scholarly journals Endothelial inflammation correlates with subject triglycerides and waist size after a high-fat meal

2011 ◽  
Vol 300 (3) ◽  
pp. H784-H791 ◽  
Author(s):  
Ying I. Wang ◽  
John Schulze ◽  
Nadine Raymond ◽  
Tyler Tomita ◽  
Kayan Tam ◽  
...  
Keyword(s):  
Waist Circumference ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
High Fat ◽  
Membrane Expression ◽  
Serum Triglycerides ◽  
Endothelial Inflammation ◽  
Tnf Α ◽  
Postprandial Triglyceride ◽  
Fat Meal

A rise in postprandial serum triglycerides (PP-sTG) can potentiate inflammatory responses in vascular endothelial cells (ECs) and thus serves as an independent risk factor for predicting increased cardiovascular morbidity. We examined postprandial triglyceride-rich lipoproteins (PP-TGRLs) in subjects ranging from normal to hypertriglyceridemic for their capacity to alter EC acute inflammatory responses. Cultured human aortic ECs (HAECs) were conditioned with PP-TGRLs isolated from human serum at the peak after a moderately high-fat meal. VLDL particle size increased postprandially and varied directly with the subject's PP-sTG level and waist circumference. PP-TGRL particles bound to HAECs and were internalized via LDL receptor-mediated endocytosis. PP-TGRL alone did not induce an inflammatory response over the range of individuals studied. However, combined with low-dose TNF-α stimulation (0.3 ng/ml), it elicited a net 10–15% increase above cytokine alone in the membrane expression of VCAM-1, ICAM-1, and E-selectin, which was not observed with fasting TGRLs. In contrast to upregulation of ICAM-1 and E-selectin, VCAM-1 transcription and expression varied in direct proportion with individual PP-sTG and waist circumference. The extent of monocyte arrest on inflamed HAECs under shear stress also correlated closely with VCAM-1 expression induced by conditioning with PP-TGRL and TNF-α stimulation. This ex vivo approach provides a quantitative means to assess an individual's inflammatory potential, revealing a greater propensity for endothelial inflammation in hypertriglyceridemic individuals with abdominal obesity.

scholarly journals Casein Compared with Whey Proteins Affects the Organization of Dietary Fat during Digestion and Attenuates the Postprandial Triglyceride Response to a Mixed High-Fat Meal in Healthy, Overweight Men

2015 ◽  
Vol 145 (12) ◽  
pp. 2657-2664 ◽  
Author(s):  
François Mariotti ◽  
Marion Valette ◽  
Christelle Lopez ◽  
Hélène Fouillet ◽  
Marie-Hélène Famelart ◽  
...  
Keyword(s):  
Dietary Fat ◽  
Whey Proteins ◽  
High Fat ◽  
Postprandial Triglyceride ◽  
Fat Meal

scholarly journals The Postprandial Effect of Spice Consumption Delivered in a High-Fat Meal on Pro-Inflammatory Cytokine Secretion in Overweight/Obese Men (OR12-06-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Ester Oh ◽  
Kristina Petersen ◽  
Penny Kris-Etherton ◽  
Connie Rogers
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Inflammatory Cytokine ◽  
Mononuclear Cells ◽  
Controlled Trial ◽  
High Fat ◽  
Science Institute ◽  
Tnf Α ◽  
Postprandial Inflammation ◽  
Fat Meal

Abstract Objectives Postprandial lipidemia is a risk factor for cardiovascular disease. The postprandial inflammation that occurs concurrently with lipidemia following ingestion of a high-fat meal (HFM) may contribute to this association. Numerous individual spices have anti-inflammatory properties in vitro and in vivo in animal models and humans. However, the effect of consumption of a spice blend on inflammatory mediators has not been examined in humans in a randomized controlled trial. The objective of this study was to investigate the postprandial effect of spice consumption delivered in a HFM on inflammatory cytokine responses. Methods Overweight/obese (BMI ≥25 and ≤35 kg/m2), nonsmoking, men (40–65 years old) with elevated waist circumference (≥94 cm) and at least one other risk factor for cardiovascular disease were recruited for a 3-period crossover study (n = 12). In random order, participants consumed the following dietary interventions: 1) a HFM (1076 kcal, 39% kcal from saturated fat), 2) a HFM containing 2 g of spice blend, or 3) a HFM containing 6 g of spice blend with a ≥3-day washout period between each test meal. The spice blend consisted of black pepper, basil, bay leaf, cinnamon, coriander, cumin, ginger, oregano, parsley, rosemary, red pepper, thyme and turmeric. Participants fasted overnight and blood was collected before, and hourly for four hours after the HFM. Peripheral blood mononuclear cells (PBMCs) were isolated at each time point, and the number of monocytes (CD14+/HLA-DR+) were quantified by flow cytometry. PBMCs were stimulated with lipopolysaccharide (LPS) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8, MCP-1) were quantified by ELISA in the supernatants. Results Monocyte number (P = 0.001), and the secretion of IL-1β (P = 0.036) and TNF-α (P = 0.046) from LPS-stimulated PBMCs were significantly elevated during the four-hour time period after HFM consumption compared to the baseline. However, the presence of 6 g of spice in the HFM reduced the secretion of IL-6 (P = 0.046), IL-8 (P = 0.031), TNF-α (P = 0.001) and MCP-1 (P = 0.063) from PBMCs at 60 min after the meal. Conclusions Consumption of a HFM containing a spice blend attenuated postprandial inflammation in overweight/obese men. Funding Sources McCormick Science Institute; Penn State Clinical and Translational Science Institute

scholarly journals Organ Injury and Cytokine Release Caused by Peptidoglycan Are Dependent on the Structural Integrity of the Glycan Chain

2004 ◽  
Vol 72 (3) ◽  
pp. 1311-1317 ◽  
Author(s):  
Anders E. Myhre ◽  
Jon Fredrik Stuestøl ◽  
Maria K. Dahle ◽  
Gunhild Øverland ◽  
Christoph Thiemermann ◽  
...  
Keyword(s):  
Structural Integrity ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Organ Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cytokine Release ◽  
Ex Vivo Model ◽  
Glycan Chain ◽  
Tnf Α ◽  
Glutamyl Transferase

ABSTRACT Several studies have implicated a role of peptidoglycan (PepG) as a pathogenicity factor in sepsis and organ injury, in part by initiating the release of inflammatory mediators. We wanted to elucidate the structural requirements of PepG to trigger inflammatory responses and organ injury. Injection of native PepG into anesthetized rats caused moderate but significant increases in the levels of alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, and bilirubin (markers of hepatic injury and/or dysfunction) and creatinine and urea (markers of renal dysfunction) in serum, whereas PepG pretreated with muramidase to digest the glycan backbone failed to do this. In an ex vivo model of human blood, PepG containing different amino acids induced similar levels of the cytokines tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-8, and IL-10, as determined by plasma analyses (enzyme-linked immunosorbent assay). Hydrolysis of the Staphylococcus aureus cross-bridge with lysostaphin resulted in moderately reduced release of TNF-α, IL-6, IL-8, and IL-10, whereas muramidase digestion nearly abolished the ability to induce cytokine release and IL-6 mRNA accumulation in CD14+ monocytes compared to intact PepG. However, additional experiments showed that muramidase-treated PepG synergized with lipopolysaccharide to induce TNF-α and IL-10 release in whole blood, despite its lack of inflammatory activity when administered alone. Based on these studies, we hypothesize that the structural integrity of the glycan chain of the PepG molecule is very important for the pathogenic effects of PepG. The amino acid composition of PepG, however, does not seem to be essential for the inflammatory properties of the molecule.

scholarly journals Expression of AXL receptor tyrosine kinase relates to monocyte dysfunction and severity of cirrhosis

2019 ◽  
Vol 3 (1) ◽  
pp. e201900465 ◽  
Author(s):  
Robert Brenig ◽  
Oltin T Pop ◽  
Evangelos Triantafyllou ◽  
Anne Geng ◽  
Arjuna Singanayagam ◽  
...  
Keyword(s):  
Disease Severity ◽  
T Cell Activation ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Infectious Complications ◽  
Receptor Expression ◽  
Tnf Α ◽  
Acute Decompensation

Infectious complications in patients with cirrhosis frequently initiate episodes of decompensation and substantially contribute to the high mortality. Mechanisms of the underlying immuneparesis remain underexplored. TAM receptors (TYRO3/AXL/MERTK) are important inhibitors of innate immune responses. To understand the pathophysiology of immuneparesis in cirrhosis, we detailed TAM receptor expression in relation to monocyte function and disease severity prior to the onset of acute decompensation. TNF-α/IL-6 responses to lipopolysaccharide were attenuated in monocytes from patients with cirrhosis (n = 96) compared with controls (n = 27) and decreased in parallel with disease severity. Concurrently, an AXL-expressing (AXL+) monocyte population expanded. AXL+ cells (CD14+CD16highHLA-DRhigh) were characterised by attenuated TNF-α/IL-6 responses and T cell activation but enhanced efferocytosis and preserved phagocytosis of Escherichia coli. Their expansion correlated with disease severity, complications, infection, and 1-yr mortality. AXL+ monocytes were generated in response to microbial products and efferocytosis in vitro. AXL kinase inhibition and down-regulation reversed attenuated monocyte inflammatory responses in cirrhosis ex vivo. AXL may thus serve as prognostic marker and deserves evaluation as immunotherapeutic target in cirrhosis.

scholarly journals Determinants of the postprandial triglyceride response to a high-fat meal in healthy overweight and obese adults

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Stephanie M. Wilson ◽  
Adam P. Maes ◽  
Carl J. Yeoman ◽  
Seth T. Walk ◽  
Mary P. Miles
Keyword(s):  
Insulin Resistance ◽  
Aerobic Exercise ◽  
Substrate Utilization ◽  
Visceral Adiposity ◽  
High Fat ◽  
Obese Adults ◽  
Exercise Frequency ◽  
Explanatory Variables ◽  
Postprandial Triglyceride ◽  
Fat Meal

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.

scholarly journals Elevated Levels of Apolipoprotein CIII Increase the Risk of Postprandial Hypertriglyceridemia

2021 ◽  
Vol 12 ◽  
Author(s):  
Yunpeng Guan ◽  
Xiaoyu Hou ◽  
Peipei Tian ◽  
Luping Ren ◽  
Yong Tang ◽  
...  
Keyword(s):  
Waist Circumference ◽  
Venous Blood ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Model Assessment ◽  
High Fat ◽  
Clinical Trial Registry ◽  
Postprandial Hypertriglyceridemia ◽  
Group 2 ◽  
Fat Meal

BackgroundTo investigate possible mechanisms of postprandial hypertriglyceridemia (PPT), we analyzed serum lipid and apolipoprotein (Apo) AI, B, CII and CIII levels before and after a high-fat meal.MethodsThe study has been registered with the China Clinical Trial Registry (registration number:ChiCTR1800019514; URL: http://www.chictr.org.cn/index.aspx). We recruited 143 volunteers with normal fasting triglyceride (TG) levels. All subjects consumed a high-fat test meal. Venous blood samples were obtained during fasting and at 2, 4, and 6 hours after the high-fat meal. PPT was defined as TG ≥2.5 mmol/L any time after the meal. Subjects were divided into two groups according to the high-fat meal test results: postprandial normal triglyceride (PNT) and PPT. We compared the fasting and postprandial lipid and ApoAI, ApoB, ApoCII and ApoCIII levels between the two groups.ResultsSignificant differences were found between the groups in fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR), TG, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), TG-rich lipoprotein remnants (TRLRs), ApoB, ApoCIII, ApoAI/ApoB and ApoCII/ApoCIII. The insulin, HOMA-IR, TG, TC, LDL-C, non-HDL-C, TRLRs, ApoB, ApoCIII and ApoCII/ApoCIII values were higher in the PPT group, while the ApoAI/ApoB ratio was higher in the PNT group. The postprandial TG level peaked in the PNT group 2 hours after the meal but was significantly higher in the PPT group and peaked at 4 hours. TRLRs gradually increased within 6 hours after the high-fat meal in both groups. The area under the curve (AUC) of TG and TRLRs and the AUC increment were higher in the PPT group (P &lt; 0.001). ApoCIII peaked in the PNT group 2 hours after the meal and gradually decreased. ApoCIII gradually increased in the PPT group within 6 hours after the meal, exhibiting a greater AUC increment (P &lt; 0.001). Fasting ApoCIII was positively correlated with age, systolic and diastolic blood pressure, body mass index (BMI), waist circumference, TC, TG, LDL-C, non-HDL-C, TRLRs, and ApoB (P&lt;0.05). ApoCIII was an independent risk factor of PPT after adjustment for BMI, waist circumference, TC, LDL-C, and ApoB (P &lt; 0.001, OR=1.188).ConclusionsElevated ApoCIII levels may cause PPT.

scholarly journals High fat meals increases postprandial fat oxidation rate but not postprandial lipemia

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Chih-Hui Chiu ◽  
Tsung-Jen Yang ◽  
Che-Hsiu Chen ◽  
Ming-Jing Zeng
Keyword(s):  
Oxidation Rate ◽  
Postprandial Lipemia ◽  
Random Order ◽  
Fat Oxidation ◽  
Calorie Intake ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Postprandial Triglyceride ◽  
Fat Meal

Abstract Background This study investigated the effects of ingesting meals with the same calorie intake but distinct nutritional contents after exercise on postprandial lipemia the next day. Methods Eight healthy male participants completed two 2-day trials in a random order. On day 1, the participants underwent five 12 min bouts of cycling exercise with a bout of higher intensity exercise (4 min) after each and then a bout of lower intensity cycling (2 min). The total exercise time was 90 min. After the exercise, the participants ingested three high-fat or low-fat meals. On Day 2, the participants were asked to rest in the laboratory and ingest a high-fat meal. Their postprandial reaction after a high-fat meal was observed. Results Postprandial triglyceride concentrations in the high-fat diet trial and low-fat diet trial exhibited nonsignificant differences. Total TG AUC were no significantly different on HF trial and LF trial (HF: 6.63 ± 3.2; LF: 7.20 ± 3.4 mmol/L*4 h. p = 0.586). However, the postprandial fat oxidation rate total AUC (HF: 0.58 ± 0.1; LF: 0.39 ± 0.2 g/min*4 h. p = 0.045), plasma glucose, and insulin concentration of the high-fat trial were significantly higher than those of the low-fat trial. Conclusions This study revealed that meals with distinct nutritional contents after a 90-min exercise increased the postprandial fat oxidation rate but did not influence the postprandial lipemia after a high-fat meal the next day.

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