In an attempt to assess the role of metabolic acidosis in the glucose intolerance of uremia, we have estimated insulinmediated glucose uptake in normal dogs, in acidotic dogs with normal renal function, and in uremic dogs. Mean steady state plasma glucose and insulin levels were measured in eighteen dogs (pH 7.4 ± .01) during constant infusion of glucose and insulin, while endogenous insulin secretion was suppressed by infusion of propranolol and epinephrine. The dogs were then divided into three groups: moderate acidosis was produced by giving 7 gm. NH4Cl/ day for four days; severe acidosis, 12 gm. NH4Cl/day for four days; and uremia (serum creatinine 15.7 ± 0.2 mg. per cent) by anastomosing both ureters to the vena cava. Duplicate infusions were then performed and the results compared to control values. Plasma insulin levels were identical, despite the presence of either acidosis or uremia. The mean increase in plasma glucose in moderate acidosis (pH 7.2 ± 0.1) over controls was 39 mg./l00 ml. (p < .05); in severe acidosis (pH 7.0 ± .04) plasma glucose increased by 69 mg,/100 ml. (p < .01). However, the mean increase in plasma glucose (149 mg./100 ml.) in uremia (pH 7.3 ± .03) was significantly greater (p < .005) than that following acidosis, although the pH did not significantly fall. Thus, although metabolic acidosis results in deterioration of glucose tolerance, the magnitude of the change does not seem able to account for the carbohydrate intolerance of uremia.

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