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ABSTRACT: BackgroundA high intake of whole grains containing soluble fiber has been shown to lower glucose and insulin responses in overweight
humans and humans with type 2 diabetes.
Aim of the studyWe investigated the linearity of this response after consumption of 5 breakfast cereal test meals containing wheat and/or
barley to provide varying amounts of soluble fiber, β-glucan (0, 2.5, 5, 7.5 and 10g).
MethodsSeventeen normoglycemic, obese women at increased risk for insulin resistance consumed 5 test meals within a randomized cross-over
design after consuming controlled diets for 2days. Blood samples for glucose and insulin response were obtained prior to
and 30, 60, 120 and 180min after consuming the test meals.
ResultsConsumption of 10g of β-glucan significantly reduced peak glucose response at 30min and delayed the rate of glucose response.
Area under the curve for 2h-postprandial glycemic response was not affected by β-glucan content. However, peak and area under
the curve of insulin responses were significantly affected by the β-glucan amount in an inverse linear relationship.
ConclusionThese data suggest that acute consumption of 10g of β-glucan is able to induce physiologically beneficial effects on postprandial
insulin responses in obese women at risk for insulin resistance.
European Journal of Nutrition 04/2012; 48(3):170-175. · 2.75 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: A high intake of whole grains containing soluble fiber has been shown to lower glucose and insulin responses in overweight humans and humans with type 2 diabetes.
We investigated the linearity of this response after consumption of 5 breakfast cereal test meals containing wheat and/or barley to provide varying amounts of soluble fiber, beta-glucan (0, 2.5, 5, 7.5 and 10 g).
Seventeen normoglycemic, obese women at increased risk for insulin resistance consumed 5 test meals within a randomized cross-over design after consuming controlled diets for 2 days. Blood samples for glucose and insulin response were obtained prior to and 30, 60, 120 and 180 min after consuming the test meals.
Consumption of 10 g of beta-glucan significantly reduced peak glucose response at 30 min and delayed the rate of glucose response. Area under the curve for 2 h-postprandial glycemic response was not affected by beta-glucan content. However, peak and area under the curve of insulin responses were significantly affected by the beta-glucan amount in an inverse linear relationship.
These data suggest that acute consumption of 10 g of beta-glucan is able to induce physiologically beneficial effects on postprandial insulin responses in obese women at risk for insulin resistance.
European Journal of Nutrition 03/2009; 48(3):170-5. · 2.75 Impact Factor
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ABSTRACT: Abstract
Background
Activity monitors (AM) are small, electronic devices used to quantify the amount and intensity of physical activity (PA). Unfortunately, it has been demonstrated that data loss that occurs when AMs are not worn by subjects (removals during sleeping and waking hours) tend to result in biased estimates of PA and total energy expenditure (TEE). No study has reported the degree of data loss in a large study of adults, and/or the degree to which the estimates of PA and TEE are affected. Also, no study in adults has proposed a methodology to minimize the effects of AM removals.
Methods
Adherence estimates were generated from a pool of 524 women and men that wore AMs for 13 – 15 consecutive days. To simulate the effect of data loss due to AM removal, a reference dataset was first compiled from a subset consisting of 35 highly adherent subjects (24 HR; minimum of 20 hrs/day for seven consecutive days). AM removals were then simulated during sleep and between one and ten waking hours using this 24 HR dataset. Differences in the mean values for PA and TEE between the 24 HR reference dataset and the different simulations were compared using paired t -tests and/or coefficients of variation.
Results
The estimated average adherence of the pool of 524 subjects was 15.8 ± 3.4 hrs/day for approximately 11.7 ± 2.0 days. Simulated data loss due to AM removals during sleeping hours in the 24 HR database (n = 35), resulted in biased estimates of PA (p < 0.05), but not TEE. Losing as little as one hour of data from the 24 HR dataset during waking hours results in significant biases (p < 0.0001) and variability (coefficients of variation between 7 and 21%) in the estimates of PA. Inserting a constant value for sleep and imputing estimates for missing data during waking hours significantly improved the estimates of PA.
Conclusion
Although estimated adherence was good, measurements of PA can be improved by relatively simple imputation of missing AM data.
BMC Medical Research Methodology. 01/2008;
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Kim S Stote,
David J Baer, Karen Spears,
David R Paul,
G Keith Harris,
William V Rumpler,
Pilar Strycula,
Samer S Najjar,
Luigi Ferrucci,
Donald K Ingram,
Dan L Longo,
Mark P Mattson
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ABSTRACT: Although consumption of 3 meals/d is the most common pattern of eating in industrialized countries, a scientific rationale for this meal frequency with respect to optimal health is lacking. A diet with less meal frequency can improve the health and extend the lifespan of laboratory animals, but its effect on humans has never been tested.
A pilot study was conducted to establish the effects of a reduced-meal-frequency diet on health indicators in healthy, normal-weight adults.
The study was a randomized crossover design with two 8-wk treatment periods. During the treatment periods, subjects consumed all of the calories needed for weight maintenance in either 3 meals/d or 1 meal/d.
Subjects who completed the study maintained their body weight within 2 kg of their initial weight throughout the 6-mo period. There were no significant effects of meal frequency on heart rate, body temperature, or most of the blood variables measured. However, when consuming 1 meal/d, subjects had a significant increase in hunger; a significant modification of body composition, including reductions in fat mass; significant increases in blood pressure and in total, LDL-, and HDL-cholesterol concentrations; and a significant decrease in concentrations of cortisol.
Normal-weight subjects are able to comply with a 1 meal/d diet. When meal frequency is decreased without a reduction in overall calorie intake, modest changes occur in body composition, some cardiovascular disease risk factors, and hematologic variables. Diurnal variations may affect outcomes.
American Journal of Clinical Nutrition 05/2007; 85(4):981-8. · 6.67 Impact Factor
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ABSTRACT: Watermelon is a rich source of citrulline, an amino acid that can be metabolized to arginine, a conditionally essential amino acid for humans. Arginine is the nitrogenous substrate used in the synthesis of nitric oxide and plays an essential role in cardiovascular and immune functions. No detailed studies have been conducted to evaluate plasma arginine response in humans after long-term feeding of citrulline from natural plant sources. This study investigated if watermelon juice consumption increases fasting concentrations of plasma arginine, ornithine, and citrulline in healthy adult humans.
Subjects (n = 12-23/treatment) consumed a controlled diet and 0 (control), 780, or 1560 g of watermelon juice per day for 3 wk in a crossover design. The treatments provided 1 and 2 g of citrulline per day. Treatment periods were preceded by washout periods of 2 to 4 wk.
Compared with the baseline, fasting plasma arginine concentrations increased 12% after 3 wk of the lower-dose watermelon treatment; arginine and ornithine concentrations increased 22% and 18%, respectively, after 3 wk of the higher-dose watermelon treatment. Fasting citrulline concentrations did not increase relative to the control but remained stable throughout the study.
The increased fasting plasma concentrations of arginine and ornithine and stable concentrations of plasma citrulline in response to watermelon juice consumption indicated that the citrulline from this plant origin was effectively converted into arginine. These results demonstrate that plasma concentration of arginine can be increased through intake of citrulline from watermelon.
Nutrition 04/2007; 23(3):261-6. · 3.03 Impact Factor
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ABSTRACT: The effect of inadequate vitamin A during the neonatal period on lung status is still unknown.
We tested the hypothesis that low plasma retinol concentrations during the first month of life are independently associated with bronchopulmonary dysplasia (BPD) and long-term respiratory morbidity at 6 mo gestationally corrected age (ie, the age the infant would be had the pregnancy gone to term).
Respiratory outcome information was obtained to 6 mo corrected age for a historical cohort of very-low-birth-weight neonates (<1250 g) who were admitted to intensive care over a 7-y period. Neonates with one or more plasma measurements of retinol concentrations < 0.35 micromol/L (<100 microg/L) on days 1-28 were classified as having low vitamin A. BPD was defined at day 28 by clinical and radiologic criteria and by use of supplemental oxygen at 36 wk postmenstrual age (PMA). Dependence on supplemental oxygen was used to identify long-term respiratory disability at 6 mo corrected age. Multivariate logistic regression analyses were conducted.
Of the 350 study infants, 192 (55%) had low vitamin A status. BPD occurred in 52% of survivors at day 28 (173/331) and at 36 wk PMA (147/285). Fourteen percent (33/244) required oxygen support at 6 mo corrected age. Adjusted odds ratios of BPD with low vitamin A were 3.5 (95% CI: 1.7, 7.2) at day 28 and 1.7 (1.0, 2.7) at 36 wk PMA. At 6 mo corrected age, the adjusted odds ratio was 2.6 (1.1, 6.4) for respiratory disability with low vitamin A.
Poor vitamin A status during the first month of life significantly increased the risk of developing BPD and long-term respiratory disability.
American Journal of Clinical Nutrition 01/2005; 80(6):1589-94. · 6.67 Impact Factor
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Karen Spears
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ABSTRACT: Thesis (Ph. D.)--University of Washington, 2001 Bronchopulmonary dysplasia (BPD), the consequence of abnormal lung growth and healing from injury, affects 25--50% of infants born weighing <1500gm. Strong biological evidence supports poor vitamin A status as a factor in the pathogenesis of BPD but clinical findings are conflicting. A large, historical cohort study was undertaken to evaluate the association of plasma retinol status during the first postnatal month and the risk of developing BPD among very low birth weight infants (VLBW < 1250g). VLBW infants admitted to the University of Washington Hospital Neonatal Intensive Care Unit from 1993--1999 surviving for >72 hours were eligible; 352 infants (71% of eligible) had available retinol levels and caregiver's consent. The cohort was followed for evidence of BPD at day 28 (defined by clinical and radiological criteria), at 36 weeks postconception age (PCA) (based on supplemental oxygen use), and supplemental oxygen use at 6 months PCA.Plasma retinol concentrations, assessed by high performance liquid chromatography, ranged from 31 to 760 mug/L (median 95 mug/L). One hundred and ninety two infants exhibited low retinol levels (one or more <100mug/L) during the first 28 days. Among survivors, 52% (173/331) developed BPD at day 28 and at 36 weeks PCA (147/285), with 14% (33/244) still dependent on oxygen support at 6 months PCA. Potential confounding factors, such as: carrier protein levels, gestational age, duration of parenteral nutrition, surfactant and steroid use, and other neonatal diseases, were included in multiple logistic regression analyses.After adjusting for confounding, infants with retinol concentrations <100 mug/L during the first month of life had a 3.5 times greater odds of BPD at day 28 (95% CI 1.68, 7.23) and 1.7 times greater odds of BPD at 36 weeks PCA (95% CI 1.02, 2.73) compared to those with levels ≥100 mug/L Low retinol levels were associated with long-term respiratory disability. At 6 months PCA, the adjusted odds for oxygen use with low retinol levels was 2.6 (1.09, 6.39) in survivors and 1.2 (0.62, 2.23) for death or oxygen use. A significant dose-response relationship between retinol levels and BPD was also evident at day 28. These findings support poor vitamin A status as a contributing factor to the risk of BPD. Optimal vitamin A dose and mode of administration for VLBW infants needs to be defined.
