Dietary fat modifies the postprandial inflammatory state in subjects with metabolic syndrome: the LIPGENE study (original) (raw)
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British Journal of …, 2010
Subjects with the metabolic syndrome (MetS) have enhanced oxidative stress and inflammation. Dietary fat quality has been proposed to be implicated in these conditions. We investigated the impact of four diets distinct in fat quantity and quality on 8-iso-PGF 2a (a major F 2 -isoprostane and oxidative stress indicator), 15-keto-13,14-dihydro-PGF 2a (15-keto-dihydro-PGF 2a , a major PGF 2a metabolite and marker of cyclooxygenasemediated inflammation) and C-reactive protein (CRP). In a 12-week parallel multicentre dietary intervention study (LIPGENE), 417 volunteers with the MetS were randomly assigned to one of the four diets: two high-fat diets (38 % energy (%E)) rich in SFA or MUFA and two low-fat high-complex carbohydrate diets (28 %E) with (LFHCC n-3) or without (LFHCC) 1·24 g/d of very long chain n-3 fatty acid supplementation. Urinary levels of 8-iso-PGF 2a and 15-keto-dihydro-PGF 2a were determined by RIA and adjusted for urinary creatinine levels. Serum concentration of CRP was measured by ELISA. Neither concentrations of 8-iso-PGF 2a and 15-keto-dihydro-PGF 2a nor those of CRP differed between diet groups at baseline (P.0·07) or at the end of the study (P. 0·44). Also, no differences in changes of the markers were observed between the diet groups (8-iso-PGF 2a , P¼ 0·83; 15-keto-dihydro-PGF 2a , P¼0·45; and CRP, P¼ 0·97). In conclusion, a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study.
The role of dietary fatty acid intake in inflammatory gene expression: a critical review
Sao Paulo Medical Journal, 2017
CONTEXT AND OBJECTIVE: Diet is an important modifiable factor involved in obesity-induced inflammation. We reviewed clinical trials that assessed the effect of consumption of different fatty acids on the expression of inflammation-related genes, such as cytokines, adipokines, chemokines and transcription factors. DESIGN AND SETTING: Narrative review study conducted at a research center. METHODS: This was a review on the effect of fat intake on inflammatory gene expression in humans. RESULTS: Consumption of saturated fatty acids (SFAs) was related to postprandial upregulation of genes associated with pro-inflammatory pathways in peripheral blood mononuclear cells (PBMCs), in comparison with monounsaturated fatty acid (MUFA) or polyunsaturated fatty acid (PUFA) intake. In addition, acute intake of a high-SFA meal also induced a postprandial pro-inflammatory response for several inflammatory genes in subcutaneous adipose tissue. Both high-MUFA and high-PUFA diets showed anti-inflammato...
Atherosclerosis, 2009
Background: Inflammation is crucial in all stages of atherosclerosis, and few studies have investigated the effect of dietary fat on markers of inflammation related to this disease during the postprandial period. Objective: To evaluate the chronic effects of dietary fat on the postprandial expression of proinflammatory genes in peripheral blood mononuclear cells (PBMCs) in healthy subjects. Design: 20 healthy men followed three different diets for 4 weeks each, according to a randomized crossover design: Western diet: 15% protein, 47% carbohydrates (CHO), 38% fat (22% saturated fatty acid (SFA)); Mediterranean diet: 15% protein, 47% CHO, 38% fat (24% monounsaturated fatty acid (MUFA)); CHO-rich and n-3 diet: 15% protein, 55% CHO, <30% fat (8% polyunsaturated fatty acid (PUFA)). After 12h fast, volunteers were given a breakfast with a fat composition similar to that consumed in each of the diets-butter breakfast: 35% SFA; olive oil breakfast: 36% MUFA; walnut breakfast: 16% PUFA, 4% ␣-linolenic acid (LNA). Results: The butter breakfast induced a higher increase in tumor necrosis factor (TNF)-␣ messenger RNA (mRNA) expression than the olive oil or walnut breakfasts (P = 0.014) in PBMCs. Moreover, we found a higher postprandial response in the mRNA of interleukin (IL)-6 with the intake of butter and olive oil breakfasts than with the walnut breakfast (P = 0.025) in these cells. However, the effects of the three fatty breakfasts on the plasma concentrations of these proinflammatory parameters showed no significant differences (P = N.S.). Conclusion: Consumption of a butter-enriched meal elicits greater postprandial expression of proinflammatory cytokine mRNA in PBMCs, compared to the olive oil and walnut breakfasts.
Diabetology & Metabolic Syndrome, 2019
Background: The rising incidence of metabolic syndrome (MetS) is a major public health problem. The inflammatory potential of diet contributes to the development of MetS. The aim of this study was to investigate the relationship between empirical dietary inflammatory pattern (EDIP) and risk of MetS among the Tehranian population. Our hypothesis was that high EDIP would increase the risk of MetS and its components. Methods: In this prospective study, 2216 adults were selected from among the Tehran Lipid and Glucose Study participants. The usual dietary intakes were estimated using a valid and reliable food frequency questionnaire. Biochemical and anthropometric measurements were assessed at baseline and over 6.2 years of follow up. MetS components were defined according to the modified national Cholesterol Education Program Adult Treatment Panel III. The inflammatory potential of diet was calculated using EDIP score; more positive scores means higher pro-inflammatory diet. Adjusted logistic regression models were used to estimate the occurrence of MetS and its components across quartiles of EDIP score. Results: Mean ± SD for EDIP score was 0.61 ± 0.40 (range − 2.3 to 6.9). Participants with the highest EDIP scores, had a higher risk of MetS incidence compared to those with the lowest score (OR: 1.75, 95% CI 1.21-2.54, P trend = 0.003). Among the MetS components, hyperglycemia, abdominal obesity, and low HDL-C had a significant positive association with EDIP score; (OR: 1.46, 95% CI 1.03-2.08, P trend = 0.026), (OR: 1.43, 95% CI 1.03-1.97, P trend = 0.046), and (OR: 1.57, 95% CI 1.34-2.19, P trend = 0.015), respectively. No significant association was found between EDIP score, hypertension and hypertriglyceridemia. Conclusion: Our finding indicated that higher intake of the pro-inflammatory diet may be an independent risk factor for the development of MetS, hyperglycemia, low HDL-C and abdominal obesity in Tehranian adults.
Lipids, 2013
Individuals with metabolic syndrome (MetS) have a higher risk of type 2 diabetes and cardiovascular disease, therefore, research has been directed at reducing various components that contribute to MetS and associated metabolic impairments, including chronic low-grade inflammation. Epidemiological, human, animal and cell culture studies provide evidence that dietary n-3 polyunsaturated fatty acids (n-3 PUFA), including alpha-linolenic acid (18:3n-3, ALA), eicosapentaenoic acid (20:5n-3, EPA) and/or docosahexaenoic acid (22:6n-3, DHA) may improve some of the components associated with MetS. The current review will discuss recent evidence from human observational and intervention studies that focused on the effects of ALA, EPA or DHA on inflammatory markers in healthy adults and those with one or more features of MetS. Observational studies in healthy adults support the recommendation that a diet rich in n-3 fatty acids may play a role in preventing and reducing inflammation, whereas intervention studies in healthy adults have yielded inconsistent results. The majority of intervention studies in adults with features of MetS have reported a benefit for some inflammatory measures; however, other studies using high n-3 fatty acid doses and long supplementation periods have reported no effect. Overall, the data reviewed herein support recommendations for regular fatty fish consumption and point toward health benefits in terms of lowering inflammation in adults with one or more features of MetS.
Inflammation, obesity and comorbidities: the role of diet
Public health …, 2007
The adipocyte metabolism has been shown to change during the fat enlargement process associated to obesity. Several procoagulant proteins such as plasminogen activator inhibitor type 1, tissue factor or factor VII and also inducible nitric oxide synthase show higher expression in adipose tissue of obese people in comparison to lean. This overexpression could explain at least a part of the atherogenic and cardiovascular risk associated with obesity. In addition to cytokine secretion, many other features have been observed to be common to adipocyte and monocyte/macrophage lines: for example, phagocytic and microbicidal activities, and possibly a cellular plasticity of adipose precursors. Overweight and obesity are associated with an increased risk of such metabolic abnormalities as dyslipidemia, hypertension or type 2 diabetes mellitus and cardiovascular diseases, common features of the metabolic syndrome. Initially, insulin resistance or hyperinsulinemia was suggested as the origin of these abnormalities. More recent studies indicate that adipokynes have an important role in obesity-associated metabolic complications, and suggest that chronically elevated local or systemic concentrations of adipokynes contribute to the development of complications associated with obesity and metabolic syndrome. Considering all the evidence relating to diet and inflammation, the best diet for protecting against the metabolic derangements associated with obesity and metabolic syndrome would be high in fibre-rich cereals, fruit, vegetables, fish, virgin olive oil and nuts; moderate in wine; and low in meat, processed meat foods and trans-fatty acids.
Applied Physiology, Nutrition, and Metabolism, 2007
Metabolic syndrome (MetS) comprises an array of metabolic risk factors including abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Individuals with MetS are at elevated risk for diabetes and cardiovascular disease. Central to the etiology of MetS is an interrelated triad comprising inflammation, abdominal obesity, and aberrations in fatty acid metabolism, coupled with the more recently recognized changes in metabolism during the postprandial period. We review herein preliminary evidence regarding the role of dietary n-3 polyunsaturated fatty acids in modulating each of the components of the triad of adiposity, inflammation, and fatty acid metabolism, with particular attention to the role of the postprandial period as a contributor to the pathophysiology of MetS.
The Journal of Nutrition, 2010
Dietary fat intake plays a critical role in the development of metabolic syndrome (MetS). This study addressed the hypothesis that dietary fat quantity and quality may differentially modulate postprandial lipoprotein metabolism in MetS patients. A multicenter, parallel, randomized, controlled trial conducted within the LIPGENE study randomly assigned MetS patients to 1 of 4 diets: high-SFA [HSFA; 38% energy (E) from fat, 16% E as SFA], high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA], and 2 low-fat, high-complex carbohydrate [LFHCC; 28% E from fat] diets supplemented with 1.24 g/d of long-chain (LC) (n-3) PUFA (ratio 1.4 eicosapentaenoic acid:1 docosahexaenoic acid) or placebo (1.24 g/d of high-oleic sunflower-seed oil) for 12 wk each. A fat challenge with the same fat composition as the diets was conducted pre-and postintervention. Postprandial total cholesterol, triglycerides (TG), apolipoprotein (apo) B, apo B-48, apo A-I, LDL-cholesterol, HDL-cholesterol and cholesterol, TG, retinyl palmitate, and apo B in TG-rich lipoproteins (TRL; large and small) were determined pre-and postintervention. Postintervention, postprandial TG (P , 0.001) and large TRL-TG (P = 0.009) clearance began earlier and was faster in the HMUFA group compared with the HSFA and LFHCC groups. The LFHCC (n-3) group had a lower postprandial TG concentration (P , 0.001) than the other diet groups. Consuming the LFHCC diet increased the TG (P = 0.04), large TRL-TG (P = 0.01), TRL-cholesterol (P , 0.001), TRL-retinyl palmitate (P = 0.001), and TRL-apo B (P = 0.002) area under the curve compared with preintervention values. In contrast, long-term ingestion of the LFHCC (n-3) diet did not augment postprandial TG and TRL metabolism. In conclusion, postprandial abnormalities associated with MetS can be attenuated with LFHCC (n-3) and HMUFA diets. The adverse postprandial TG-raising effects of long-term LFHCC diets may be avoided by concomitant LC (n-3) PUFA supplementation to weight-stable MetS patients.
Nutrition in Clinical Practice, 2010
I nflammation has recently emerged as an important aspect of the pathophysiology of age-related infirmity and the major chronic diseases of industrialized societies, including cardiovascular disease, type 2 diabetes mellitus, Alzheimer's disease, and many types of cancer. Most observational studies and clinical trials have used high-sensitivity C-reactive protein (HS-CRP) as a biochemical marker of inflammation, because it is relatively stable and easy to measure. Elevation of HS-CRP predicts future development of diabetes mellitus and hypertension more accurately than body mass index (BMI). Any attempt to create a diet for optimal health must consider the impact of the dietary prescription on systemic inflammation. Part of this impact results from visceral adiposity, because of the inflammatory effects of abdominal obesity. Part of this impact can be attributed to direct or indirect effects of nutrients and dietary pattern on components of the inflammatory response itself. This overview will first consider the relationship between nutrient intake and inflammatory mediators, relying mainly on human observational data, and will then describe observational and interventional trials, primarily