1. Serum postheparin lipolytic activities (PHLA), triglyceride and free fatty acid concentrations were determined in children with kwashiorkor before and after treatment and also in normal control children.

2. Using the range (571–1650 μmol/l) of serum triglyceride of the control children as normal, five (20%) of the twenty-five children with kwashiorkor had low (less than 570μmol/l), thirteen (52%) had normal (571–1650, μmol/l) and seven (28%) had high (more than 1650 μmol/l) serum triglyceride levels.

3. The serum PHLA did not show any definite correlation with the level of circulating triglycerides, although the lowest levels of PHLA were found in the malnourished children with highest triglyceride level.

4. While the hepatic PHLA in the malnourished children was significantly less than control value, the extrahepatic PHLA did not differ significantly.

5. After treatment, serum PHLA rose significantly and the mean levels were within normal range.

6. Our findings suggest that a defect in catabolism of very-low-density lipoprotein caused by a low hepatic PHLA may cause hypertriglyceridaemia in children with kwashiorkor.

1.The anthropometric measurements and neurointegrative performance of seventy-nine children aged 6–12 years who had survived kwashiorkor in early childhood were compared to those of 142 children who served as controls.

2. For the boys the differences in height and weight between those who had survived protein-energy malnutrition (PEM) and the controls were significant (P < 0.01).

3. For the girls the differences in height and weight between those who had survived PEM and the controls were not significant.

4. In the tests chosen, the performances of the survivors of PEM was significantly poorer than that of the controls.

5. There was no improvement in the performance when thirteen survivors were reassessed at 10 years of age.

6. There was a significant difference in scholastic performance between the survivors of PEM and the normal controls. The scholastic performance of the siblings of PEM survivors was also significantly better than that of the PEM survivors.

7. The dietary intakes at the time of reassessment were unsatisfactory in 25% of the survivors, but did not relate to their scholastic abilities.

1. The heart-rate (HR) method for determining the energy expenditure of free-living subjects has been evaluated using a whole-body calorimete in which individuals lived continuously for 27 h while carrying out normal daily activities. Eight male volunteers each occupied the calorimeter on at least two occasions when HR and energy expenditure were measured continously.

2. After each session in the calorimeter a calibration was obtained using standard techniques by determining HR and heat production (HP) over periods of 10–15 min at several levels of activity. Energy expenditure in the calorimeter was then predicted, by each of five methods, from the mean HR in the calorimeter. Additionally, one session in the calorimeter was used to obtain a calibration and was used for predicting the subject's energy expenditure while in the calorimeter on other occasions.

3. Standard methods of prediction using one calibration point at rest and several points during activity were unreliable for predicting the energy expenditure of an individual. The 24 h HR was at the lower end of the calibration scale and there were considerable over-estimates or underestimates of energy expenditure, particularly during the night when the mean (±SD) difference between the actual and predicted HP was −66±38±6%. A linear regression fitted to points at the lower levels of activity improved the prediction of 24 h HP while a logistic plot reduced the error even further. The best estimate of energy expenditure was that obtained from a calibration over 24 h within the calorimeter; the mean (±SD) difference between the actual and predicted 24 h HP was +3+10.5% for light activity and −3±6.7% for moderate activity. Thus current procedures for calibrating subjects may lead to large errors which could be reduced by using a respiratory chamber.

1. Ascorbic acid was absorbed across the mucosa of the human mounth.

2. Omission of sodium ions from the medium decreased the absorption of ascorbic acid.

3. The presence of D-glucose, or 3-O-methyl-D-glucose, incrased the absorption of ascorbic acid but D-fructose had little effect and D-mannitol had no effect.

4. Calcium ions also increased ascorbic acid absorption probably by a secondary effect on Na+ fluxes.

5. Buccal mucosa was also premeable to dehydroascorbic acid and D-isoascorbic. acid

1. The effect of pectin on the structure and function of the rat small intestine was compared with that of a standard pellet diet and of a fibre-free basal diet.

2. The length and wet weight of the small bowel was significantly greater inpect in-fed rats than in either pellet- or basal-diet-fed rats.

3. Histological measurements of longitudinal sections from the small bowel showed a significantly greater crypt depth and muscle layer thickness in the mid-jejunum and ileum of the pectin fed rats. Villous height showed less variation.

4. The specific activity of alkaline phosphatase (EC 3.1.3.1)and leucyl-P-naphthylamidase (EC 3.4.11.1) in mucosal scrapings was significantly lower in the upper jejunum of pectin-fed rats compared with either of the other dietary groups. The differences were not so marked in mid-jejunum or ileum.

5. Glucose absorption measured in vivo from jejunal and ileal loops was similar in all three dietary groups.

6. With two minor exceptions there were no significant differences in any of these measurements between the pellet- and basal-diet-fed rats.

7. These findings could be explained by increased epithelial cell turnover caused by pectin. The possible mechanisms of this are discussed.

8. The effect of pectin on the human small bowel requires study before it can be widely prescribed in man.

1. A new apparatus is described with which it is possible to measure the volume (and hence density) of obese patients without requiring them to immerse totally in water. Replicate measurements of subjects with 6, 23 and 38 kg body fat had a standard deviation not greater than 0.3 kg fat.

2. In nineteen obese women body fat was measured by density, total body water, and total body potassium at the beginning, and again at the end, of a period of 3–4 weeks on a reducing diet, during which they lost 5.43 (SD 1.83) kg in weight. The composition of weight loss was also estimated both by energy balance and nitrogen balance during the interval between the two measurements of body composition.

3. The estimates of fat content of the nineteen women at the start of the balance period were 45.63 (SD 14.50)kg by density, 48.07 (SD 13.88) kg by K and 47.09 (SD 13.85) kg by water. The correlation coefficient between the density and K estimate was 0–949, and for the density and water estimate it was 0.971.

4. It is concluded that measurement of density by the new method provides a convenient method for estimating body fatness, and change in fat content, which compares favourably with estimates based on total body water or total body K. However, these methods cannot be used to provide an accurate estimate of the composition of a small weight loss in an individual since deviations up to 4 kg fat occur between fat loss based on change in density and those based on the more reliable (but more tedious) energy balance method.

1. Rats were made oedematous by feeding them low-protein diets (protein: energy (P:E) 0.005) ad lib., and measurements were made of plasma and interstitial fluid colloid osmotic pressures (πp and πi respectively) and interstitial fluid hydrostatic pressure (Pi) before, and at the onset of, oedema formation. Taken together as (πp − πi + Pi) these forces oppose capillary pressure (Pc) and thus determine rates of transcapillary water filtration. Interstitial fluid was sampled, in non-oedematous and oedematous animals, from perforated capsules implanted subcutaneously for the measurement of Pi. Blood, plasma and interstitial fluid volumes were also determined.

2. In Expt I comparisons were made between animals fed on a control diet (P:E 0.210) and the lowprotein diet. In normal animals the ratio πp:πi was approximately 2, but in protein deficiency it was increased since reductions in the absolute value of πi matched those in πp. These changes were observed 2 weeks after the start of the experiment and became more exaggerated when oedema appeared (weeks 18–22).

3. Pi was normally negative with respect to atmospheric pressure but increased to values close to zero when oedema formation occurred.

4. Despite the reductions in πp that were seen in the protein-deficient animals the sum of the forces opposing filtration (πp − πi + Pi) did not change significantly during the experiment.

5. Plasma and interstitial fluid volumes expressed per kg body-weight (measured using 125I-albumin and 35SO42−) were unchanged as πp initially decreased in the protein-deficient animals but increased markedly with the onset of oedema.

6. In Expt 2 comparisons were made between animals fed the low-protein diet ad lib. and others fed on the control diet in restricted amounts so that weight loss was the same in the two groups of animals.

7. The wasting induced by restriction of the control diet did not produce reductions in πp or πi and values for Pi were normal. Changes in the animals fed on the low-protein diet were similar to those observed in Expt I. By using 51Cr-labelled erythrocytes it was shown that the expansion in plasma volume that occurred when oedema appeared in the protein-deficient animals was mainly due to a reduction in total erythrocyte volume. Blood volume did not increase significantly.

8. It was concluded that in the hypoproteinaemia induced in the experimental animals reductions in the value of πp, which might otherwise result in an imbalance of forces that would produce excessive rates of transcapillary water filtration, were compensated for by reductions in πi. Increases in Pi also compensated but were quantitatively less important.

9. The significance of the results is discussed in terms of the pathogenesis of oedema in kwashiorkor and the concept of an oncotic threshold for oedema formation in hypoproteinaemia.

1. Groups of lean and genetically obese (ob/ob) mice were adapted to varying energy intakes and the rates of total protein turnover in liver, gut and kidney were measured.

2. Lean mice gained less weight when fed above maintenance and lost less weight when fed below maintenance than obese mice.

3. Hepatic protein turnover (mg/d) was sigmoidally related to digestible energy intake in lean mice but showed no significant changes with dietary intake in obese mice.

4. The changes in protein turnover resulted from changes in both the half-lives of protein synthesis and catabolism and in tissue protein content.

5. In the lean mice, protein turnover in kidney and gut was not significantly changed with increasing energy intake until the highest level was reached.

6. The findings suggest that protein turnover may be an important cycle for the regulation of energy balance in mice and that this cycle is impaired in the genetically obese (ob/ob) mice.

1. The effects on body composition, measured by direct techniques, of a controlled 25% body-surfacearea thermal injury have been studied in two groups of forty male Wistar rats.

2. The extent of weight loss in the animals was directly related to their energy deficit resulting from a combination of injury, food intake and rate of wound healing.

3. Body fat proved the most labile source of tissue energy, decreasing to a minimum of approximately 30 g/kg body-weight.

4. Relationships between water and fat, and water and protein seen in control animals were not significantly different in the traumatized group.

1. Long-term clinical and biochemical riboflavin status and dietary intake of riboflavin were monitored for 18 months in a group of twenty-three relatively-healthy elderly subjects living at home in the north of England.

2. Both dietary intake and biochemical status, as measured by the activation coefficient (stimulated: basal activity) of NAD(P)H2: glutathione oxidoreductase (EC 1.6.4.2), remained fairly constant for each individual and for most subjects the usual intake and biochemical status were characterized quite accurately by a single week's intake dietary record and a single measurement of the activation coefficient.

The expected relationship between biochemical status and dietary intake was present, but not strongly evident. There was a significant within-subject correlation between α values and the immediately preceding dietary intake; however the between-subject correlation between α values and dietary intake approached zero if the two subjects receiving long-term riboflavin supplements were omitted. Over the limited range of intakes observed in unsupplemented subjects, non-dietary factors evidently obscure the relationship.

4. Although eight subjects had average values above 1.2 for the activation coefficient, no excessively high values were observed, and no subject showed any clear-cut clinical deficiency symptoms.

1. In order to quantitatively assess the energetic significance of reduced thermoregulatory thermogenesis in the accumulation of excess body fat in genetically-obese (ob/ob) mice experiments have been conducted at four environmental temperatures (17, 23, 28 and 33°) in which young growing obese animals were pair-fed for 10 d to the ad lib. intake of lean siblings.

2. The food intake of the lean mice increased with decreasing environmental temperature: at 17° the intake was 86% higher than that at 33°.

3. The estimated gain in carcass energy of lean mice rose with increasing temperature, from 82 kJ at 17° to 150 kJ at 33°. The energy gain of the pair-fed obese mice was higher than that of the lean at all temperatures but showed a slight decrease with increasing temperature, from 231 kJ at 17° to 191 kJ at 33°.

4. Environmental temperature affected the ‘excess’ energy gain of the obese mice. At 17° the obese mice deposited 182% more energy than the lean but this difference decreased progressively with increasing temperature to 127, 62 and 27% more energy at 23, 28 and 33° respectively.

5. At all environmental temperatures the pair-fed obese mice deposited considerably less protein than their lean controls. The deposition ranged from 32% (at 17°) to 56% (at 28°) of that of the lean mice.

6. It is concluded that environmental temperature plays a major role in determining the excess energy gain of ob/ob mice receiving the same amount of food as lean controls, and that the low energy expenditure and consequent high metabolic efficiency of this mutant is due primarily to reduced thermoregulatory thermogenesis.

1. Erythrocyte, plasma and whole blood selenium concentrations and glutathione peroxidase (EC I.11. 1.9; GSHPx) activities were measured (1) in 104 healthy New Zealand residents living in Otago, a low-soil-Se area (2) in sixty-four surgical patients, including nineteen patients on total parenteral nutrition and twenty-three cancer patients (3) in fifty-two ‘overseas subjects’ (twenty-five visitors to Otago from outside New Zealand and twenty-seven Otago residents on return from overseas travel).

2. Blood Se concentrations reflected dietary Se intake; means for Otago patients, healthy subjects and overseas subjects were different (0043, 0.059, 0.136 μg Se/ml blood respectively) and mean for overseas residents was greater than for New Zealand overseas travellers.

3. Erythrocyte Se concentration was always greater than plasma Se, and plasma Se was a smaller pro- portion of erythrocyte Se for patients compared with the controls.

4. GSHPx activities were different in the three groups, and vaned directly with erythrocyte Se until a plateau was reached at approximately 0.14 μg Se/ml erythrocytes.

5. Overseas subjects showed no relationship between erythrocyte Se and GSHPx activity. This agrees with some overseas studies and the significance of this finding is discussed.

6. Plasma Se concentration remained the most sensitive index of short-term changes in Se status, and erythrocyte Se and GSHPx activities for long-term changes in New Zealand subjects. Use of these measure- ments for overseas subjects with higher blood levels is discussed.

1. The effects of feeding isolated saponins on plasma lipid concentrations and on concentrations of biliary and faecal bile acids and neutral sterols were studied in the rat.

2. The animals were given one of four diets, i.e. a standard low-cholesterol synthetic diet, the diet+10 g saponins/kg, the diet+10 g cholesterol/kg, the diet+10 g cholesterol+10 g saponins/kg.

3. Saponins partially reversed the hypercholesterolaemia caused by the high-cholesterol diet and increased both the rate of bile acid secretion and the faecal excretion of bile acids and neutral sterols. The proportionate contribution of the primary bile acids (particularly chenodeoxycholic) to faecal excretion was also increased by saponins.

4. The results are discussed in relation to the hypothesis that saponins act by inducing the adsorption of bile acids by dietary fibre.

1. Long-term clinical and biochemical vitamin C (ascorbic acid and dehydroascorbic acid) status and dietary intake of vitamin C were monitored for 18 months in twenty-three relatively-healthy elderly subjects living at home in the north of England.

2. Plasma vitamin C showed a strong positive correlation with buffy-coat vitamin C both cross-sectionally between subjects and longitudinally within subjects; plasma levels, therefore, were almost as good an index of long-term status as buffy-coat levels.

3. Vitamin C intake was strongly correlated with plasma and with buffy-coat levels both between subjects and within subjects. This contrasts with the poor correlation observed between riboflavin intake and biochemical riboflavin status in the same subjects.

4. Subjects with relatively high average intakes showed considerable seasonal variation, and several widely-spaced measurements would be needed to characterize their long-term status accurately. Those with low average intakes and blood levels showed little variation during the study.

5. The strongest within-subject correlation was obtained by relating the biochemical values to the 7 d dietary intake directly preceding the biochemical analysis. Blood and tissue levels therefore appear to be strongly related to the current dietary intake.

6. Although some subjects had blood vitamin C levels consistently within the region associated with biochemical deficiency, none showed clinical evidence of specific deficiency symptoms.

7. After the main study, fifteen of the subjects received supplementary vitamin C for 2 months. Plasma and buffy-coat levels rose sharphy, but fell to presupplementation levels within 1 month of withdrawal, emphasizing the transitory nature of increased tissue levels. No significant changes were detected in the following collagen-related urinary ratios: hydroxyproline: creatinine, proline: creatinine, proline: total amino-nitrogen and proline: hydroxyproline in hydrolysates either of whole urine or of various fractions. These variables thus appear to be insensitive to short-term changes in vitamin C status over the ranges encountered in this study.

1. Plasma tyrosine and urinary p-hydroxyphenyl lactic acid (PHPLA) and p-hydroxyphenyl acetic acid (PHPAA) were studied in thirty patients with marasmus and twenty normal controls in the same age group.

2. In the control group conventional tyrosyluria was not observed but 30% of the group excreted high levels of PHPAA. In the group with marasmus, plasma tyrosine and urinary PHPLA and PHPAA values were significantly higher than the control values. However only 13.3% of the patients were considered to have conventional tyrosyluria and 52.3% were found to excrete high levels of PHPAA.

3. Administration of ascorbic acid resulted in a reduction of PHPLA excretion while it had no effect on PHPAA excretion.

4. It was inferred that (a) tyrosyluria in marasmus is due to the reduced activity of the hepatic enzyme 4-hydroxyphenyl pyruvate: oxygen oxidoreductase (hydroxylating, decarboxylating) (PHPPA-oxidase; EC 1. 13. 11. 27) due to the deficiency of ascorbic acid and (b) high excretion of PHPAA is related to age and nutrition of the child and is unaffected by the administration of ascorbic acid.

5. It was further inferred that urinary excretion of PHPLA is a reliable index of tyrosyluria.

1. It is shown that a basal roughage diet can be successfully supplemented with glucose, as long as nitrogen is not limiting. Lack of N depresses the digestibility of the basal ration, results in incomplete fermentation and the increased recoveries of N are consistent with fixation of atmospheric N2.

2. Using a complex, but soluble supplement (whey powder) it is shown that reproducible incremental measurements can be made and that the supplement used gives increases in production of characteristic end-products only (carbon dioxide, methane, acetic and butyric acids).

3. The location of the solid dietary components within the reaction vessel is not important and it is possible to measure changes in a particular component in the presence of others. It is shown that there is sequestration of bacteria and protozoa on the solid digesta.

1. Adipose tissue samples were obtained by needle biopsy from three subcutaneous sites (thigh, abdomen and upper arm) in twenty-two obese women. The fatty acid composition was determined using gas-liquid chromatography and the results presented relate to eleven component fatty acids.

2. The fatty acid composition of adipose tissue obtained from the arm and abdomen was remarkably similar, with the exception of the levels of lauric acid.

3. The analyses showed that the majority of the saturated fatty acids were present in smaller proportions whilist the majority of unsaturated fatty acids were present in larger proportions in the thigh than in the two other sites. Highly significant inter-site differences were demonstrated for six of the major fatty acids and also for both the total amounts of saturated and unsaturated fatty acids and their ratios.

4. No marked differences in the fatty acid composition of adipose tissue from obese subjects were revealed during this study when compared with previously reported results obtained from ‘normal-weight’ subjects.