Preference for and sensitivity to flavanol mean degree of polymerization in model wines is correlated with body composition.

Bitterness and astringency (dryness) are characteristic sensory attributes of flavanol-rich foods. The degree of polymerization (DP) of flavanols influences their bitter and astringent sensations. Smaller DP compounds can enter the papillae on the tongue, eliciting a bitter response. Larger DP compounds are sterically inhibited from entering papillae and instead interact with oral proteins, cause precipitation, and elicit astringent sensations. Previous research has indicated that bitterness preference is related to health status, density of fungiform papillae on the tongue, and sensitivity to bitter compounds such as 6-n-propyl-thiouracil (PROP). The purpose of this study was to examine trends in liking, bitterness intensity, and astringency intensity of wine-like products with flavanols of different DP using a consumer sensory panel. Participants (n = 102) were segmented by phenotypes: body fat percentage (BF%), body mass index (BMI), PROP sensitivity, and stated bitter food preference. Differences in wine liking, perceived bitterness intensity, and astringency intensity were observed between three model wine samples of varying flavanol mean degrees of polymerization (mDP, i.e. the average size (polymer length) of flavanol compounds in a mixture). Specifically, with increased mDP, overall liking and bitterness liking decreased, with concurrent increased perception of bitterness and astringency intensity. Greater differences between phenotypes were observed when participants were segmented by BF% and BMI classification, than when segmented by PROP sensitivity classification. Reduced ability to detect differences in bitterness and astringency were noted in participants of higher weight status. Overall, these data suggest that weight status in adults is a greater predictor of liking of flavanol-rich foods than bitterness sensitivity (as determined by PROP classification), and that reduced perception of bitterness and astringency associated with weight gain may impact selection and preference for these foods.

Methylsulfonylmethane decreases inflammatory response to tumor necrosis factor-α in cardiac cells.

The development of various cardiovascular diseases (CVDs) are associated with chronic inflammation. Tumor necrosis factor α (TNF-α) is a pro-inflammatory cytokine that activates the nuclear factor-κB (NF-κB) signaling pathway, leading to increased inflammatory cytokine expression, such as interleukin-6 (IL-6). Interventions to reduce each of these factors have been demonstrated to reduce the development of CVD. Methylsulfonylmethane (MSM) is a naturally occurring compound that demonstrates anti-inflammatory effects in humans and various animal and cell culture models. The effects of MSM include decreased NF-κB activation, decreased expression of TNF-α, and IL-6. However, the effects of MSM within the heart have not yet been examined. Therefore, the purpose of this investigation was to determine whether MSM protects cardiac cells from inflammation that occurs in response to pro-inflammatory stimuli. A novel immortalized human ventricular cardiomyocyte cell line, designated Ac16, developed and characterized in the laboratory of Dr. Mercy Davidson, Columbia Invention Report No. 823, U.S. patent No. 7,223,599 were utilized. Cells were treated with TNF-α, alone or in combination with MSM. To confirm an appropriate dosage of MSM, the effect of various concentrations on cell viability, and IL-6 production were examined. The effect of MSM on transcript expression of pro-inflammatory markers and activation of NF-κB were examined with the established dose by real-time quantitative PCR and western blot, respectively. MSM treatment combined with TNF-α significantly decreased IL-6 production and transcript expression compared to TNF-α alone. These findings indicate that MSM may protect against inflammation in the heart, and thereby protect against inflammation-linked CVDs. Further study is warranted to determine the effect of MSM on cardiovascular health outcomes.

Involvement of the δ-opioid receptor in exercise-induced cardioprotection.

NEW FINDINGS: What is the central question of this study? Does the δ-opioid receptor trigger exercise-induced cardioprotection against ischaemia-reperfusion injury? What is the main finding and its importance? In exercised hearts, the δ-opioid receptor appears to trigger cardioprotection against ischaemia-reperfusion-induced tissue necrosis but not apoptosis. ABSTRACT: Endogenous opioids mediate exercise-induced cardioprotection against ischaemia-reperfusion (IR) injury, although the opioid receptor subtype mediating this effect is unknown. We investigated whether the δ-opioid receptor mediates exercise-induced cardioprotection against IR injury. Endogenous opioids are produced in various tissues, including the heart and skeletal muscle; therefore, we also sought to identify the effect of exercise on circulating endogenous opioid as well as transcript, protein and receptor expression in heart and skeletal muscle. Male Sprague-Dawley rats (n = 73) were assigned randomly to treadmill exercise or sedentary treatments. Cardiac tissue and serum were harvested 0, 20 and 120 min following exercise and from sedentary animals (n = 32) to quantify effects on proenkephalin and δ-opioid receptor mRNA and protein levels, as well as serum enkephalin. Skeletal muscle (soleus) was harvested at identical time points for determination of proenkephalin protein and mRNA. A separate group of rats (n = 41) were randomly assigned to sham operation (Sham; surgical control), sedentary (Sed), exercise (Ex) or exercise + Î´-opioid receptor antagonist (ExD; naltrindole, 5 mg kg(-1) i.p.) and received IR by left anterior descending coronary artery ligation in vivo. After IR, tissues were harvested to quantify treatment effects on necrosis and apoptosis. Cardiac proenkephalin mRNA expression increased following exercise (0 min, P = 0.03; 120 min, P = 0.021), while soleus expression was unaffected. Exercise-induced changes in serum enkephalin were undetectable. After IR, tissue necrosis was elevated in Sed and ExD hearts (P < 0.001 and P = 0.003, respectively) compared with the Sham group, while the Ex group was partly protected. After IR, apoptosis was evident in Sed hearts (P = 0.016), while Ex and ExD hearts were protected. Data suggest that cardioprotective opioids are produced by the heart, but not by the soleus. After IR, the δ-opioid receptor may mediate, in part, cardioprotection against necrosis but not apoptosis.

Consuming a Western diet for two weeks suppresses fetal genes in mouse hearts.

Diets high in sugar and saturated fat (Western diet) contribute to obesity and pathophysiology of metabolic syndrome. A common physiological response to obesity is hypertension, which induces cardiac remodeling and hypertrophy. Hypertrophy is regulated at the level of chromatin by repressor element 1-silencing transcription factor (REST), and pathological hypertrophy is associated with reexpression of a fetal cardiac gene program. Reactivation of fetal genes is commonly observed in hypertension-induced hypertrophy; however, this response is blunted in diabetic hearts, partially due to upregulation of the posttranslational modification O-linked-ß-N-acetylglucosamine (O-GlcNAc) to proteins by O-GlcNAc transferase (OGT). OGT and O-GlcNAc are found in chromatin-modifying complexes, but it is unknown whether they play a role in Western diet-induced hypertrophic remodeling. Therefore, we investigated the interactions between O-GlcNAc, OGT, and the fetal gene-regulating transcription factor complex REST/mammalian switch-independent 3A/histone deacetylase (HDAC). Five-week-old male C57BL/6 mice were fed a Western (n = 12) or control diet (n = 12) for 2 wk to examine the early hypertrophic response. Western diet-fed mice exhibited fasting hyperglycemia and increased body weight (P < 0.05). As expected for this short duration of feeding, cardiac hypertrophy was not yet evident. We found that REST is O-GlcNAcylated and physically interacts with OGT in mouse hearts. Western blot analysis showed that HDAC protein levels were not different between groups; however, relative to controls, Western diet hearts showed increased REST and decreased ANP and skeletal α-actin. Transcript levels of HDAC2 and cardiac α-actin were decreased in Western diet hearts. These data suggest that REST coordinates regulation of diet-induced hypertrophy at the level of chromatin.

Effect of resveratrol and quercetin supplementation on redox status and inflammation after exercise.

Resveratrol and quercetin function as antioxidants and anti-inflammatories in vitro, but these mechanisms have been minimally examined in combination in exercising humans. The purpose of this investigation was to examine supplementation as a countermeasure against oxidative stress and inflammation in response to exercise. Fourteen athletes were randomly assigned, in a double-blind crossover design, to a resveratrol and quercetin combination (RQ) (120 mg resveratrol and 225 mg quercetin for 6 days and 240 mg resveratrol and 450 mg quercetin on day 7 just prior to exercise) or to placebo (P). There was a 1-week washout between trials. Blood was taken at baseline, pre-exercise, immediately after exercise, and 1 h after exercise. Plasma was analyzed for oxidative stress (F2-isoprostanes and protein carbonyls), antioxidant capacity (ferric-reducing ability of plasma (FRAP), Trolox equivalent antioxidant capacity (TEAC), oxygen radical absorptive capacity (ORAC)), and inflammation (cytokine interleukin (IL)-8 and C-reactive protein (CRP)). Statistical design utilized a 2 × 3 ANOVA and Student's t test. Pre-exercise values were not different from baseline for any measure. The postexercise increase in F2-isoprostanes was significantly less (p = 0.039 interaction) with RQ (68%) than with P (137%). Protein carbonyls, FRAP, ORAC, and TEAC significantly increased after exercise but were not affected by treatment. IL-8 and CRP increased significantly immediately after exercise but were not affected by treatment. These data indicate that RQ significantly reduces exercise-induced lipid peroxidation without associated changes in inflammation or plasma antioxidant status.

Blood oxidative-stress markers during a high-altitude trek.

UNLABELLED: Oxidative stress occurs as a result of altitude-induced hypobaric hypoxia and physical exercise. The effect of exercise on oxidative stress under hypobaric hypoxia is not well understood. PURPOSE: To determine the effect of high-altitude exercise on blood oxidative stress. Nine male participants completed a 2-d trek up and down Mt Rainer, in North America, at a peak altitude of 4,393 m. Day 1 consisted of steady-pace climbing for 6.25 hr to a final elevation of 3,000 m. The 4,393-m summit was reached on Day 2 in approximately 5 hr. Climb-rest intervals varied but were consistent between participants, with approximately 14 hr of total time including rest periods. Blood samples were assayed for biomarkers of oxidative stress and antioxidant potential at the following time points: Pre (before the trek), 3Kup (at ascent to 3,000 m), 3Kdown (at 3,000 m on the descent), and Post (posttrek at base elevation). Blood serum variables included ferric-reducing antioxidant potential (FRAP), Trolox equivalent antioxidant capacity (TEAC), protein carbonyls (PC), and lipid hydroperoxides. Serum FRAP was elevated at 3Kup and 3Kdown compared with Pre and Post values (p = .004, 8% and 11% increase from Pre). Serum TEAC values were increased at 3Kdown and Post (p = .032, 10% and 18% increase from Pre). Serum PC were elevated at 3Kup and 3Kdown time points (p = .034, 194% and 138% increase from Pre), while lipid hydroperoxides were elevated Post only (p = .004, 257% increase from Pre). CONCLUSIONS: Findings indicate that high-altitude trekking is associated with increased blood oxidative stress.

Evaluation of arrhythmia scoring systems and exercise-induced cardioprotection.

INTRODUCTION: Exercise is protective against ventricular arrhythmias induced by ischemia (I), the condition of inadequate blood flow, and reperfusion (R), the reestablishment of blood flow. This protection is observed clinically and scientifically by decreased incidence in ECG abnormalities. Numerous scoring systems exist for the quantification of ventricular arrhythmia severity. On the basis of preventricular contractions, ventricular tachycardia, and ventricular fibrillation frequency, these scoring systems are intended to provide more robust ECG outcome indicators than individual arrhythmia variables. Scoring systems vary primarily on continuous versus discontinuous treatment of the data, which should be considered when matching these arrhythmia metrics to scientific applications. PURPOSE: The aim of this investigation was to evaluate seven ECG scoring systems in the assessment of ventricular arrhythmia severity after IR in male Sprague-Dawley rats. METHODS: Animals remained sedentary or exercised (3 d of treadmill exercise for 60 min) before surgically induced IR. A subset of sedentary animals served as sham, undergoing surgical procedure without IR. ECGs were evaluated under blinded conditions by three trained individuals. Single arrhythmia data and the parametric score were analyzed by one-way ANOVA, whereas the Kruskal-Wallis was used to compare group means for all nonparametric scoring systems between groups. RESULTS: IR produced a significant arrhythmic response in exercised and sedentary rats as determined by all arrhythmia scoring systems. Four arrhythmia metrics resulted in significant differences between exercised and sedentary treatments (P < 0.001), whereas three metrics did not. CONCLUSIONS: Continuous versus discontinuous treatment of the data may account for variation in scoring system outcomes. These data confirm that exercise protects against IR-induced arrhythmias, and care must be taken when selecting an arrhythmia scoring system for ECG evaluation.