Search

OBJECTIVE: Breakfast-eating frequency declines through adolescence and has been inversely associated with body weight in cross-sectional studies, with few prospective studies on this topic. This study was conducted to examine the association between breakfast frequency and 5-year body weight change in 2216 adolescents. PATIENTS AND METHODS: Project EAT (Eating Among Teens) was a 5-year longitudinal study of eating patterns and weight concerns among adolescents. Surveys were completed in 1998-1999 (time 1) and 2003-2004 (time 2). Multivariable linear regression was used to examine the association between breakfast frequency and change in BMI, with adjustment for age, socioeconomic status, race, physical activity, time 1 BMI and breakfast category, and time 1 dietary and weight-related variables. RESULTS: At time 1, frequency of breakfast was directly associated with intake of carbohydrate and fiber, socioeconomic status, white race, and physical activity and inversely associated with smoking and alcohol consumption and dieting and weight-control behaviors. In cross-sectional analyses at times 1 and 2, inverse associations between breakfast frequency and BMI remained largely independent of all of the confounding and dietary factors. Weight-related factors (concerns, behaviors, and pressures) explained little of the breakfast-BMI association. In prospective analyses, frequency of breakfast was inversely associated with BMI in a dose-response manner. Further adjustment for confounding and dietary factors did not seem to explain the association, but adjustment for weight-related variables seemed to partly explain this finding. CONCLUSIONS: Although experimental studies are needed to verify whether the association between breakfast and body weight is of a causal nature, our findings support the importance of promoting regular breakfast consumption among adolescents. Future studies should further examine the role of breakfast habits among youth who are particularly concerned about their weight. [ABSTRACT FROM AUTHOR]

Many pharmacists report they lack nutritional knowledge and believe the best time to educate pharmacists about nutrition is during pharmacy school., Purpose: This study was conducted to determine if today's pharmacy students receive education in nutrition and if they realize the importance of a nutrition course., Methods: Ninety-five pharmacy students attending pharmacy school were surveyed in two pharmacy schools in the United States., Results: The survey showed only 13.7% received nutrition education and 82.9% of students believed nutrition education should be incorporated into the pharmacy degree curriculum. When the pharmacy-related experience was taken into account, 73.3% of students believed that a nutrition course should be incorporated into the curriculum., Conclusion: This study suggests that pharmacy students from two major universities in Alabama and Illinois realize the importance of nutrition education and believe a nutrition course should be incorporated into the pharmacy degree curriculum.

The goal of this study was to determine the magnitude by which acute consumption of fructose in a morning bolus would stimulate lipogenesis (measured by infusion of 13C1-acetate and analysis by GC-MS) immediately and after a subsequent meal. Six healthy subjects [4 men and 2 women; aged (mean +/- SD) 28 +/- 8 y; BMI, 24.3 +/- 2.8 kg/m(2); and serum triacylglycerols (TG), 1.03 +/- 0.32 mmol/L] consumed carbohydrate boluses of sugars (85 g each) in a random and blinded order, followed by a standardized lunch 4 h later. Subjects completed a control test of glucose (100:0) and a mixture of 50:50 glucose:fructose and one of 25:75 (wt:wt). Following the morning boluses, serum glucose and insulin after 100:0 were greater than both other treatments (P < 0.05) and this pattern occurred again after lunch. In the morning, fractional lipogenesis was stimulated when subjects ingested fructose and peaked at 15.9 +/- 5.4% after the 50:50 treatment and at 16.9 +/- 5.2% after the 25:75 treatment, values that were greater than after the 100:0 treatment (7.8 +/- 5.7%; P < 0.02). When fructose was consumed, absolute lipogenesis was 2-fold greater than when it was absent (100:0). Postlunch, serum TG were 11-29% greater than 100:0 and TG-rich lipoprotein-TG concentrations were 76-200% greater after 50:50 and 25:75 were consumed (P < 0.05). The data demonstrate that an early stimulation of lipogenesis after fructose, consumed in a mixture of sugars, augments subsequent postprandial lipemia. The postlunch blood TG elevation was only partially due to carry-over from the morning. Acute intake of fructose stimulates lipogenesis and may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate TG synthesis postprandially.

The present study quantified dietary fatty acid flux in healthy men (n = 6) who were fed a liquid formula through a duodenal feeding tube (continuous feeding group) or who consumed the same formula in meals (meal feeding group). A triacylglycerol (TAG) stable isotope was added to the formula to determine the entry of dietary fatty acids into the serum and its clearance to the liver and resecretion into serum via VLDL. The contribution of dietary fatty acids to serum nonesterified fatty acids (NEFAs) was higher with meal feeding (24.4 +/- 2.6%) compared with continuous feeding (10.8 +/- 2.9%, P < 0.01) and, when multiplied by the NEFA concentration, resulted in similar absolute fatty acid spillover. Diet-derived NEFAs subsequently represented 10.6 +/- 1.2% and 4.7 +/- 1.3% of hepatic VLDL-TAG (meal feeding vs. continuous feeding, respectively, P = 0.004). Chylomicron remnant uptake by the liver contributed 9.3 +/- 1.9% of fatty acids to hepatic VLDL-TAG synthesis with meal feeding compared with continuous feeding (4.4 +/- 0.8%, P < 0.03). These data suggest that the extent of dietary fatty acid recycling via serum NEFAs and VLDL-TAG is determined by the rate of delivery of dietary fat to the intestine. The inefficient removal of dietary fat from the circulation may maintain VLDL-TAG production but may also result in prolonged postprandial lipemia.

Sources of fatty acids flowing to the liver may be used for triacylglycerol (TAG) synthesis. Our objective was to quantify contributions of nonesterified fatty acids (NEFAs), de novo lipogenesis, and dietary fatty acids to VLDL-TAG in the fed state after meal feeding in healthy subjects (n = 6). The effect of substrate delivery rate was also determined by comparison with data obtained under a continuous-feeding regimen. A liquid diet was administered by mouth or via feeding tube. Contributions of NEFAs, de novo lipogenesis, and dietary fatty acids to VLDL-TAG were quantified using stable isotopes and gas chromatography-mass spectrometry. Contribution of NEFAs to VLDL-TAG was similar under meal feeding and continuous feeding, although insulin area under the curve (AUC) was greater under meal feeding (1,597 +/- 455 vs. 471 +/- 484 pmol . h . l(-1), P < 0.004). Lipogenesis achieved a higher AUC with meal feeding versus continuous feeding (88.7 +/- 84.4 vs. 1.9 +/- 19.3 mumol . h . l(-1), P = 0.03) supporting greater stimulation of de novo lipogenesis from increased glucose delivery rate. The contribution of dietary fatty acids to VLDL-TAG was also greater with meal feeding. These data demonstrate for the first time in humans the well-coordinated use of fatty acids by the liver during the transition from fasted to fed states and highlight the dominant role of NEFAs for VLDL-TAG synthesis in both states.

Background: Recent data suggest that hepatic de novo lipogenesis (DNL) is elevated in the fed state compared with the fasting state, but the rate at which lipogenesis can increase with meal consumption is currently unknown., Objective: The objective was to quantify the diurnal pattern of lipogenesis after 2 consecutive mixed meals were fed to healthy men (n = 8)., Design: A liquid diet was administered after a 12-h fast. During the fasting and postprandial periods, serum insulin, glucose, triacylglycerol, and nonesterified fatty acid concentrations were measured, and rates of DNL were quantified via intravenous infusion of [1-(13)C] sodium acetate and mass isotopomer distribution analysis., Results: The temporal pattern of postprandial lipogenesis was similar in all subjects. Lipogenesis rose significantly from 4.7 +/- 3.3% at fasting, peaked at 18.2 +/- 7.1% after meal 1 (P = 0.003 compared with fasting), rose further to 23.1 +/- 8.9% after meal 2 (P = 0.01 for difference between meals), and then decreased toward baseline (P < 0.001). Lipogenesis peaked 4.2 h after the meals; lipoprotein-triacylglycerol concentrations peaked sooner, 2.0 h after the meals (P < 0.02). Maximum postprandial DNL ranged from 10.3% to 37.5%. Peak insulin concentrations after meal 1 correlated with peak DNL (R = 0.838, P = 0.037), although the leanest subjects had some of the highest rates of postprandial DNL., Conclusion: These data confirm the acute stimulation of DNL after meals in healthy subjects and validate the contribution of this pathway to elevations in triacylglycerol concentration.