort comparisons of glucose‐insulin homeostasis and indices of insulin secretion and sensitivity.ResultsDuring the oral glucose tolerance test, the 2‐h glucose (6.75 vs 4.93 mmol/l; P = 0.029), insulin concentrations (285.6 vs 148.5 pmol/l; P = 0.043), incremental area under the curve for glucose (314 vs 161 mmol/l/min; P = 0.036) and incremental area under the curve for insulin (37,720 vs 18,080 pmol/l/min; P = 0.03) were higher in participants with ataxia telangiectasia than in the controls. There were no significant differences between groups in fasting glucose, insulin concentrations or insulinogenic index measurement (0.94 vs 0.95; P = 0.95). The Matsuda index, reflecting whole‐body insulin sensitivity, was lower in participants with ataxia telangiectasia (5.96 vs 11.03; P = 0.019) than in control subjects.ConclusionsMutations in Ataxia Telangiectasia Mutated (ATM) that cause ataxia telangiectasia are associated with elevated glycaemia and low insulin sensitivity in participants without diabetes. This indicates a role of ATM in glucose and insulin metabolic pathways.

Rainbow trout fed a normal salt diet (1.3% NaCl) or a high salt diet (12% NaCl for at least 6 months) were chronically cannulated in the dorsal aorta and received 10 μg kg(-1) ANP (1-28 human, UBC-Bioproducts) infused over a 10 min period. This had an insignificant influence on sodium balance, blood electrolytes and branchial sodium fluxes. In fish given a normal diet, the blood pressure and heart rate were uninfluenced by ANP, but pulse pressure was reduced by on average 60% and in some cases was not evident at all. Blood pressure in the fish fed a high salt diet was significantly higher than in the control fish; this together with heart rate and pulse pressure was not affected by ANP administration.

Dietary Na+ loads (0.5­70 mmol kg-1 fish) were almost completely absorbed within 7 h, and branchial Na+ excretion commenced within 1 h. Na+ loads of less than 1 mmol kg-1 were lost through the gills through a significant decrease in Na+ influx with unaltered Na+ efflux rate (compared with Na+ fluxes in unfed fish). At higher salt loads (>18 mmol kg-1), Na+ loss increased as a result of significantly higher Na+ efflux rates, with no further decrease in Na+ influx rate. Tissue Na+ concentrations were unchanged, apart from a significant increase in blood plasma Na+ concentration in fish loaded above 18 mmol kg-1. The results show that branchial Na+ fluxes may be rapidly adjusted in response to prevailing conditions, and possible control mechanisms are discussed.