Biomedical subjects

Alan Lucas

Publications and source records attributed to Alan Lucas.

21 records · Page 2Linked to original sources

PubMed2002

Influence of leptin on arterial distensibility: a novel link between obesity and cardiovascular disease?

BACKGROUND: The mechanisms by which obesity increases the risk of atherosclerotic cardiovascular disease (CVD) are poorly understood. In experimental models, leptin, a hormone produced by adipose tissue, has been shown adversely to affect vascular health. Therefore, we tested the hypothesis that high leptin concentrations are associated with lower arterial distensibility, an index of circulatory function relevant to the atherosclerotic process. METHODS AND RESULTS: Noninvasive, high-resolution, vascular ultrasound was used to measure brachial artery distensibility in 294 healthy adolescents (aged 13 to 16 years) who had a broad range of body mass indexes. Fat mass was measured by bioelectric impedance analysis; fasting serum leptin concentration by radioimmunoassay; and lipid profile, fasting insulin, glucose, and C-reactive protein concentrations by standard laboratory techniques. Higher leptin concentrations were associated with impaired arterial distensibility (regression coefficient, -1.3% change in arterial distension per 10% increase in leptin; 95% CI, -1.9% to -0.8%; P<0.001). This association was independent of fat mass, blood pressure, and C-reactive protein, fasting insulin, or LDL cholesterol concentrations. CONCLUSIONS: Elevation in leptin was associated with impaired vascular function, independent of the metabolic and inflammatory disturbances associated with obesity. Our observations are consistent with data from experimental models and suggest that high leptin concentration is an important mechanism for the adverse influence of body fatness on CVD.

Adipose Tissue↗

PubMed2002

Early nutrition and leptin concentrations in later life.

BACKGROUND: Formula feeding or overweight in infancy may increase the later risk of obesity, but the mechanisms involved are uncertain. Because obesity is associated with high leptin concentrations relative to fat mass, programming of leptin concentrations may be one mechanism by which early nutrition influences later obesity. OBJECTIVE: We tested the hypothesis that high nutrient intake or formula feeding in infancy programs greater leptin concentrations relative to fat mass in later life. DESIGN: Serum leptin concentrations were measured by radioimmunoassay in 197 adolescents aged 13-16 y who were born preterm and randomly assigned at birth to receive either a nutrient-enriched preterm formula or banked donated breast milk (trial 1) or a preterm formula or a standard formula (trial 2). Fat mass was estimated with the use of bioelectrical impedance analysis. RESULTS: After combining the results of trials 1 and 2 as planned, the ratio of leptin to fat mass was significantly greater in the children who received the preterm formula (geometric : 0.84 microg x L(-1) x kg(-1)) than in those who received standard formula or banked breast milk (0.62 microg x L(-1) x kg(-1); mean difference: 30.8%; 95% CI for difference: 8.4%, 53.2%; P = 0.007). The difference between the diet groups remained significant after adjustment for age, sex, Tanner stage, social class, and fat mass. Human milk intake was significantly associated with lower leptin concentrations relative to fat mass in adolescence (P = 0.023), independent of potential confounding factors. CONCLUSION: Programming of relative leptin concentrations by early diet may be one mechanism that links early nutrition with later obesity.

Adolescent↗

PubMed2002

Double-blind, randomized trial of long-chain polyunsaturated fatty acid supplementation in formula fed to preterm infants.

OBJECTIVE: We tested the hypothesis that balanced addition of long-chain polyunsaturated fatty acid (LCPUFA) to preterm formula during the first weeks of life would confer long-term neurodevelopmental advantage in a double-blind, randomized, controlled trial of preterm formula with and without preformed LCPUFA. METHODS: The participants were 195 formula-fed preterm infants (birth weight <1750 g, gestation <37 weeks) from 2 UK neonatal units and 88 breast milk-fed infants. Main outcome measures were Bayley Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) at 18 months and Knobloch, Passamanick and Sherrard's Developmental Screening Inventory at 9 months' corrected age. Safety outcome measures were anthropometry at 9 and 18 months, tolerance, infection, necrotizing enterocolitis, and death. RESULTS: There were no significant differences in developmental scores between randomized groups, although infants who were fed LCPUFA-supplemented formula showed a nonsignificant 2.6-point (0.25 standard deviation) advantage in MDI and PDI at 18 months, with a greater (nonsignificant) advantage (MDI: 4.5 points; PDI: 5.8 points) in infants below 30 weeks' gestation. LCPUFA-supplemented infants were shorter than control infants at 18 months (difference in length standard deviation score: 0.44; 95% confidence interval: 0.08-0.8). No other significant short- or long-term differences in safety outcomes were observed. Breastfed infants had significantly higher developmental scores at 9 and 18 months than both formula groups and were significantly heavier and longer at 18 months than LCPUFA-supplemented but not control infants. CONCLUSIONS: With the dose, duration, and preparation of LCPUFA used, efficacy was not demonstrated, although an advantage in later neurodevelopment cannot be excluded by global tests of development up to 18 months, particularly in infants below 30 weeks' gestation. The surprising effect of LCPUFA-supplemented formula on growth 18 months beyond the intervention period needs to be confirmed in other studies using similar supplementation strategies. Additional follow-up of this cohort is critical at an age when more specific tests of cognitive function are possible.

Age Factors↗