Alex K Chen Posted January 15, 2016 Report Share Posted January 15, 2016 and is it a non-linear function of postprandial glucose increase? Link to comment Share on other sites More sharing options...
Dean Pomerleau Posted January 15, 2016 Report Share Posted January 15, 2016 Alex, Yes, inflammation does peak after meals, and it appears to be more a function of the meal's fat content than its influence on blood glucose, although glucose levels may play a factor in triggering inflammation as well [1]. Endotoxins, particularly in animal products, are another cause of postprandial inflammation, as discussed in this Nutritionfacts.org video. Below is a picture from this review [2] of the factors that most affect postprandial lipemia (fat in the blood) resulting in inflammation, ranging from most beneficial at the top to most detrimental at the bottom: Note - these authors say: Since humans are postprandial most of the day, the continuous generation of [lipoproteins] remnants after each meal may be one of the triggers for the development of atherosclerosis. This might help you get motivated to cut back from three meals per day, as you asked about on this other thread! --Dean ------ [1] Adv Exp Med Biol. 2014;824:161-70. doi: 10.1007/978-3-319-07320-0_12. Postprandial inflammation: targeting glucose and lipids. de Vries MA(1), Klop B, Janssen HW, Njo TL, Westerman EM, Castro Cabezas M. Author information: (1)Department of Internal Medicine, Center for Diabetes and Vascular Medicine, Sint Franciscus Gasthuis, 10900, Rotterdam, 3004 BA, The Netherlands, m.devries@sfg.nl. Many risk factors have been identified as being responsible for the process of atherogenesis. Several of these risk factors are related to inflammation, which is an obligatory feature of the atherosclerotic plaque. Increasing evidence suggests that postprandial lipoproteins and glucose may be involved in the inflammatory process preceding the development of atherosclerosis. During the postprandial situation, remnants of chylomicrons and very low-density lipoproteins bind to circulating leukocytes and endothelial cells, leading to a state of acute activation with the expression of integrins on different cells, the generation of oxidative stress, production of cytokines and complement activation. Elevated plasma glucose levels may also induce leukocyte activation in humans. In addition, advanced glycation end products, formed during hyperglycemia, cause inflammation and endothelial damage. This chain of events results in a situation of acute inflammation causing endothelial dysfunction, which may be one of the earliest defects in atherogenesis. Interestingly, while this may occur several times each day after each meal, there is only limited information on the contribution of different nutrients on the postprandial inflammatory processes. In this review, we will focus on the available evidence and we will discuss the role of lifestyle and pharmaceutical interventions in modulating postprandial inflammation. PMID: 25038999 ------------ [2] Int J Vasc Med. 2012;2012:947417. doi: 10.1155/2012/947417. Epub 2011 Sep 25. Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases. Klop B(1), Proctor SD, Mamo JC, Botham KM, Castro Cabezas M. Author information: (1)Department of Internal Medicine, Center for Diabetes and Vascular Medicine, Sint Franciscus Gasthuis, 3004 BA Rotterdam, The Netherlands. Postprandial hyperlipidemia with accumulation of remnant lipoproteins is a common metabolic disturbance associated with atherosclerosis and vascular dysfunction, particularly during chronic disease states such as obesity, the metabolic syndrome and, diabetes. Remnant lipoproteins become attached to the vascular wall, where they can penetrate intact endothelium causing foam cell formation. Postprandial remnant lipoproteins can activate circulating leukocytes, upregulate the expression of endothelial adhesion molecules, facilitate adhesion and migration of inflammatory cells into the subendothelial space, and activate the complement system. Since humans are postprandial most of the day, the continuous generation of remnants after each meal may be one of the triggers for the development of atherosclerosis. Modulation of postprandial lipemia by lifestyle changes and pharmacological interventions could result in a further decrease of cardiovascular mortality and morbidity. This paper will provide an update on current concepts concerning the relationship between postprandial lipemia, inflammation, vascular function, and therapeutic options. PMCID: PMC3179890 PMID: 21961070 Link to comment Share on other sites More sharing options...
Alex K Chen Posted January 15, 2016 Author Report Share Posted January 15, 2016 Hmm interesting. Is this just restricted to saturated fats though? Wouldn't MUFAs decrease inflammation after meals? Or is there a certain limit after which MUFAs would start increasing it again? Link to comment Share on other sites More sharing options...
Dean Pomerleau Posted January 16, 2016 Report Share Posted January 16, 2016 Wouldn't MUFAs decrease inflammation after meals? Or is there a certain limit after which MUFAs would start increasing it again? You would think MUFA would decrease (or at least not increase) post-meal inflammation. Michael may correct me if I'm wrong, but I'm not sure this is the case however. Study [1] suggests little difference between MUFA and SFA on post-meal lipid metabolism - e.g. ApoB was similarly elevated by the two type of fats. In study [2], carbohydrates were better than MUFA for post meal inflammation markers like ApoB, at least in Type 1 diabetics: Our data suggest that in patients with type 1 diabetes, a CHO diet might be preferable to a Mono diet, since adherence to the former results in a lower number of circulating postprandial lipoprotein particles that are potentially atherogenic. --Dean -------- [1] Br J Nutr. 1998 May;79(5):419-24. The effect of test meal monounsaturated fatty acid: saturated fatty acid ratio on postprandial lipid metabolism. Roche HM(1), Zampelas A, Jackson KG, Williams CM, Gibney MJ. Author information: (1)Unit of Nutrition, Trinity Centre for Health Sciences, St James's Hospital, Dublin, Ireland. hmroche@tcd.ie Epidemiological evidence shows that a diet high in monounsaturated fatty acids (MUFA) but low in saturated fatty acids (SFA) is associated with reduced risk of CHD. The hypocholesterolaemic effect of MUFA is known but there has been little research on the effect of test meal MUFA and SFA composition on postprandial lipid metabolism. The present study investigated the effect of meals containing different proportions of MUFA and SFA on postprandial triacylglycerol and non-esterified fatty acid (NEFA) metabolism. Thirty healthy male volunteers consumed three meals containing equal amounts of fat (40 g), but different proportions of MUFA (12, 17 and 24% energy) in random order. Postprandial plasma triacylglycerol, apolipoprotein B-48, cholesterol, HDL-cholesterol, glucose and insulin concentrations and lipoprotein lipase (EC 3.1.1.34) activity were not significantly different following the three meals which varied in their levels of SFA and MUFA. There was a significant difference in the postprandial NEFA response between meals. The incremental area under the curve of postprandial plasma NEFA concentrations was significantly (P = 0.03) lower following the high-MUFA meal. Regression analysis showed that the non-significant difference in fasting NEFA concentrations was the most important factor determining difference between meals, and that the test meal MUFA content had only a minor effect. In conclusion, varying the levels of MUFA and SFA in test meals has little or no effect on postprandial lipid metabolism. PMID: 9682660 ---------- [2] Arterioscler Thromb Vasc Biol. 1998 May;18(5):773-82. Differences in the metabolism of postprandial lipoproteins after a high-monounsaturated-fat versus a high-carbohydrate diet in patients with type 1 diabetes mellitus. Georgopoulos A(1), Bantle JP, Noutsou M, Swaim WR, Parker SJ. Author information: (1)Minneapolis Veterans Affairs Medical Center, MN 55417, USA. georg003@maroon.tc.umn.edu There is little information comparing the effects of a high-monounsaturated (Mono)-fat versus a high-carbohydrate (CHO) diet in patients with type 1 diabetes mellitus. In the present study, the effects of these diets on a number of metabolic parameters were compared. Seventeen normolipidemic, nonobese patients with type 1 diabetes were provided with the diets for 4 weeks each in a randomized, crossover design. The percentages of Mono fat of the two diets were 25 Mono versus 9 CHO, with a corresponding total fat content of 40% versus 24% and a total CHO content of 45% versus 61%. At the end of each dietary period, parameters of glycemic control, coagulation factors, and fasting and postprandial lipoproteins were assessed. There were no differences in weight, glycemia, insulin dose, fasting lipid profile, or coagulation factors between the two diets. However, the metabolism of postprandial lipoproteins after a fat load differed; viz, after the Mono diet compared with the CHO diet, mean plasma triglyceride levels over 10 hours were higher (P=.0025, by repeated-measures ANOVA). The levels of triglyceride (P=.0045) and retinyl esters (P=.0046) in chylomicrons (Sf>400) and chylomicron remnants (Sf 100 to 400) (P=.0047 and P=.043, respectively), and the total particle number (apolipoprotein B levels) in chylomicron remnants (P=.001) and small, very low density lipoprotein (Sf 20 to 100, P=.016) were also higher. Our data suggest that in patients with type 1 diabetes, a CHO diet might be preferable to a Mono diet, since adherence to the former results in a lower number of circulating postprandial lipoprotein particles that are potentially atherogenic. PMID: 9598837 Link to comment Share on other sites More sharing options...
Dean Pomerleau Posted January 16, 2016 Report Share Posted January 16, 2016 Qualifier - to avoid Michael jumping down my throat. MUFA, including low phenolic olive oil, appears to increase postprandial inflammation as mentioned above, but high phenolic content, extra virgin olive oil appears not to, or at least not as much, according to [1]. --Dean ---------- [1] Food Chem. 2014 Nov 1;162:161-71. doi: 10.1016/j.foodchem.2014.04.047. Epub 2014 Apr 24. Olive oil phenolic compounds decrease the postprandial inflammatory response by reducing postprandial plasma lipopolysaccharide levels. Camargo A(1), Rangel-Zuñiga OA(2), Haro C(2), Meza-Miranda ER(2), Peña-Orihuela P(2), Meneses ME(2), Marin C(2), Yubero-Serrano EM(2), Perez-Martinez P(2), Delgado-Lista J(2), Fernandez-Real JM(3), Luque de Castro MD(4), Tinahones FJ(5), Lopez-Miranda J(2), Perez-Jimenez F(2). Full text via sci-hub.io: http://www.sciencedirect.com.sci-hub.io/science/article/pii/S0308814614006049 We investigated the molecular mechanisms by which phenolic compounds (phenols) in virgin olive oil reduce the postprandial inflammatory response with the aim of identifying the transcription factor involved and the downstream effects. Olive oil-based breakfasts prepared with virgin olive oil (VOO) with high (398 ppm), intermediate (149 ppm) and low (70 ppm) phenol content were administered to 49 metabolic syndrome patients following a randomized crossover design. The consumption of a high-phenol VOO-based breakfast limited the increase of lipopolysaccharide plasma levels, TLR4, and SOCS3 proteins (p<0.001, p=0.041 and p=0.008, respectively), the activation of NF-κB (p=0.016) and the IL6 (p=0.007 and p=0.048, low and intermediate oil, respectively), IL1B (p=0.002, intermediate oil), and CXCL1 (p=0.001) postprandial gene expression, in peripheral blood mononuclear cells, as compared with the consumption of a breakfast prepared with the same oil but with low or intermediate phenol content. Virgin olive oil phenolic compounds reduce the postprandial inflammatory response in association with postprandial plasma lipopolysaccharide levels. Copyright © 2014 Elsevier Ltd. All rights reserved. PMID: 24874372 Link to comment Share on other sites More sharing options...
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