OBJECTIVES: To examine the hypothesis that a sustained rise in plasma acylation stimulating protein (ASP, C3a desarg) accompanies the elevation in triacylglycerol that follows the ingestion of an oral fat load. DESIGN: Following an overnight fast, blood samples were obtained from healthy volunteers while fasting and 15 min, 1, 2, 4, 6 and 8 h following ingestion of: (i) a liquid meal, rich in dairy fat (eight subjects) and (ii) a semi-liquid meal, with higher total fat content and rich in polyunsaturated fat (six subjects). SUBJECTS AND METHODS: Four male and four female volunteers (age range: 22 ± 51 y; body mass index (BMI): 17.9 ± 26.9 kgam 2 ) received the ®rst meal. Six subjects (age range: 32 ± 60 y; BMI: 18.0 ± 28.4 kgam 2 ), including three from the ®rst study, received the second meal using the same protocol. ASP and C5a were measured by radioimmunoassay (RIA) and the complement proteins C3, factor B and C5 by radial immunodiffusion or nephelometry. Tumour necrosis factor (TNF)-a was measured by enhanced ELISA, and plasma cholesterol and triacylglycerol by an automated enzymatic method. The presence of chylomicrons was assessed in post-prandial plasma samples taken after the second meal. RESULTS: There was no signi®cant change in mean ASP concentration in either group at any time point, following ingestion of either meal. However, there was a signi®cant positive linear trend in ASP following the second fat challenge (ANOVA; P`0.05). There was also no change in complement proteins, plasma cholesterol or TNF-a. Plasma triacylglycerol rose signi®cantly after the ®rst and second meals (P`0.05 and P`0.001 at 2 h post-prandially); the mean maximum rise above the fasting level was 58 AE 41% and 89 AE 38% respectively (mean AE s.d.). Chylomicrons were detected in samples taken from each subject after the second meal. Analysis of individual ASP data showed a sustained rise in one subject after the ®rst meal and two subjects after the second meal. Substantial variation in ASP concentration was observed in samples taken in the ®rst 2 h post-prandially. CONCLUSION: There was no signi®cant change in ASP nor other complement proteins for either group of subjects following ingestion of the lipid loads. Individual data showed substantial variation in post-prandial ASP, but multiple plasma sampling did not de®ne the basis for this variation.

Almost all cystic fibrosis patients develop hyperglycaemia after lung transplantation, but patients with prior diabetes have more complication-related admissions to hospital and a higher mortality rate.

Central adiposity carries an increased risk of non-insulin dependent diabetes mellitus (NIDDM), cardiac disease, hypertension and death, and is closely related to insulin resistance. Genetic factors explain a large proportion of the population variance in central adiposity, although the genotypic characteristics remain obscure. Hormonal factors such as endogenous sex steroid levels, the menopause, hormone replacement therapy and cortisol may in¯uence body fat partitioning. The link between dietary factors and central adiposity is controversial, with contradictory results in the literature. Smoking is associated with lower total body fat, but investigations of its in¯uence on central adiposity have also yielded contradictory results. Higher levels of physical activity are associated with lesser amounts of central fat, both cross-sectionally and in intervention studies. Some of the contradictory results regarding putative in¯uences on central adiposity may be due to limitations of some of the anthropometric parameters of central adiposity, such as the waist-hip ratio. Further research is required to clarify the relationships between many of these factors and with both compartments of central adiposity: subcutaneous abdominal and intraabdominal adipose tissue.

A low reported EI and greater BMI may help identify energy underreporters. However, whilst underreporters may more frequently be 'bigger' (by BMI), they are not necessarily fatter (using direct measures of body fat). As underreporting was present among all tertiles of BMI and adiposity, these results emphasise the importance of following past recommendations to identify and exclude energy underreporters in nutritional studies. Where underreporters have not been excluded, reported nutrition-disease relationships must remain in doubt.

OBJECTIVE:To construct a simple physiological model of leptin kinetics, based on measures of body size and composition, which is suitable for investigating the influence of genetic and other influences on circulating leptin levels in humans. METHODS: Consideration of the kinetics of the secretion and clearance of leptin led to a predicted linear relationship between ln(leptin), ln(fat mass), and a function of non-fat body compartments. Results obtained from this model were compared with those from two published empirical models based on adjustment for fat mass alone or for body mass index. Overnight fasted leptin levels, body composition data (dual-energy X-ray absorptiometry) and questionnaire responses were obtained from 527 twin pairs (127 monozygotic, 400 dizygotic; 37 male (age 18 -68 y, BMI 18 -32 kg=m 2 ), 489 female (age 18 -71, BMI 17 -44) drawn from the St Thomas' UK Adult Twin Registry. RESULTS: In a partial correlation analysis ln(fat mass) and ln(height) (r ¼ 0.80, P < 0.0001) and r ¼ 70.22, P < 0.0001 respectively) were independent predictors of ln(leptin) in females but ln(lean mass) was not (r ¼ 70.01). A regression model incorporating ln(fat mass), ln(height) and a second order polynomial in age provided an adequate fit of the ln(leptin) data in females (r 2 ¼ 71%). ln(Leptin) values adjusted for body size and composition using the model were not significantly heritable (P ¼ 0.11), were significantly related to gender (r 2 ¼ 2.3%) and to ln(insulin) (r 2 ¼ 5.7%), but not to menopausal status (r 2 ¼ 0.7%), hormone replacement therapy (r 2 ¼ 0.4%), past or current smoking (r 2 ¼ 1.1%), or percentage trunk fat (r 2 ¼ 0.5%). Both empirical models found significant heritability (h 2 ¼ 36 -42%), overestimated the effect of gender in the data (r 2 ¼ 14 -16%), and produced significant relationships between adjusted ln(leptin) and percentage trunk fat (r 2 ¼ 4 -12%). CONCLUSIONS: We conclude that our physiologically based model provides an adequate description of the relationship between leptin and body composition and provides a more reliable framework than current empirical approaches for the investigation of other influences on circulating leptin levels. Heritable variations in the control of leptin secretion are unlikely to contribute significantly to variations in leptin levels at the population level.