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      The effect of two iso-caloric meals containing equal amounts of fats with a different fat composition on the inflammatory and metabolic markers in apparently healthy volunteers

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          Abstract

          Background

          Little is known about the time-course of the postprandial appearance of macronutrient-induced inflammatory response. Our aim was to investigate the postprandial inflammatory and metabolic response following high fat, high caloric popular meals in apparently healthy participants.

          Methods

          Fifty four apparently healthy normal weight volunteers (BMI of 25.9±0.9) were given two iso-caloric meals with similar amounts but different composition of fats: a meal high in monounsaturated fats (MUFA), and a meal high in saturated fat (SFA). Three main effects and the interactions between them were analyzed: the time (before and 2 and 4 hours following the meals), the meal (MUFA or SFA) and the gender.

          Results

          The effect of time from the meal on hs-CRP level was highly significant ( p=0.004). The highest responses were observed 2 hours after the meal ( p=0.002). A statistically significant interaction was found between the time and the meal ( p≤0.0001), which reflects the higher increase in hs-CRP values 2 hours after the SFA meal, with no effect by the MUFA meal. The white blood cell counts were affected significantly by the time ( p≤0.0001) however, other inflammatory markers (fibrinogen, IL-6, TNFα, ICAM and VICAM) were not. All the metabolic markers (insulin, glucose, HOMA-R, QUICKI and triglycerides) were affected by the time ( p≤0.0001), with no interactions observed.

          Conclusions

          Metabolic and modest inflammatory changes occur within a few hours after the ingestion of a high SFA meal in apparently healthy adults.

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          Most cited references46

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          C-reactive protein: a critical update.

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            Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage.

            Insulin resistance contributes to the pathophysiology of diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resistance in humans and animal models is of great importance for epidemiological studies, clinical and basic science investigations, and eventual use in clinical practice. Direct and indirect methods of varying complexity are currently employed for these purposes. Some methods rely on steady-state analysis of glucose and insulin, whereas others rely on dynamic testing. Each of these methods has distinct advantages and limitations. Thus, optimal choice and employment of a specific method depends on the nature of the studies being performed. Established direct methods for measuring insulin sensitivity in vivo are relatively complex. The hyperinsulinemic euglycemic glucose clamp and the insulin suppression test directly assess insulin-mediated glucose utilization under steady-state conditions that are both labor and time intensive. A slightly less complex indirect method relies on minimal model analysis of a frequently sampled intravenous glucose tolerance test. Finally, simple surrogate indexes for insulin sensitivity/resistance are available (e.g., QUICKI, HOMA, 1/insulin, Matusda index) that are derived from blood insulin and glucose concentrations under fasting conditions (steady state) or after an oral glucose load (dynamic). In particular, the quantitative insulin sensitivity check index (QUICKI) has been validated extensively against the reference standard glucose clamp method. QUICKI is a simple, robust, accurate, reproducible method that appropriately predicts changes in insulin sensitivity after therapeutic interventions as well as the onset of diabetes. In this Frontiers article, we highlight merits, limitations, and appropriate use of current in vivo measures of insulin sensitivity/resistance.
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              C-Reactive Protein, the Metabolic Syndrome, and Risk of Incident Cardiovascular Events: An 8-Year Follow-Up of 14 719 Initially Healthy American Women

              The metabolic syndrome describes a high-risk population having 3 or more of the following clinical characteristics: upper-body obesity, hypertriglyceridemia, low HDL, hypertension, and abnormal glucose. All of these attributes, however, are associated with increased levels of C-reactive protein (CRP). We evaluated interrelationships between CRP, the metabolic syndrome, and incident cardiovascular events among 14 719 apparently healthy women who were followed up for an 8-year period for myocardial infarction, stroke, coronary revascularization, or cardiovascular death; 24% of the cohort had the metabolic syndrome at study entry. At baseline, median CRP levels for those with 0, 1, 2, 3, 4, or 5 characteristics of the metabolic syndrome were 0.68, 1.09, 1.93, 3.01, 3.88, and 5.75 mg/L, respectively (P(trend) <0.0001). Over the 8-year follow-up, cardiovascular event-free survival rates based on CRP levels above or below 3.0 mg/L were similar to survival rates based on having 3 or more characteristics of the metabolic syndrome. At all levels of severity of the metabolic syndrome, however, CRP added prognostic information on subsequent risk. For example, among those with the metabolic syndrome at study entry, age-adjusted incidence rates of future cardiovascular events were 3.4 and 5.9 per 1000 person-years of exposure for those with baseline CRP levels less than or greater than 3.0 mg/L, respectively. Additive effects for CRP were also observed for those with 4 or 5 characteristics of the metabolic syndrome. The use of different definitions of the metabolic syndrome had minimal impact on these findings. These prospective data suggest that measurement of CRP adds clinically important prognostic information to the metabolic syndrome.
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                Author and article information

                Journal
                J Inflamm (Lond)
                J Inflamm (Lond)
                Journal of Inflammation (London, England)
                BioMed Central
                1476-9255
                2013
                31 January 2013
                : 10
                : 3
                Affiliations
                [1 ]The Departments of Diet and Nutrition, The Tel-Aviv Sourasky Medical Center, 6 Weizman St, Tel Aviv, Israel
                [2 ]Cardiology, Tel Aviv University, Tel Aviv, Israel
                [3 ]Internal Medicine “D” & “E” the Tel Aviv Sourasky Medical Center affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
                [4 ]The Department of Molecular Biology at the Faculty of Natural Sciences, the Ariel University of Samaria, Samaria, Israel
                [5 ]Department on Nutritional Sciences, the Ariel University of Samaria, Israel
                Article
                1476-9255-10-3
                10.1186/1476-9255-10-3
                3599567
                23369030
                239f6275-2e98-405c-89aa-5a5bd477e4e9
                Copyright ©2013 Raz et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 November 2012
                : 25 January 2013
                Categories
                Research

                Immunology
                inflammation,monounsaturated fats,nutrition,saturated fat
                Immunology
                inflammation, monounsaturated fats, nutrition, saturated fat

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