Growth rates in children recovering from protein-calorie malnutrition

Compensatory, or 'catch-up', growth in eight malnourished children has been studied in relation to foods intake, efficiency of food utilization and changes in body composition. During recovery, growth rates were fifteen times as fast as those of normal children of similar age, and five times as fast as those of normal children of a similar height or weight. Rapid growth was associated with a high food intake. When the expected weight for height was reached food intakes fell abruptly by 30 percent and growth rates dropped to a level comparable with those of normal children of that height and weight. Food conversion figures suggest an over-all increase in the efficiency of food utilization during rapid growth. The percentage body fat increased, once the expected weight for height was reached. Differences in the rates of weight gain from those predicted by the Miller-Payne equation were difficult to interpret: problems associated with the equation are discussed. (AU)

Studies on the effect of diet on hepatic lipogenesis

This thesis is an account of investigation in which special diets were fed to rats and the resulting effects on hepatic lipogenesis studied. The carbohydrate and fat contents of the diets were varied and groups of rats on the different diets compared. It was shown in a test system consisting of liver slices that rats, which were previously fed for two days on a relatively high carbohydrate diet, incorporated the carbon of 14C labelled glucose into fatty acids and carbon dioxide at an increased rate when compared with rats fed a relatively low and a control diet. Hepatic glucose - 6 - phosphatase activity was not altered by feeding the different diets. Liver glycogen concentrations was also unaltered. The ratio of this concentrations of oxidised to reduced diphosphopyridine nucleotide in liver was higher for rats on the "high" carbohydrate diet than for rats on the "low" carbohydrate and the control diets. The concentration of reduced triphosphopyridine nucleotide in liver was decreased by feeding the "high" carbohydrate diet. The plasma "insulin activity" of the rats on the "high" carbohydrate diet was less than that of rats on the "low" carbohydrate diet. There was no significant difference between the "insulin binding" capacity of the livers of rats fed the "high" and "low" carbohydrate diets. It was not possible to offer any explanation, from the experimental results, of how the "high" carbohydrate diet caused an increase in hepatic lipogenesis (AU)