Special report on Quebec creates controversy.
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Biomedical subjects
Publications and source records attributed to M Golden.
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Our pilot study compared the short-term glycemic effects of a traditional "sucrose free" diet (Suc-Free, 2% total calories from sucrose) to a sucrose-containing diet (Suc-Con, 10% total calories from sucrose) in a clinical research center. Both weighed diets were isocaloric and included 50% carbohydrate, 30% fat, and 20% protein in three meals and three snacks; glucose, fructose, and dietary fiber were identical. Sucrose isocalorically replaced complex carbohydrate at each meal and for the afternoon snack. Ten children (7 to 12 years of age; mean total hemoglobin A1 level 8.9 +/- 0.3%) were randomly assigned, in a crossover design, to one of the two orders (Suc-Free followed by Suc-Con or Suc-Con followed by Suc-Free) for consecutive 2-day diet periods; insulin doses remained constant. Preprandial and postprandial blood glucose levels were measured for each meal and snack (18 measurements per day). To account for baseline differences, we calculated the change in blood glucose levels from baseline to 30 minutes and 1 hour for each meal and snack (mean +/- SEM). No differences were detected between diets. Total area under the glucose response curve (levels measured hourly from 8 AM to 9:30 PM in milligrams per deciliter) was not significantly different for the two diets (Suc-Free 3672 +/- 240; Suc-Con 3574 +/- 285; p = 0.74). No difference in 24-hour urinary glucose levels (measured in grams per day) was detected between the two diets (Suc-Free 35.6 +/- 7.5; Suc-Con 34.5 +/- 7.5; p = 0.84). Incidences of hyperglycemia that required supplemental short-acting insulin and of mild hypoglycemia were similar for both diet periods. Thus, in a controlled setting and during a short study period, children with insulin-dependent diabetes mellitus had a similar glycemic response to diets with and without a moderate amount of sucrose.
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Red cells in oedematous malnutrition (kwashiorkor) have an increased sodium content, 'leakiness' to sodium and enhanced sodium pumping. In non-oedematous malnutrition (marasmus) there is a reduction in the sodium pump activity. The explanation has hitherto been unknown but the glutathione content of red cells is low in kwashiorkor and normal in marasmus. We artificially lowered the glutathione content of normal red cells to values characteristic of mild oedematous malnutrition, using the enzyme inhibitors bischloronitrosourea (BCNU) and buthionine sulfoximine (BSOX). After preincubation, the cells were washed to remove the inhibitors and oxidized glutathione. Cellular content of sodium and potassium, and 86Rb influx were then measured. The reduction in glutathione reproduced the abnormalities of sodium content and flux observed in kwashiorkor. We suggest that oxidant stress in kwashiorkor, by reducing cellular glutathione, may affect cell membrane electrolyte transport. This may act through alterations in membrane sulfhydryl groups. Glutathione depletion may therefore play an important role in the clinical picture and natural history of oedematous malnutrition and may have relevance to other conditions where oxidant stress occurs.
Sequential neurological and intellectual recovery after childhood near-drowning is discussed. Decisions concerning the persistence and intensity of resuscitation require a knowledge of the natural history of intellectual improvement after rescue from near-drowning. A severe case of fresh-water immersion, leading to recovery, is described. Evidence is presented to suggest that the time interval of one hour before the first spontaneous respiratory gasp forms the upper limit of the apnoeic time bracket after which survival can still be expected, and to indicate that intellectual improvement (to a measured IQ of 97) can occur even after initial decerebrate signs if vigorous therapy is prosecuted. The proportion of cases capable of sequential neurological improvement is unknown. A time base for sequential clinical and intellectual improvement after near-drowning is presented to form a yardstick with which future cases may be compared.
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We have examined the relationships between protein turnover, protein synthesis, and protein breakdown and dietary intake, weight change, and nitrogen balance in children who were recovering and had recovered from severe protein-energy-malnutrition. Protein metabolism was measured by giving [15N]glycine and measuring the enrichment of urinary urea. The level of dietary protein did not affect protein metabolism. There were highly significant correlations between both protein flux and protein synthesis and the ad libitum dietary intake, nitrogen balance, and weight change. Over the range of dietary intake, 60 to 270 cal/kg per day, the protein synthesis rate increased 5-fold. Large changes in dietary intake resulted in small changes in protein breakdown, with breakdown being least on an inadequate intake. Changes in the rate of protein breakdown did not contribute to changes in nitrogen balance or body weight.
Intracellular electrolytes and sodium transport were measured in leukocytes obtained from malnourished children. In the presence of edema, leukocyte sodium and potassium were raised. The total flux and the glycoside-sensitive portion were increased. Loss of edema was associated with reductions in all these measurements. In marasmus, glycoside-sensitive sodium efflux was reduced compared to recovered values. Sodium was increased and potassium reduced. It is concluded that at least two defects in sodium transport may occur in protein energy malnutrition, an increased passive permeability in kwashiorkor and a reduced active transport for sodium in marasmus.
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