Carbohydrate depletion has profound effects on the muscle amino acid and glucose metabolism during hyperinsulinaemia.

AIM: We investigated the effect of carbohydrate availability and euglycaemic hyperinsulinaemia on intramuscular and plasma amino acids in 14 healthy men (age 26.5 +/- 0.9 years, b.m.i. 22.9 +/- 0.5 kg/m2). METHODS: Insulin was infused (1.5 mU/kg/min) for 240 min both after a carbohydrate depleting exercise and after carbohydrate loading. Muscle samples were taken before and after hyperinsulinaemia. Plasma and intramuscular amino acid concentrations were measured. RESULTS: Insulin-mediated glucose disposal was similar after carbohydrate depletion (65.2 +/- 1.9 micromol/kg/min) and loading (66.9 +/- 2.8 micromol/kg/min). Carbohydrate depletion was associated with decreased alanine and increased branched chain amino acid (BCAA) concentrations in muscle and plasma. Blood lactate was lower after carbohydrate depletion (477 +/- 25 micromol/l) than loading (850 +/- 76 micromol/l, p < 0.001). In carbohydrate depletion, hyperinsulinaemia resulted in a greater increase in intramuscular (from 927 +/- 48 nmol/g muscle to 2029 +/- 104 nmol/g muscle, p < 0.001), than plasma (from 197 +/- 6.7 micromol/l to 267 +/- 11 micromol/l, p < 0.001) alanine. After carbohydrate loading muscle alanine did not rise significantly (from 1546 +/- 112 nmol/g muscle to 1781 +/- 71 nmol/g muscle) whereas plasma alanine decreased (from 339 +/- 26 micromol/l to 272 +/- 13 micromol/l, p < 0.05). CONCLUSIONS: (1) Carbohydrate availability has profound effects on the interrelationship between glucose and amino acid metabolism and on the form of storage for glucose-derived carbons. (2) For most amino acids changes in plasma levels of amino acids are not related to changes in concentrations of intramuscular amino acids during hyperinsulinaemia.

Fibronectin concentration in cerebrospinal fluid reflects early central nervous system involvement in children with acute lymphoblastic leukemia.

We measured concentrations of fibronectin (FN) in the cerebrospinal fluid (CSF) in long-term follow-up patients with acute lymphoblastic leukemia (ALL). In 11 patients with neuroleukemia the CSF-FN level was elevated already at the time of diagnosis of ALL, 3.8 +/- 0.6 mg/l, increased during therapy to 4.7 +/- 0.5 mg/l, and at the time of concurrent blast cell finding it was 5.5 +/- 1.0 mg/l. In 11 patients with no subsequent CNS leukemia, the mean CSF-FN level was 2.4 +/- 0.6 mg/l at the time of diagnosis of ALL and 2.8 +/- 0.6 mg/l during therapy, and increased to 3.2 +/- 0.8 mg/l. The neuroleukemia rate was 43% in patients with initial CSF-FN levels greater than 2 mg/l, compared with 5% in patients with CSF-FN levels less than or equal to 2 mg/l (p less than 0.005) in a group of 45 long-term follow-up patients with ALL. Regression analysis on the 21 clinical or laboratory parameters studied showed that the only variable independently associated with CSF-FN was the total protein concentration in the CSF; this, however, explained only 14% of the observed variation in the CSF-FN concentration and did not show any correlation with CNS involvement. We conclude that the CSF-FN test at diagnosis of ALL showed significant differences between groups of patients with and without CNS leukemia, and may prove to be a new early marker for neuroleukemia.

Proteinuria in congenital nephrotic syndrome of the Finnish type.

The pattern of urinary protein excretion was followed for 2 to 19 months in 15 children with the congenital nephrotic syndrome of the Finnish type. The duration of the disease and the renal histopathological changes were correlated with the urinary total protein and albumin excretion, the sieving coefficients of five proteins, the selectivity angle based on relative clearances of four proteins, and the excretion of beta-2-microglobulin. Total urinary protein excretion increased with time; in general, the proteinuria was of glomerular type and highly selective. With advancing histological lesions selectivity declined corresponding to the increases in individual sieving coefficients, and there were signs of secondary tubular impairment as shown by increased beta-2-microglobulin excretion. Of the histopathological changes, tubular atrophy correlated best with the various measures of proteinuria. The findings support the concept of a primary glomerular disease with secondary tubular injury.