14 research outputs found

    The Effect of the TyG Index on Liver Steatosis, Immune Activation, Oxidative Stress, Liver Fibrosis Pathways and Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort

    Get PDF
    The purpose of this study was to establish the Triglyceride-Glucose (TyG) Index Ln (fasting TG x fasting glucose/2) as a predictor of liver steatosis in People Living with HIV (PLWH) and determine the effect of increased TyG Index on biomarkers of immune activation, inflammation, oxidative stress, apoptosis, and liver fibrosis. Four-hundred and eighty participants were selected from the Miami Adult Studies on HIV (MASH) cohort, two-hundred and eleven were PLWH, and two-hundred and sixty-nine were uninfected controls. Biomarkers were analyzed from blood samples collected at the FIU Borinquen Clinic. Primary research outcomes were analyzed using multiple linear and logistic regression, pairwise analyses, and ROC curves. The TyG Index was determined to be a good predictor of liver steatosis among PLWH and uninfected controls (AUC=0.738 and AUC=0.702), respectively. Participants in the High TyG Risk category were 4.638 times more likely to have liver steatosis than those in the Low TyG Risk category [95% CI:(2.075, 10.368)]. Greater TyG Index was associated with higher immune activation markers Ln sCD14 (β=0.080, P=0.050) and Ln sCD163 (β=0.164, P=0.008). Linear regression analysis found HIV infection to be associated with higher levels sCD27 (β=0.181, P=0.005), and liver fibrosis pathway biomarkers LnTGF- β (β=0.915, P These data indicate a consistent relationship between increased TyG Index and biological pathways that lead to liver fibrosis. As liver disease becomes a more prominent concern among PLWH, it is crucial for health care professionals to address markers of metabolic health, such as the TyG Index, as a means to effectively manage liver steatosis and avoid the development of liver fibrosis

    Does moderate intensity exercise in the postprandial period attenuate the inflammatory response to a high-fat meal?

    Get PDF
    Master of ScienceDepartment of Human NutritionSara K. RosenkranzBackground: High-fat meals (HFM) have been shown to increase postprandial lipemia (PPL) and inflammation. Acute exercise both pre and post-meal has been shown to attenuate PPL and inflammation. However, studies examining the interaction of HFMs and exercise on PPL and inflammation have used meal and exercise conditions more extreme than typical for average adults. The purpose of this study was to determine if moderate intensity exercise following a "true-to-life" HFM would attenuate PPL and inflammation. Methods: Participants were thirty-nine young adults (18-40 years) with no known metabolic disease. Inclusion criteria consisted of participants meeting physical activity guidelines of ≥ 150 min/week of moderate-to-vigorous physical activity or ≥ 75 min/week of vigorous activity, or < 30 min of planned physical activity per week. Participants were block randomized to EX or CON groups. Participants consumed a HFM of 10 kcal/kgbw. The EX group walked at 60% VO[subscript 2peak] to expend ≈ 5 kcal/kgbw beginning one-hour following the HFM. The CON group remained sedentary during the postprandial period. Blood samples were collected at baseline and 2, and 4hrs postprandially. Results: At baseline, there were no differences between EX and CON groups for any metabolic or inflammatory markers (p>0.05). Postprandial TRG increased ≈ 100% (p0.05). The EX group increased sVCAM-1 from baseline to 4hr (p=0.003), while the CON group did not. Change in TRG was associated with change IL-6, IL-8, IL-10 and TNF-α from baseline to 2hrs when controlling for VO[subscript 2peak] and body fat%. No other associations were seen between change scores for TRG and inflammatory markers. Conclusions: Despite significant increases in PPL following a HFM, moderate intensity exercise in the postprandial period did not mitigate the PPL nor the inflammatory response to the HFM. These results indicate PPL and inflammation following a HFM are not directly related in a young, healthy population with low metabolic risk

    Summation of blood glucose and TAG to characterise the 'metabolic load index'

    Get PDF
    Citation: Emerson, S. R., Haub, M. D., Teeman, C. S., Kurti, S. P., & Rosenkranz, S. K. (2016). Summation of blood glucose and TAG to characterise the 'metabolic load index'. British Journal of Nutrition, 116(9), 1553-1563. doi:10.1017/s0007114516003585Research points to postprandial glucose and TAG measures as preferable assessments of cardiovascular risk as compared with fasting values. Although elevated postprandial glycaemic and lipaemic responses are thought to substantially increase chronic disease risk, postprandial glycaemia and lipaemia have historically only been considered separately. However, carbohydrates and fats can generally 'compete' for clearance from the stomach, small intestine, bloodstream and within the peripheral cell. Further, there are previous data demonstrating that the addition of carbohydrate to a high-fat meal blunts the postprandial lipaemic response, and the addition of fat to a high-carbohydrate meal blunts the postprandial glycaemic response. Thus, postprandial glycaemia and lipaemia are interrelated. The purpose of this brief review is 2-fold: first, to review the current evidence implicating postprandial glycaemia and lipaemia in chronic disease risk, and, second, to examine the possible utility of a single postprandial glycaemic and lipaemic summative value, which will be referred to as the metabolic load index. The potential benefits of the metabolic load index extend to the clinician, patient and researcher

    The effect of moderate intensity exercise in the postprandial period on the inflammatory response to a high-fat meal: an experimental study

    Get PDF
    Citation: Teeman, C. S., Kurti, S. P., Cull, B. J., Emerson, S. R., Haub, M. D., & Rosenkranz, S. K. (2016). The effect of moderate intensity exercise in the postprandial period on the inflammatory response to a high-fat meal: an experimental study. Nutrition Journal, 15, 13. doi:10.1186/s12937-016-0134-4Background: Consuming a high-fat meal (HFM) may lead to postprandial lipemia (PPL) and inflammation. Postprandial exercise has been shown to effectively attenuate PPL. However, little is known about the impact of postprandial exercise on systemic inflammation and whether PPL and inflammation are associated. The purpose of this study was to determine whether moderate intensity exercise performed 60 min following a true-to-life HFM would attenuate PPL and inflammation. Methods: Thirty-nine young adults (18-40 year) with no known metabolic disease were randomized to either a control group (CON) who remained sedentary during the postprandial period or an exercise (EX) group who walked at 60 % VO2peak to expend approximate to 5 kcal/kgbw one-hour following the HFM. Participants consumed a HFM of 10 kcal/kgbw and blood draws were performed immediately before, 2 h and 4 h post-HFM. Results: At baseline, there were no differences between EX and CON groups for any metabolic or inflammatory markers (p > 0.05). Postprandial triglycerides (TRG) increased from baseline to 4 h in the EX and CON groups (p 0.05). There was an increase in soluble vascular adhesion molecule (sVCAM-1) from baseline to 4 h (p = 0.027) for all participants along with a group x time interaction (p = 0.020). Changes in TRG were associated with changes in interleukin-10 (IL-10) from 0 to 2 h (p = 0.007), but were not associated with changes in any other inflammatory marker in the postprandial period (p > 0.05). Conclusions: Despite significant increases in PPL following a HFM, moderate intensity exercise in the postprandial period did not mitigate the PPL nor the inflammatory response to the HFM. These results indicate that in populations with low metabolic risk, PPL and inflammation following a HFM may not be directly related

    Wildcat wellness coaching feasibility trial: protocol for home-based health behavior mentoring in girls

    Get PDF
    Citation: Cull, B. J., Rosenkranz, S. K., Dzewaltowski, D. A., Teeman, C. S., Knutson, C. K., & Rosenkranz, R. R. (2016). Wildcat wellness coaching feasibility trial: protocol for home-based health behavior mentoring in girls. Pilot and Feasibility Studies, 2(1), 26. https://doi.org/10.1186/s40814-016-0066-yChildhood obesity is a major public health problem, with one third of America’s children classified as either overweight or obese. Obesity prevention and health promotion programs using components such as wellness coaching and home-based interventions have shown promise, but there is a lack of published research evaluating the impact of a combined home-based and wellness coaching intervention for obesity prevention and health promotion in young girls. The main objective of this study is to test the feasibility of such an intervention on metrics related to recruitment, intervention delivery, and health-related outcome assessments. The secondary outcome is to evaluate the possibility of change in health-related psychosocial, behavioral, and biomedical outcomes in our sample of participants

    Does moderate intensity exercise attenuate the postprandial lipemic and airway inflammatory response to a high-fat meal?

    Get PDF
    Citation: Stephanie P. Kurti, Sara K. Rosenkranz, Morton Levitt, et al., “Does Moderate Intensity Exercise Attenuate the Postprandial Lipemic and Airway Inflammatory Response to a High-Fat Meal?,” BioMed Research International, vol. 2015, Article ID 647952, 10 pages, 2015. doi:10.1155/2015/647952We investigated whether an acute bout of moderate intensity exercise in the postprandial period attenuates the triglyceride and airway inflammatory response to a high-fat meal (HFM) compared to remaining inactive in the postprandial period. Seventeen (11 M/6 F) physically active (≥150 min/week of moderate-vigorous physical activity (MVPA)) subjects were randomly assigned to an exercise (EX; 60% VO[subscript 2peak]) or sedentary (CON) condition after a HFM (10 kcal/kg, 63% fat). Blood analytes and airway inflammation via exhaled nitric oxide (eNO) were measured at baseline, and 2 and 4 hours after HFM. Airway inflammation was assessed with induced sputum and cell differentials at baseline and 4 hours after HFM. Triglycerides doubled in the postprandial period (~113 ± 18%, P < 0.05 ), but the increase did not differ between EX and CON. Percentage of neutrophils was increased 4 hours after HFM (~17%), but the increase did not differ between EX and CON. Exhaled nitric oxide changed nonlinearly from baseline to 2 and 4 hours after HFM (P < 0.05, ƞ² = 0.36) . Our findings suggest that, in active individuals, an acute bout of moderate intensity exercise does not attenuate the triglyceride or airway inflammatory response to a high-fat meal

    Lipemic and Airway Inflammatory Response to a High-Fat Meal?

    Get PDF
    We investigated whether an acute bout of moderate intensity exercise in the postprandial period attenuates the triglyceride and airway inflammatory response to a high-fat meal (HFM) compared to remaining inactive in the postprandial period. Seventeen (11 M/6 F) physically active (≥150 min/week of moderate-vigorous physical activity (MVPA)) subjects were randomly assigned to an exercise (EX; 60% VO 2peak ) or sedentary (CON) condition after a HFM (10 kcal/kg, 63% fat). Blood analytes and airway inflammation via exhaled nitric oxide (eNO) were measured at baseline, and 2 and 4 hours after HFM. Airway inflammation was assessed with induced sputum and cell differentials at baseline and 4 hours after HFM. Triglycerides doubled in the postprandial period (∼113 ± 18%, &lt; 0.05), but the increase did not differ between EX and CON. Percentage of neutrophils was increased 4 hours after HFM (∼17%), but the increase did not differ between EX and CON. Exhaled nitric oxide changed nonlinearly from baseline to 2 and 4 hours after HFM ( &lt; 0.05, 2 = 0.36). Our findings suggest that, in active individuals, an acute bout of moderate intensity exercise does not attenuate the triglyceride or airway inflammatory response to a high-fat meal

    Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise

    Full text link

    Realistic Test-Meal Protocols Lead to Blunted Postprandial Lipemia but Similar Inflammatory Responses Compared with a Standard High-Fat Meal

    No full text
    BACKGROUND: A substantial increase in triglycerides (TGs) after a meal is associated with an increased risk of cardiovascular disease. Most studies investigating the effects of a meal on TGs have not used meals that reflect typical consumption. OBJECTIVE: The objective of this study was to compare the TG and inflammatory responses of true-to-life meals, containing moderate fat and energy contents, with a high-fat, high-energy, low-carbohydrate meal (HFM) typically used to test TG responses. METHODS: Nine healthy, insufficiently active men [mean ± SD age: 25.1 ± 6.7 y; body mass index (in kg/m2): 25.8 ± 7.0; &lt;150 min moderate- to vigorous-intensity physical activity/wk] completed 3 meal trials in random order: an HFM (17 kcal/kg, 60% fat), a moderate-fat meal (MFM; 8.5 kcal/kg, 30% fat), and a biphasic meal (BPM), in which participants consumed the full MFM at baseline and 3 h postmeal. Blood samples were collected via an indwelling catheter at baseline and hourly for 6 h. RESULTS: Peak blood TGs were significantly greater (P = 0.003) after the HFM (285.2 ± 169.7 mg/dL) than after the MFM (156.0 ± 98.7 mg/dL), but the BPM (198.3 ± 182.8 mg/dL) was not significantly different from the HFM (P = 0.06) or the MFM (P = 0.99). Total area under the curve for TGs was greater after the HFM (1348.8 ± 783.7 mg/dL × 6 h) than after the MFM (765.8 ± 486.8 mg/dL × 6 h; P = 0.0005) and the BPM (951.8 ± 787.7 mg/dL × 6 h; P = 0.03), although the MFM and BPM were not significantly different (P = 0.72). There was a significant time-by-meal interaction for interferon γ, but not for interleukins 6, 8, or 10. CONCLUSION: These findings in insufficiently active, healthy young men suggest that the large TG response after HFMs in previous studies may not reflect the metabolic state of many individuals in daily life

    Does chronic physical activity level modify the airway inflammatory response to an acute bout of exercise in the post-prandial period?

    No full text
    Recent studies have confirmed that a single high-fat meal (HFM) leads to increased airway inflammation. However exercise is a natural anti-inflammatory and may modify post-prandial airway inflammation. The post-prandial airway inflammatory response is likely to be modified by chronic physical activity (PA) level. PURPOSE: To investigate whether chronic PA modifies the airway inflammatory response to an acute bout of exercise in the post-prandial period in both insufficiently active and active subjects. METHODS: Thirty-nine non-asthmatic subjects (twenty active (ACT), 13M/7F) who exceeded PA guidelines (>150 min moderate-vigorous PA/week) and (nineteen insufficiently active (IN), 6M/13F) underwent an incremental treadmill test to exhaustion to determine VO2peak. Subjects were then randomized to a condition (COND), either remaining sedentary (CON) or exercising (EX) post-HFM. Exercise was performed at the heart rate corresponding to 60% VO2peak on a treadmill one-hour post-HFM (63% fat, 10kcal/kg bw). Blood lipids and exhaled nitric oxide (eNO: marker of airway inflammation) were measured at baseline, 2 h and 4 h post-HFM. Sputum differential cell counts were performed at baseline and 4 h post-HFM. RESULTS The mean eNO response for all groups increased at 2 h post-HFM (~6%) and returned to baseline by 4 h (p=0.03). There was a time*COND interaction (p=0.04), where EX had a greater eNO response at 4 hours compared to CON. Sputum neutrophils increased at 4 hours post-HFM (pThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author
    corecore