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High-fat Meal (high-fat + meal)
Selected AbstractsEffect of raisin consumption on oxidative stress and inflammation in obesityDIABETES OBESITY & METABOLISM, Issue 11 2008J. W. Rankin Aim:, Oxidative stress can initiate increased inflammation that elevates risk for cardiovascular disease. The objective of this study was to determine the effects of daily consumption of raisins on markers of oxidative stress, inflammation and endothelial activation in response to an acute high-fat meal in overweight individuals. Methods:, Seventeen overweight men and women consumed 90 g raisins or isocaloric placebo (264 kcal/day) for 14 days in a randomized, crossover design while following a low-flavonoid diet. The oxidative [urinary 8-iso-prostaglandin-F2, (8-epi PGF2,) and serum oxygen radical absorbance capacity (ORAC)], inflammatory (serum C-reactive protein and interleukin-6), endothelial (serum soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1, sVCAM-1) and metabolic [free fatty acids (FFAs), triacylglycerol, glucose and insulin] response to four high-fat (53%) meals was tested pre- and postintervention. Results:, Urinary 8-epi PGF2, decreased (,22%) and fasting ORAC increased (+3%) after both interventions combined. Fasting protein-free ORAC was modestly (+3.5%) higher during the raisin than the placebo intervention. Neither the meals nor the raisins consistently induced fasted markers of inflammation or endothelial dysfunction. Gender influenced postprandial metabolic responses in that males responded with higher serum FFAs, sVCAM-1 and glucose compared with females. Conclusions:, Serum antioxidant capacity was modestly increased by daily raisin consumption, but this did not alter fasted or postprandial inflammatory response in these relatively healthy but overweight individuals. Providing all food in regular pattern reduced measures of oxidative stress. [source] Transcription factor 7,like 2 polymorphism modulates glucose and lipid homeostasis, adipokine profile, and hepatocyte apoptosis in NASH,HEPATOLOGY, Issue 2 2009Giovanni Musso Genetic factors underlying the association of NAFLD with diabetes and atherosclerosis are unknown. Recent human studies suggest transcription factor 7,like 2 (TCF7L2) polymorphism predisposes to diabetes through modulation of ,-cell function and modulates lipid levels in familial dyslipidemia. Emerging experimental evidence connects TCF7L2 to adipocyte metabolism and lipid homeostasis, as well. We tested if TCF7L2 polymorphism is a risk factor for nonalcoholic fatty liver disease (NAFLD) and if it modulates liver injury, glucose homeostasis, lipoprotein, and adipokine profiles in NASH. TCF7L2 genotype and dietary habits of 78 nondiabetic normolipidemic NAFLD subjects and 156 age-, body mass index,, sex-matched healthy controls were assessed. In 39 biopsy-proven nonalcoholic steatohepatitis (NASH) and matched controls TCF7L2 polymorphism was correlated to liver histology and oral glucose tolerance test,derived parameters of glucose homeostasis. Patients with NASH and controls consumed a high-fat meal and TCF7L2 genotype was correlated to postprandial circulating lipoproteins, adipokines, and cytokeratin-18 fragments. The TCF7L2 CT/TT genotype was more frequent in NAFLD and predicted the presence and severity of liver disease, of ,-cell dysfunction, of reduced incretin effect and hepatic insulin resistance in NASH; it also modulated postprandial hepatocyte apoptosis, lipoproteins, and adipokine profiles in both groups. Conclusion: TCF7L2 polymorphism predisposes to NAFLD and significantly impacts liver injury, glucose homeostasis, and postprandial lipoprotein and adipokine responses to fat ingestion. This polymorphism also modulates a fat-induced increase in circulating markers of hepatocyte apoptosis in NASH. Targeting postprandial lipemia, at least in at-risk TCF7L2 genotypes, may improve liver disease and glucose dysmetabolism in these patients. (HEPATOLOGY 2008.) [source] Three-dimensional sonographic evaluation of gallbladder contractility: Comparison with cholescintigraphyJOURNAL OF CLINICAL ULTRASOUND, Issue 3 2006Hei Ja Yoon MD Abstract Purpose: To compare three-dimensional sonography (3D US) with quantitative cholescintigraphy for assessing gallbladder contractility. Methods: Gallbladder radioactivity was assessed in 35 patients with suspected gallbladder disease using a gamma camera 5, 30, 60, and 90 minutes after technetium 99m (Tc-99m) DISIDA injection and 30 and 60 minutes after ingestion of a high-fat meal. Immediate gallbladder images were obtained via 3D US. Gallbladder radioactivity at 120 minutes after injection of Tc-99m DISIDA was defined as 100%, and gallbladder contractility was calculated. Gallbladder volume on 3D US was calculated using a dedicated software. Pearson correlation analysis and simple linear regression analysis were used. Results: The mean gallbladder volume on 3D US was 25.3 ml after fasting and 6.6 ml after a high-fat meal. The mean gallbladder contractility index was 77.7% on cholescintigraphy (range, 18,99) and 73.4 on 3D US (range, 16.7,97.3). A linear correlation between cholescintigraphy and 3D US contractility indices was observed. The r value on Pearson analysis was 0.92 and R2 of the coefficient of determination was 0.85. The difference in measured contractility between the 2 methods ranged from +21.5% to ,15.0% (mean ± SD, 4.4 ± 8.7%). Conclusions: 3D US is a reliable and easy method for clinical measurement of the volume of the gallbladder and its contractility. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:123,127, 2006 [source] A population pharmacokinetic meta-analysis of maraviroc in healthy volunteers and asymptomatic HIV-infected subjectsBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 2008Phylinda L. S. Chan AIMS To develop a population pharmacokinetic model for maraviroc, a noncompetitive CCR5 antagonist, after oral administration of tablets to healthy volunteers and asymptomatic HIV-infected subjects and to quantify the inherent variability and influence of covariates on the parameters of the model. METHODS Rich pharmacokinetic data available from 15 studies in healthy volunteers (n = 365) and two studies in asymptomatic HIV-infected subjects (n = 48) were analysed using NONMEM. Maraviroc was administered as single or multiple oral tablet doses under fasted and fed conditions. Doses ranged from 100 to 1800 mg day,1. RESULTS A two-compartment model parameterized to separate out absorption and clearance components on bioavailability was used. Absorption was described by a lagged first-order process. A sigmoid Emax model described the effect of dose on absorption. A visual predictive check and nonparametric bootstrap evaluation confirmed that the model was a good description of the data. Typical CL, Vc and Vp values for a 30-year-old non-Asian are 51.5 l h,1, 132 l and 277 l, respectively. CONCLUSIONS For the typical non-Asian subject, fasted bioavailability increased asymptotically with dose from 24% at 100 mg to 33% at 600 mg. A high-fat meal taken with maraviroc reduced exposure by 43% for a 100-mg dose to approximately 25% at doses of 600 mg. The typical Asian subject had a 26.5% higher AUC than the typical non-Asian subject irrespective of dose, a difference not considered to be clinically relevant. None of the other covariates tested had any clinically relevant effects on exposure. [source] Effects of a high-fat meal on resistance vessel reactivity and on indicators of oxidative stress in healthy volunteersCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2001Andreas Schinkovitz High fat meals postprandially impair macrovascular endothelial function and a link to increased oxidative stress is suggested. Few information, on the other hand, exists on the effect of postprandial hyperlipidaemia on resistance vessel function. Under normal circumstances this vascular bed regulates tissue perfusion and, by controlling flow, impacts on macrovascular nitric oxide formation. The impact of a high fat meal (1200 kcal, 90 g fat, 46 g protein and 47 g carbohydrates) on postprandial resistance vessel reactivity and on indicators of oxidative stress was studied in 11 healthy subjects by venous-occlusion plethysmography using another six subjects as time control group. Ingestion of the test meal resulted in a pronounced increase of serum triglycerides from 1·05 ± 0·61 mmol l,1 in the fasting state to peak postprandial values of 1·94 ± 0·41 mmol l,1 (P < 0·001) reached after 4 h and a return to baseline after 8 h. Fasting peak reactive hyperaemia (RH) was 19·6 ± 2·4 ml min,1 (100 ml),1. Two hours after ingestion of the test meal peak RH was transiently reduced to 16·8 ± 2·2 ml min,1 (100 ml),1 (P < 0·05). No alteration of resting forearm perfusion was observed. The time course of peak RH suggested a potential biphasic effect of the test meal with an early impairment and a late increase of RH. Ingestion of a lipid rich test meal did not exert any influence on either total plasma antioxidant capacity given in trolox equivalents (513 ± 26 ,mol l,1 at baseline) or on plasma peroxides measured as H2O2 equivalents (469 ± 117 ,mol l,1). Our results suggest that ingestion of a meal containing 90 g of fat results in a transient impairment of reactive hyperaemia in healthy subjects but these vascular alterations are not accompanied by signs of systemically increased oxidative stress. [source] | ||||||||||