Schlienger J L, Sapin R, Imler M
C R Seances Soc Biol Fil. 1980;174(2):199-204.
In order to investigate the controverted effect of ammonia on insulin and glucagon secretion 3 groups of 55 rats were perfused either by Na+ acetate (controls), either by NH4+ acetate: in the first group plasma insulin (IRI) and glucagon (IRG) levels were compared before and after perfusion; the second group was supplemented by glucose perfusion (1 g/100 g/hour); in the last group an arginine perfusion (1 g/kg/min) was started 15 min after the beginning of NH4+ or Na acetate and IRI and IRG levels were determined in the portal blood. Hyperammonemia, which reached about 500 microgram/dl, reduced significantly the IRI portal level and the IRI secretion induced by glucose or arginine, whereas basal or stimulated IRG levels are not modified. The ratio IRI:IRG is diminished in each group perfused with NH4+ acetate. Our results show that ammonia inhibits insulin without modifications in the glucagon secretion; hyperglucagonemia and hyperinsulinism reported in hepatic encephalopathy with chronic hyperammonemia may not be attributed to an effect of ammonia.
为了研究氨对胰岛素和胰高血糖素分泌的争议性作用，将3组每组55只大鼠分别用乙酸钠（对照组）或乙酸铵进行灌注：第一组在灌注前后比较血浆胰岛素（IRI）和胰高血糖素（IRG）水平；第二组通过葡萄糖灌注（1 g/100 g/小时）进行补充；在最后一组中，在开始乙酸铵或乙酸钠灌注15分钟后开始精氨酸灌注（1 g/kg/分钟），并测定门静脉血中的IRI和IRG水平。高氨血症达到约500微克/分升，显著降低了门静脉IRI水平以及葡萄糖或精氨酸诱导的IRI分泌，而基础或刺激后的IRG水平未改变。在每组用乙酸铵灌注的大鼠中，IRI:IRG比值降低。我们的结果表明，氨抑制胰岛素分泌而不改变胰高血糖素分泌；在慢性高氨血症性肝性脑病中报道的高胰高血糖素血症和高胰岛素血症可能不能归因于氨的作用。
