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      Risks of Misinterpretation in the Evaluation of the Effect of Fruit-Based Drinks in Postprandial Studies

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      Author(s): 1 , * , 2
      Publication date (Electronic):
      Journal: Gastroenterology Research and Practice
      Publisher: Hindawi Publishing Corporation

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          Abstract

          It has been suggested that some fruit-based drinks (FBD) may delay the onset of postprandial stress, which is involved in the pathogenesis of many diseases. The majority of the studies, which have investigated the effects of FBD on postprandial stress, involved a placebo that was a drink with the same content in sugars or carbohydrates of the FBD, but without the bioactive antioxidant compounds. These studies were aimed more at evaluating the effect of the antioxidants rather than the effect of the FBD as a whole. Only 4 studies compared the effect of FBD with water as control and did not support the hypothesis that FBD could inhibit postprandial dysmetabolism, as well as the studies that compared the effect of orange juice and cola. Overall, the results suggest a complex relationship between postprandial dysmetabolism, inflammation, and oxidative stress. Furthermore, the inflammatory and oxidative stress markers need further analytical validation and normal ranges should be established in order to reach a firm conclusion. Finally, caution should be taken in the interpretation of the effect of FBD in postprandial studies and the reviewed results suggest that dietary recommendations should aim to limit rather than increase sugar-sweetened beverages consumption.

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          Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

          Karen Teff, Sharon S Elliott, Matthias Tschöp … (2004)
          Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.
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            Breaking prolonged sitting reduces postprandial glycemia in healthy, normal-weight adults: a randomized crossover trial.

            C Murray Skeaff, R. Gray, C Peddie … (2013)
            Sedentary behavior is a risk factor for cardiometabolic disease. Regularly interrupting sedentary behavior with activity breaks may lower this risk. We compared the effects of prolonged sitting, continuous physical activity combined with prolonged sitting, and regular activity breaks on postprandial metabolism. Seventy adults participated in a randomized crossover study. The prolonged sitting intervention involved sitting for 9 h, the physical activity intervention involved walking for 30 min and then sitting, and the regular-activity-break intervention involved walking for 1 min 40 s every 30 min. Participants consumed a meal-replacement beverage at 60, 240, and 420 min. The plasma incremental area under the curve (iAUC) for insulin differed between interventions (overall P < 0.001). Regular activity breaks lowered values by 866.7 IU · L(-1) · 9 h(-1) (95% CI: 506.0, 1227.5 IU · L(-1) · 9 h(-1); P < 0.001) when compared with prolonged sitting and by 542.0 IU · L(-1) · 9 h(-1) (95% CI: 179.9, 904.2 IU · L(-1) · 9 h(-1); P = 0.003) when compared with physical activity. Plasma glucose iAUC also differed between interventions (overall P < 0.001). Regular activity breaks lowered values by 18.9 mmol · L(-1) · 9 h(-1) (95% CI: 10.0, 28.0 mmol · L(-1) · 9 h(-1); P < 0.001) when compared with prolonged sitting and by 17.4 mmol · L(-1) · 9 h(-1) (95% CI: 8.4, 26.3 mmol · L(-1) · 9 h(-1); P < 0.001) when compared with physical activity. Plasma triglyceride iAUC differed between interventions (overall P = 0.023). Physical activity lowered values by 6.3 mmol · L(-1) · 9 h(-1) (95% CI: 1.8, 10.7 mmol · L(-1) · 9 h(-1); P = 0.006) when compared with regular activity breaks. Regular activity breaks were more effective than continuous physical activity at decreasing postprandial glycemia and insulinemia in healthy, normal-weight adults. This trial was registered with the Australian New Zealand Clinical Trials registry as ACTRN12610000953033.
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              A consideration of biomarkers to be used for evaluation of inflammation in human nutritional studies.

              Luis A. Marcos, J Moreines, N Bosco … (2013)
              To monitor inflammation in a meaningful way, the markers used must be valid: they must reflect the inflammatory process under study and they must be predictive of future health status. In 2009, the Nutrition and Immunity Task Force of the International Life Sciences Institute, European Branch, organized an expert group to attempt to identify robust and predictive markers, or patterns or clusters of markers, which can be used to assess inflammation in human nutrition studies in the general population. Inflammation is a normal process and there are a number of cells and mediators involved. These markers are involved in, or are produced as a result of, the inflammatory process irrespective of its trigger and its location and are common to all inflammatory situations. Currently, there is no consensus as to which markers of inflammation best represent low-grade inflammation or differentiate between acute and chronic inflammation or between the various phases of inflammatory responses. There are a number of modifying factors that affect the concentration of an inflammatory marker at a given time, including age, diet and body fatness, among others. Measuring the concentration of inflammatory markers in the bloodstream under basal conditions is probably less informative compared with data related to the concentration change in response to a challenge. A number of inflammatory challenges have been described. However, many of these challenges are poorly standardised. Patterns and clusters may be important as robust biomarkers of inflammation. Therefore, it is likely that a combination of multiple inflammatory markers and integrated readouts based upon kinetic analysis following defined challenges will be the most informative biomarker of inflammation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Gastroenterol Res Pract
                Journal ID (iso-abbrev): Gastroenterol Res Pract
                Journal ID (publisher-id): GRP
                Title: Gastroenterology Research and Practice
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1687-6121
                ISSN (Electronic): 1687-630X
                Publication date (Print): 2014
                Publication date (Electronic): 25 December 2014
                Volume: 2014
                Electronic Location Identifier: 870547
                Affiliations
                1Food and Nutrition Center of the Agricultural Research Council (CRA-NUT), Via Ardeatina 546, 00178 Rome, Italy
                2Department of Physiology and Pharmacology “V. Erspamer”, “Sapienza” University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy
                Author notes

                Academic Editor: Gianfranco D. Alpini

                Article
                DOI: 10.1155/2014/870547
                PMC ID: 4295616
                SO-VID: 34efc061-9faf-40f4-8692-a86dae84f3b1
                Copyright © Copyright © 2014 I. Peluso and M. Palmery.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 October 2014
                Date accepted : 14 December 2014
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology

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