scholarly journals A single high-fat meal alters human soluble RAGE profiles and PBMC RAGE expression with no effect of prior aerobic exercise

2018 ◽  
Vol 6 (14) ◽  
pp. e13811 ◽  
Author(s):  
Kelly N.Z. Fuller ◽  
Rudy J. Valentine ◽  
Edwin R. Miranda ◽  
Prabhakaran Kumar ◽  
Bellur S. Prabhakar ◽  
...  
2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Stephanie M. Wilson ◽  
Adam P. Maes ◽  
Carl J. Yeoman ◽  
Seth T. Walk ◽  
Mary P. Miles

Abstract Background Dyslipidemia is a feature of impaired metabolic health in conjunction with impaired glucose metabolism and central obesity. However, the contribution of factors to postprandial lipemia in healthy but metabolically at-risk adults is not well understood. We investigated the collective contribution of several physiologic and lifestyle factors to postprandial triglyceride (TG) response to a high-fat meal in healthy, overweight and obese adults. Methods Overweight and obese adults (n = 35) underwent a high-fat meal challenge with blood sampled at fasting and hourly in the 4-hour postprandial period after a breakfast containing 50 g fat. Incremental area under the curve (iAUC) and postprandial magnitude for TG were calculated and data analyzed using a linear model with physiologic and lifestyle characteristics as explanatory variables. Model reduction was used to assess which explanatory variables contributed most to the postprandial TG response. Results TG responses to a high-fat meal were variable between individuals, with approximately 57 % of participants exceeded the nonfasting threshold for hypertriglyceridemia. Visceral adiposity was the strongest predictor of TG iAUC (β = 0.53, p = 0.01), followed by aerobic exercise frequency (β = 0.31, p = 0.05), insulin resistance based on HOMA-IR (β = 0.30, p = 0.04), and relative exercise intensity at which substrate utilization crossover occurred (β = 0.05, p = 0.04). For postprandial TG magnitude, visceral adiposity was a strong predictor (β = 0.43, p < 0.001) followed by aerobic exercise frequency (β = 0.23, p = 0.01), and exercise intensity for substrate utilization crossover (β = 0.53, p = 0.01). Conclusions Postprandial TG responses to a high-fat meal was partially explained by several physiologic and lifestyle characteristics, including visceral adiposity, insulin resistance, aerobic exercise frequency, and relative substrate utilization crossover during exercise. Trial Registration ClinicalTrials.gov, NCT04128839, Registered 16 October 2019 – Retrospectively registered.


Metabolism ◽  
2017 ◽  
Vol 71 ◽  
pp. 144-152 ◽  
Author(s):  
Kelly N.Z. Fuller ◽  
Corey M. Summers ◽  
Rudy J. Valentine

2021 ◽  
Author(s):  
Stephanie M Wilson ◽  
Adam P. Maes ◽  
Carl J. Yeoman ◽  
Seth T. Walk ◽  
Mary P. Miles

Abstract Background: Dyslipidemia is a feature of impaired metabolic health in conjunction with impaired glucose metabolism and central obesity. However, the contribution of factors to postprandial lipemia in healthy but metabolically at-risk adults is not well understood. We investigated the collective contribution of several physiologic and lifestyle factors to postprandial triglyceride (TG) response to a high-fat meal in healthy, overweight and obese adults. Methods: Overweight and obese adults (n=35) underwent a high-fat meal challenge with blood sampled at fasting and hourly in the 4-hour postprandial period after a breakfast containing 50 grams fat. Incremental area under the curve and postprandial magnitude for TG were calculated and data analyzed using a linear model with physiologic and lifestyle characteristics as explanatory variables. Model reduction was used to assess which explanatory variables contributed most to the postprandial TG response.Results: TG responses to a high-fat meal were variable between individuals, with approximately 57% of participants exceeded the nonfasting threshold for hypertriglyceridemia. Visceral adiposity was the strongest predictor of TG iAUC (β=0.53, p=0.01), followed by aerobic exercise frequency (β=0.31, p=0.05), insulin resistance based on HOMA-IR (β=0.30, p=0.04), and relative exercise intensity at which substrate utilization crossover occurred (β=0.05, p=0.04). For postprandial TG magnitude, visceral adiposity was a strong predictor (β=0.43, p<0.001) followed by aerobic exercise frequency (β=0.23, p=0.01), and exercise intensity for substrate utilization crossover (β=0.53, p=0.01). Conclusions: Postprandial TG responses to a high-fat meal was partially explained by several physiologic and lifestyle characteristics, including visceral adiposity, insulin resistance, aerobic exercise frequency, and relative substrate utilization crossover during exercise. Trial Registration: ClinicalTrials.gov, NCT04128839, Registered 16 October 2019 – Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT04128839


Retos ◽  
2015 ◽  
pp. 206-212
Author(s):  
Laurel A. Littlefield ◽  
Peter W. Grandjean

Exaggerated postprandial lipemia has been observed in metabolic and cardiovascular diseases and is associated with increased risk for cardiovascular disease (CVD). Prior aerobic exercise reduces the triglyceride response to a high-fat meal. The purpose of this review is to examine the factors contributing to metabolic dyslipidemia and to review available evidence supporting the role of aerobic exercise in reducing postprandial lipemia. The contribution of exercise intensity and excess-post exercise oxygen consumption (EPOC) to changes in postprandial lipemia is examined.Key words. lipemia, Metabolic Syndrome, exercise, EPOC.Resumen. La exagerada lipemia postprandial exagerada ha sido observada en enfermedades metabólicas y cardiovasculares, y está asociada a un mayor riesgo de enfermedad cardiovascular (ECV). Se ha encontrado que el ejercicio aeróbico previo reduce la respuesta de los triglicéridos a una comida rica en grasas. El propósito de esta revisión es examinar los factores que contribuyen a la dislipidemia metabólica y revisar la evidencia disponible que respalda el papel del ejercicio aeróbico en la reducción de la lipemia postprandial. Se examina la contribución de la intensidad del ejercicio y el exceso de consumo de oxígeno post-ejercicio (EPOC) en los cambios en la lipemia postprandial.Palabras claves. lipemia, Síndrome Metabólico, ejercicio, EPOC


Author(s):  
Bruno Costa Teixeira ◽  
Renata L. Krüger ◽  
Juliano Boufleur Farinha ◽  
Francesco P Boeno ◽  
Rodrigo Cauduro Oliveira Macedo ◽  
...  

Exercise intensity modulates postprandial lipemia. It is still unknown, however, its effect on hemostatic and pro- and anti-inflammatory markers in the postprandial state. Eleven young males perform a 2-day trial on different conditions: (i) REST: rest for 45 min; (ii) MIE: moderate-intensity exercise; and (iii) HIE: heavy-intensity exercise. Experimental conditions were performed in the evening. On the following morning, blood samples were taken in the fasted state (0 h) and at 1, 3, and 5 h after the consumption of a high-fat meal (HFM). Interleukin-10 (IL-10) levels were higher in the HIE vs. MIE trial at 0 and 1 h (p < 0.033) and IL-10 iAUC was greater in the MIE (p = 0.027) and HIE (p = 0.045) vs. REST. Lower levels of anti-coagulation factor VII (FVII) were observed at 1 h in the MIE condition vs. REST (p = 0.043). In comparison with REST, MIE improved hemostatic (FVII) and anti-inflammatory markers (IL-10 iAUC) whereas HIE enhanced IL-10 in the postprandial state. Regardless of the exercise intensity, aerobic exercise mitigates the deleterious consequences of an HFM. Novelty Bullets: • Prior aerobic exercise at moderate-intensity attenuates next day’s postprandial FVII and IL-10 levels whereas exercise performed at heavy-intensity increases IL-10 levels. • Moderate-intensity exercise may be more beneficial to improve hemostatic (FVII) and anti-inflammatory (IL-10) responses while heavy-intensity exercise may improve anti-inflammatory (IL-10) levels only.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 265-LB ◽  
Author(s):  
HELMUT O. STEINBERG ◽  
FRANKIE B. STENTZ ◽  
NANDITA K. SHANKAR
Keyword(s):  
High Fat ◽  
Apo B ◽  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 162-LB
Author(s):  
JEANIE B. TRYGGESTAD ◽  
APRIL M. TEAGUE ◽  
KEVIN R. SHORT

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