Showing papers on "Normal diet published in 2012"
TL;DR: It is found that daily injections of osteocalcin at either 3 or 30 ng/g/day significantly improved glucose tolerance and insulin sensitivity in mice fed a normal diet and when mice were fed a high-fat diet, daily injections partially restored insulin sensitivity and glucose tolerance.
376 citations
TL;DR: These results provide a new mechanism by which nitrate exerts beneficial effects on muscle function with applications to sports performance and a potential therapeutic role in conditions with muscle weakness.
Abstract: Dietary inorganic nitrate has profound effects on health and physiological responses to exercise. Here, we examined if nitrate, in doses readily achievable via a normal diet, could improve Ca(2+) handling and contractile function using fast- and slow-twitch skeletal muscles from C57bl/6 male mice given 1 mm sodium nitrate in water for 7 days. Age matched controls were provided water without added nitrate. In fast-twitch muscle fibres dissected from nitrate treated mice, myoplasmic free [Ca(2+)] was significantly greater than in Control fibres at stimulation frequencies from 20 to 150 Hz, which resulted in a major increase in contractile force at ≤ 50 Hz. At 100 Hz stimulation, the rate of force development was ∼35% faster in the nitrate group. These changes in nitrate treated mice were accompanied by increased expression of the Ca(2+) handling proteins calsequestrin 1 and the dihydropyridine receptor. No changes in force or calsequestrin 1 and dihydropyridine receptor expression were measured in slow-twitch muscles. In conclusion, these results show a striking effect of nitrate supplementation on intracellular Ca(2+) handling in fast-twitch muscle resulting in increased force production. A new mechanism is revealed by which nitrate can exert effects on muscle function with applications to performance and a potential therapeutic role in conditions with muscle weakness.
274 citations
TL;DR: Fat-laden KCs are "primed" to recruit lymphocytes and exhibit a pro-inflammatory phenotype, which is reversible with inhibition of lipogenesis, which could be reversed by inhibition oflipogenesis.
204 citations
TL;DR: It is found that in the HFD group, metformin significantly attenuated the insulin resistant condition by improving metabolic parameters, decreasing peripheral and brain oxidative stress levels, and improving learning behavior, compared to the vehicle-treated group.
197 citations
TL;DR: It is proposed that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissues through direct interplay with adipocytes and prevent insulin resistance.
Abstract: Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance.
187 citations
TL;DR: It is found that the loss of LSD1 function, either by short interfering RNA or by selective inhibitors in adipocytes, induces a number of regulators of energy expenditure and mitochondrial metabolism such as PPARγ coactivator-1α resulting in the activation of mitochondrial respiration.
Abstract: Environmental factors such as nutritional state may act on the epigenome that consequently contributes to the metabolic adaptation of cells and the organisms. The lysine-specific demethylase-1 (LSD1) is a unique nuclear protein that utilizes flavin adenosine dinucleotide (FAD) as a cofactor. Here we show that LSD1 epigenetically regulates energy-expenditure genes in adipocytes depending on the cellular FAD availability. We find that the loss of LSD1 function, either by short interfering RNA or by selective inhibitors in adipocytes, induces a number of regulators of energy expenditure and mitochondrial metabolism such as PPARγ coactivator-1α resulting in the activation of mitochondrial respiration. In the adipose tissues from mice on a high-fat diet, expression of LSD1-target genes is reduced, compared with that in tissues from mice on a normal diet, which can be reverted by suppressing LSD1 function. Our data suggest a novel mechanism where LSD1 regulates cellular energy balance through coupling with cellular FAD biosynthesis.
187 citations
TL;DR: Rosiglitazone significantly improved peripheral insulin resistance and insulin-induced long-term depression and increased neuronal Akt/PKB-ser phosphorylation in response to insulin and prevented brain mitochondrial conformational changes and attenuated brain mitochondrial swelling and brain mitochondrial ROS production.
Abstract: We previously demonstrated that a high-fat diet (HFD) consumption can cause not only peripheral insulin resistance, but also neuronal insulin resistance. Moreover, the consumption of an HFD has been shown to cause mitochondrial dysfunction in both the skeletal muscle and liver. Rosiglitazone, a peroxizome proliferator-activated receptor-γ ligand, is a drug used to treat type 2 diabetes mellitus. Recent studies suggested that rosiglitazone can improve learning and memory in both human and animal models. However, the effects of rosiglitazone on neuronal insulin resistance and brain mitochondria after the HFD consumption have not yet been investigated. Therefore, we tested the hypothesis that rosiglitazone improves neuronal insulin resistance caused by a HFD via attenuating the dysfunction of neuronal insulin receptors and brain mitochondria. Rosiglitazone (5 mg/kg · d) was given for 14 d to rats that were fed with either a HFD or normal diet for 12 wk. After the 14(th) week, all animals were euthanized, and their brains were removed and examined for insulin-induced long-term depression, neuronal insulin signaling, and brain mitochondrial function. We found that rosiglitazone significantly improved peripheral insulin resistance and insulin-induced long-term depression and increased neuronal Akt/PKB-ser phosphorylation in response to insulin. Furthermore, rosiglitazone prevented brain mitochondrial conformational changes and attenuated brain mitochondrial swelling, brain mitochondrial membrane potential changes, and brain mitochondrial ROS production. Our data suggest that neuronal insulin resistance and the impairment of brain mitochondria caused by a 12-wk HFD consumption can be reversed by rosiglitazone.
175 citations
TL;DR: This work aimed to determine which baseline characteristics and which fast track elements are independent predictors of faster postoperative recovery in patients undergoing resection for colon cancer.
Abstract: Aim It is questioned whether all separate fast track elements are essential for enhanced postoperative recovery. We aimed to determine which baseline characteristics and which fast track elements are independent predictors of faster postoperative recovery in patients undergoing resection for colon cancer. Method Data from the LAFA trial database were used. In this trial, fast track care was compared with standard perioperative care in 400 patients undergoing laparoscopic or open surgery for colonic cancer. During admission 19 fast track elements per patient were prospectively evaluated and scored whether or not they were successfully applied. To identify predictive factors six baseline characteristics and those fast track items that were successfully achieved were entered in a univariate and multivariate linear regression analysis with total postoperative hospital stay (THS) as the primary outcome. Results In 400 patients, two baseline characteristics and two fast track elements were found to be significant independent predictors of THS: female sex [B = 0.85; 95% CI 0.75‐0.96; reduction of 15% (CI 14‐25%) in THS], laparoscopic resection [B = 0.85; 95% CI 0.75‐ 0.96; reduction of 15% (CI 14‐25%) in THS], ‘normal diet at postoperative days 1, 2 and 3’ [B = 0.70; 95% CI 0.61‐0.81; reduction of 30% (CI 19‐39%) in THS] and ‘enforced mobilization at postoperative days 1, 2 and 3’ [B = 0.68; 95% CI 0.59‐0.80; reduction of 32% (CI 20‐ 41%) in THS]. Conclusion Evaluating only those fast track elements that were successfully achieved, enforced advancement of oral intake, early mobilization, laparoscopic surgery and female sex were independent determinants of early recovery.
152 citations
TL;DR: Beetroot juice will lower BP in men when consumed as part of a normal diet in free-living healthy adults when consumed in a double-blind, randomized, placebo-controlled, crossover study.
Abstract: Background: The consumption of beetroot juice on a low nitrate diet may lower blood pressure (BP) and therefore reduce the risk of cardiovascular events. However, it is unknown if its inclusion as part of a normal diet has a similar effect on BP. The aim of the study was to conduct a randomized controlled trial with free-living adults to investigate if consuming beetroot juice in addition to a normal diet produces a measureable reduction in BP. Method: Fifteen women and fifteen men participated in a double-blind, randomized, placebo-controlled, crossover study. Volunteers were randomized to receive 500 g of beetroot and apple juice (BJ) or a placebo juice (PL). Volunteers had BP measured at baseline and at least hourly for 24-h following juice consumption using an ambulatory blood pressure monitor (ABPM). Volunteers remained at the clinic for 1-h before resuming normal non-strenuous daily activities. The identical procedure was repeated 2-wk later with the drink (BJ or PL) not consumed on the first visit. Results: Overall, there was a trend (P=0.064) to lower systolic blood pressure (SBP) at 6-h after drinking BJ relative to PL. Analysis in men only (n=13) after adjustment for baseline differences demonstrated a significant (P<0.05) reduction in SBP of 4 – 5 mmHg at 6-h after drinking BJ.
137 citations
TL;DR: Data clearly demonstrate that paternal obesity has significant negative effects on the embryo at a variety of key early developmental stages, resulting in delayed development, reduced placental size and smaller offspring.
Abstract: Worldwide, 48% of adult males are overweight or obese. An association between infertility and excessive body weight is now accepted, although focus remains primarily on females. It has been shown that parental obesity results in compromised embryo development, disproportionate changes in embryo metabolism and reduced blastocyst cell number. The aim of this study was to determine whether paternal obesity has negative effects on the resultant embryo. Specifically, using in vitro fertilisation (IVF), we wanted to isolate the functional effects of obesity on sperm by examining the subsequent embryo both pre- and post-implantation. Epididymal sperm was collected from age matched normal and obese C57BL/6 mice and cryopreserved for subsequent IVF with oocytes collected from Swiss females (normal diet/weight). Obesity was induced in male mice by feeding a high fat diet of 22% fat for 10 weeks. Resultant embryos were cultured individually and development monitored using time-lapse microscopy. Paternal obesity resulted in a significant delay in preimplantation embryo development as early as syngamy (P<0.05). Metabolic parameters were measured across key developmental stages, demonstrating significant reduction in mitochondrial membrane potential (P<0.01). Blastocysts were stained to determine trophectoderm (TE) and inner cell mass (ICM) cell numbers, revealing significant differences in the ratio of cell allocation to TE and ICM lineages (P<0.01). Functional studies examining blastocyst attachment, growth and implantation demonstrated that blastocysts derived from sperm of obese males displayed significantly reduced outgrowth on fibronectin in vitro (P<0.05) and retarded fetal development in vivo following embryo transfer (P<0.05). Taken together, these data clearly demonstrate that paternal obesity has significant negative effects on the embryo at a variety of key early developmental stages, resulting in delayed development, reduced placental size and smaller offspring.
129 citations
TL;DR: Surprisingly, exercise was more effective than diet control, although both exercise and diet control ameliorated HFD-induced memory deficit and Aβ deposition, which provides solid evidence that exercise is a useful intervention to rescue H FD-induced aggravation of cognitive decline in transgenic model mice of AD.
TL;DR: Despite a large number of positive effects of selenium and selenoproteins in various model systems, there have now been some human clinical trials that have shown adverse effects of Se supplementation, according to various endpoints.
Abstract: Selenium (Se) is an essential micronutrient for humans, acting as a component of the unusual amino acids, selenocysteine (Se-Cys) and selenomethionine (Se-Met). Where Se levels are low, the cell cannot synthesise selenoproteins, although some selenoproteins and some tissues are prioritised over others. Characterised functions of known selenoproteins, include selenium transport (selenoprotein P), antioxidant/redox properties (glutathione peroxidases (GPxs), thioredoxin reductases and selenoprotein P) and anti-inflammatory properties (selenoprotein S and GPx4). Various forms of Se are consumed as part of a normal diet, or as a dietary supplement. Supplementation of tissue culture media, animal or human diets with moderate levels of certain Se compounds may protect against the formation of DNA adducts, DNA or chromosome breakage, and chromosome gain or loss. Protective effects have also been shown on mitochondrial DNA, and on telomere length and function. Some of the effects of Se compounds on gene expression may relate to modulation of DNA methylation or inhibition of histone deacetylation. Despite a large number of positive effects of selenium and selenoproteins in various model systems, there have now been some human clinical trials that have shown adverse effects of Se supplementation, according to various endpoints. Too much Se is as harmful as too little, with animal models showing a "U"-shaped efficacy curve. Current recommended daily allowances differ among countries, but are generally based on the amount of Se necessary to saturate GPx enzymes. However, increasing evidence suggests that other enzymes may be more important than GPx for Se action, that optimal levels may depend upon the form of Se being ingested, and vary according to genotype. New paradigms, possibly involving nutrigenomic tools, will be necessary to optimise the forms and levels of Se desirable for maximum protection of genomic stability in all humans.
TL;DR: Exercise training reduces hepatic inflammation, injury, and fibrosis by suppressing macrophage infiltration, which is considered the hepatic event in metabolic syndrome.
Abstract: Nonalcoholic steatohepatitis, which is considered the hepatic event in metabolic syndrome, was recently associated with the innate immune system. Although regular exercise reduces hepatic injury markers like serum alanine aminotransferase (ALT) levels, the mechanisms regulating the effects of exercise on steatohepatitis are unclear. This study aimed to clarify whether exercise training suppresses hepatic injury, inflammation, and fibrosis by suppressing macrophage infiltration. Male C57BL/6J (4-week old) mice were randomly divided into four groups: normal diet (ND) control (n=7), ND exercise (n=5), high-fat diet and high-fructose water (HFF) control (n=11), and HFF exercise (n=11) groups. Mice were fed the ND or HFF from 4 to 20 weeks of age. The exercise groups were trained on a motorized treadmill for 60 min/day, five times/week. The nonalcoholic fatty liver disease (NAFLD) activity score and plasma ALT activity, indicators of liver injury, were increased in HFF control mice but were attenuated in HFF exercise mice. Hepatic inflammation, indicated by hepatic tumor necrosis factor (TNF)-α levels and hepatic resident macrophage infiltration, was significantly lower in HFF exercise mice than in HFF control mice. Hepatic fibrosis markers (histological hepatic fibrosis detected by Sirius red and α-smooth muscle actin staining and tissue inhibitor of matrix metalloproteinase-1 mRNA) were attenuated in HFF exercise mice compared with HFF control mice. These results suggest that exercise training reduces hepatic inflammation, injury, and fibrosis by suppressing macrophage infiltration.
TL;DR: Daily consumption of a low dose of RV is effective for protecting against diet-induced obesity, hepatic steatosis and dyslipidaemia in HFD-fed mice.
Abstract: Consumption of a high-fat diet (HFD) enriched in saturated fat induces excessive weight gain due to adiposity, which can lead to metabolic complications, as well as increased risk of fatty liver disease and CVD. The present study investigated the underlying mechanism and dose–response effects of resveratrol (RV) on obesity, hepatic steatosis and dyslipidaemia in mice fed a HFD. Male C57BL/6J mice were fed a normal diet or a HFD (20 % fat, w/w) combined with 0·005 or 0·02 % (w/w) RV for 10 weeks. As expected, mice fed a HFD developed obesity, as shown by increased body weight gain, visceral fat, hepatic fat and plasma cholesterol. RV significantly reduced visceral fat and plasma NEFA. In the liver of HFD-fed mice, RV significantly reduced TAG and cholesterol, as well as lipid droplet number and size. A low dose of RV (0·005 %) appeared to be more effective than a higher dose of RV (0·02 %) for suppressing adiposity and hepatic steatosis development with a significant decrease in body weight gain, plasma TAG and total cholesterol levels. These changes were seemingly attributable to a suppression of the fatty acid (FA) synthase, glucose-6-phosphate dehydrogenase, and phosphatidate phosphohydrolase and/or an activation of FA oxidation in the liver and epididymal adipose tissue. In conclusion, daily consumption of a low dose of RV is effective for protecting against diet-induced obesity, hepatic steatosis and dyslipidaemia in HFD-fed mice.
TL;DR: It is found that a carbohydrate-free dietetic regimen that lowers the fasting glucose levels blunts p53 mutant expression and oncogenic activity relative to a normal diet in several animal model systems, indicating that the stability of mutant forms of p53 is influenced by the levels of glucose and by dietetic habits.
Abstract: The majority of human tumors express mutant forms of p53 at high levels, promoting gain of oncogenic functions and correlating with disease progression, resistance to therapy and unfavorable prognosis. p53 mutant accumulation in tumors is attributed to the ability to evade degradation by the proteasome, the only currently recognized machinery for p53 disruption. We report here that glucose restriction (GR) induces p53 mutant deacetylation, routing it for degradation via autophagy. Depletion of p53 leads, in turn, to robust autophagic activation and to cell death, while expression of degradation-defective mutant p53 blocks autophagy and enables survival to GR. Furthermore, we found that a carbohydrate-free dietetic regimen that lowers the fasting glucose levels blunts p53 mutant expression and oncogenic activity relative to a normal diet in several animal model systems. These findings indicate that the stability of mutant forms of p53 is influenced by the levels of glucose and by dietetic habits. They also unravel the existence of an inhibitory loop between autophagy and mutant p53 that can be exploited therapeutically.
TL;DR: The polyphenols resveratrol and S17834 administered concurrently with a HFHS diet prevent the development of left ventricular hypertrophy, interstitial fibrosis, and diastolic dysfunction.
Abstract: Background—Diet-induced obesity is associated with metabolic heart disease characterized by left ventricular hypertrophy and diastolic dysfunction. Polyphenols such as resveratrol and the synthetic flavonoid derivative S17834 exert beneficial systemic and cardiovascular effects in a variety of settings including diabetes mellitus and chronic hemodynamic overload. Methods and Results—We characterized the structural and functional features of a mouse model of diet-induced metabolic syndrome and used the model to test the hypothesis that the polyphenols prevent myocardial hypertrophy and diastolic dysfunction. Male C57BL/6J mice were fed a normal diet or a diet high in fat and sugar (HFHS) with or without concomitant treatment with S17834 or resveratrol for up to 8 months. HFHS diet–fed mice developed progressive left ventricular hypertrophy and diastolic dysfunction with preservation of systolic function in association with myocyte hypertrophy and interstitial fibrosis. In HFHS diet–fed mice, there was incr...
TL;DR: A systematic review of randomised controlled trials examining the impact of perioperative administration of systemic antibiotics on post-tonsillectomy morbidity in children or adults suggests that although individual studies vary in their findings, there is no evidence to support a consistent, clinically important impact of antibiotics.
Abstract: Background This is an update of a Cochrane Review first published in The Cochrane Library in Issue 2, 2008 and previously updated in 2010.Tonsillectomy continues to be one of the most common surgical procedures performed in children and adults. Despite improvements in surgical and anaesthetic techniques, postoperative morbidity, mainly in the form of pain, remains a significant clinical problem. Postoperative bacterial infection of the tonsillar fossa has been proposed as an important factor causing pain and associated morbidity, and some studies have found a reduction in morbid outcomes following the administration of perioperative antibiotics. Objectives To determine whether perioperative antibiotics reduce pain and other morbid outcomes following tonsillectomy. Search methods We searched the Cochrane Ear, Nose and Throat Disorders Group Trials Register; the Cochrane Central Register of Controlled Trials (CENTRAL); PubMed; EMBASE; CINAHL; Web of Science; BIOSIS Previews; Cambridge Scientific Abstracts; ICTRP and additional sources for published and unpublished trials. The date of the most recent search was 20 March 2012. Selection criteria All randomised controlled trials examining the impact of perioperative administration of systemic antibiotics on post-tonsillectomy morbidity in children or adults. Data collection and analysis Two authors independently collected data. Primary outcomes were pain, consumption of analgesia and secondary haemorrhage (defined as significant if patient re-admitted, transfused blood products or returned to theatre, and total (any documented) haemorrhage). Secondary outcomes were fever, time taken to resume normal diet and activities and adverse events. Where possible, we generated summary measures using random-effects models. Main results Ten trials, comprising a pooled total of 1035 participants, met the eligibility criteria. Most did not find a significant reduction in pain with antibiotics. Similarly, antibiotics were mostly not shown to be effective in reducing the need for analgesics. Antibiotics were not associated with a reduction in significant secondary haemorrhage rates (risk ratio (RR) 0.49, 95% CI 0.08 to 3.11, P = 0.45) or total secondary haemorrhage rates (RR 0.90, 95% CI 0.56 to 1.44, P = 0.66). With regard to secondary outcomes, antibiotics reduced the proportion of patients with fever (RR 0.63, 95% CI 0.46 to 0.85, P = 0.002). Authors' conclusions The present systematic review, including meta-analyses for select outcomes, suggests that although individual studies vary in their findings, there is no evidence to support a consistent, clinically important impact of antibiotics in reducing the main morbid outcomes following tonsillectomy (i.e. pain, need for analgesia and secondary haemorrhage rates). The limited benefit apparent with antibiotics may be a result of positive bias introduced by several important methodological shortcomings in the included trials. Based on existing evidence, therefore, we would advocate against the routine prescription of antibiotics to patients undergoing tonsillectomy. Whether a subgroup of patients who might benefit from selective administration of antibiotics exists is unknown and needs to be explored in future trials.
TL;DR: Elevated sympathetic drive and impaired baroreflex function appear integral to the rapid development of obesity-related hypertension, which likely lies in alterations in the response of neurons in the hypothalamus.
Abstract: Hypertension and elevated sympathetic drive result from consumption of a high-calorie diet and deposition of abdominal fat, but the etiology and temporal characteristics are unknown. Rabbits instrumented for telemetric recording of arterial pressure and renal sympathetic nerve activity (RSNA) were fed a high-fat diet for 3 weeks then control diet for 1 week or control diet for 4 weeks. Baroreflexes and responses to air-jet stress and hypoxia were determined weekly. After 1 week of high-fat diet, caloric intake increased by 62%, accompanied by elevated body weight, blood glucose, plasma insulin, and leptin (8%, 14%, 134%, and 252%, respectively). Mean arterial pressure, heart rate, and RSNA also increased after 1 week (6%, 11%, and 57%, respectively). Whereas mean arterial pressure and body weight continued to rise over 3 weeks of high-fat diet, heart rate and RSNA did not change further. The RSNA baroreflex was attenuated from the first week of the diet. Excitatory responses to air-jet stress diminished over 3 weeks of high-fat diet, but responses to hypoxia were invariant. Resumption of a normal diet returned glucose, insulin, leptin, and heart rate to control levels, but body weight, mean arterial pressure, and RSNA remained elevated. In conclusion, elevated sympathetic drive and impaired baroreflex function, which occur within 1 week of consumption of a high-fat, high-calorie diet, appear integral to the rapid development of obesity-related hypertension. Increased plasma leptin and insulin may contribute to the initiation of hypertension but are not required for maintenance of mean arterial pressure, which likely lies in alterations in the response of neurons in the hypothalamus.
TL;DR: The results indicate the beneficial effect of administering the bacteria isolated from fish gut microflora, B. amyloliquefaciens, in improving growth, FCR and immunological parameters and indicates that the probiotic colonization in the gut is essential for the best responses and economics.
Abstract: This study evaluated the effect of two bacteria, Bacillus amyloliquefaciens and the dairy yogurt (DY) Lactobacillus sp., on improving the growth performance, feed conversion ratio (FCR) and some immunological and haematological parameters. Nile tilapia (19.1 g) were stocked in 0.42 m3 tanks at 67 fish m−3 and fed with two probiotic-incorporated diets and a control diet for 99 days, followed by a normal diet for another 61 days. At the end of the probiotic feeding, the mean weight, FCR and production rate showed no significant difference among the treatments. However, after 61 days of feeding of the normal diet, the B. amyloliquefaciens fish showed significantly superior growth and better FCR than the control. The DY group had the lowest growth and the poorest FCR. Significantly higher serum lysozyme activity, head-kidney superoxide dismutase, total immunoglobulin and serum bacterial agglutination titres were recorded in the probiotic groups than the control. Haematological parameters showed no difference between treatments. The B. amyloliquefaciens fed fish showed that the gut microflora was dominated by B. amyloliquefaciens even after the withdrawal of the probiotic. On the contrary, the probiotic bacterial species isolated from the dairy yoghurt did not persist longer in the gut. These results indicate the beneficial effect of administering the bacteria isolated from fish gut microflora, B. amyloliquefaciens, in improving growth, FCR and immunological parameters. The high persistence of B. amyloliquefaciens indicates that the probiotic colonization in the gut is essential for the best responses and economics.
TL;DR: It is reported that curcumin can target the cytosolic/nuclear thioredoxin system to eventually elevate oxidative stress in HeLa cells and disclose a previously unrecognized prooxidant mechanism ofCurcumin in cells, and provide a deep insight in understanding how cur cumin works in vivo.
Journal Article•
TL;DR: Soluble ICam-1 is a reliable measure of ICAM-1 expression in the aorta, vasa vasorum and fibroblasts/smooth muscle cells and a cholesterol diet plays a role in the expression of IC AM-1 but not in that of VCAM- 1 in the rat aortA.
Abstract: Backround: Members of the immunoglobulin superfamily of endothelial adhesion molecules, vascular cell adhesion molecule (VCAM-1) and intercellular cell adhesion molecule (ICAM-1), participate in leukocyte adhesion to the endothelium and play an important role in all stages of atherosclerosis. The aim of the study was to examine the expression of VCAM-1 and ICAM-1 in the aorta of rats at the early stages of atherosclerosis and the correlation with their plasma concentrations. Materials and Methods: Male rats (n=44), 10 weeks of age, were divided in 4 groups. Groups A and C (n=12) were fed with rich cholesterol diet for 12 and 16 weeks, respectively. Group B (regression group, n=12) was fed for the first 12 weeks with rich cholesterol diet and for another 4 weeks with normal diet. Group D (control group, n=8) was fed with normal diet for 12 weeks. We measured the serum lipid profile, the concentration of soluble ICAM-1 and the immunohistochemical expression of ICAM-1 and VCAM-1 in the endothelium, media and vasa vasorum of the aorta. Results: There were significant differences (p<0.05) in the expression of ICAM-1 between group C (maximum time of rich cholesterol diet) and all other groups in the 3 groups of the aorta studied. There was regression of the expression of ICAM-1 in group B and significant differences (p<0.05) between group B and all the other groups, except group D in the expression of ICAM-1. There were no significant differences in the expression of VCAM-1 between any groups. The serum concentration of soluble ICAM-1 positively correlated with the expression of the molecule in the vasa vasorum (r=0.35, p<0.05) and fibroblasts/smooth muscular cells (r=0.34, p<0.05) of the aorta. Conclusion: A cholesterol diet plays a role in the expression of ICAM-1 but not in that of VCAM-1 in the rat aorta. The expression of ICAM-1 in the aorta regresses after the withdrawal of a cholesterol-rich diet. Soluble ICAM-1 is a reliable measure of ICAM-1 expression in the aorta, vasa vasorum and fibroblasts/smooth muscle cells. Atherosclerosis is influenced by the interactions of cellular adhesion molecules. The cell-surface expression of these molecules in response to pathophysiological stimuli mediates the interaction between the endothelium and blood cells and is central to the development of atherosclerosis (1). Atherosclerosis affects discrete regions of the vasculature, such as vessel curvatures and bifurcations. These regions are characterized by disturbed oscillatory flow that induces up- regulation of proinflammatory adhesion molecules, such as intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 (2). Chemokines then stimulate leukocytes and up-regulate α4 and β2 integrin binding to VCAM-1 and ICAM-1 respectively, which themselves mediate later steps (2). VCAM-1 and ICAM-1 are closely related in structure and function. Both are cytokine-inducible Ig gene superfamily members that bind leukocyte integrins (3). We investigated the expression of ICAM-1 and VCAM-1 in the aortic wall of Wistar rats in response to hypercholesterolemia. We also investigated the correlation between the expression of adhesion molecules, the lipid
TL;DR: The anti‐obesity effects of kimchi fermented either without starter culture or with a specific starter culture, Weissella koreensis OK1‐6, are investigated.
Abstract: Aims
In this study, we investigated the anti-obesity effects of kimchi (Korean traditional fermented vegetable) fermented either without starter culture or with a specific starter culture, Weissella koreensis OK1-6
Methods and Results
C57BL/6J mice were divided into four groups (n = 7); normal diet, HF (high-fat diet), HF-KC (high-fat diet containing 3% kimchi manufactured without starter) and HF-KCO (high-fat diet containing 3% kimchi manufactured with the starter culture W koreensis OK1-6) After 12 weeks of dietary intervention, the mice were killed, and serum and tissue samples were examined Serum and hepatic lipid profile, insulin, leptin concentration and expression level of lipid anabolic genes like peroxisome proliferator-activated receptor γ, stearoyl-CoA desaturase-1, liver X receptor α and SREBP2 were significantly decreased (<0·05) along with body and epididymal fat pad weight in the HF-KCO group compared with the HF-KC and HF group
Conclusions
These results suggested that kimchi fermented with the starter W koreensis OK1-6 has anti-obesity effects in HF-induced obese mice
Significance and Impact of the Study
These results may contribute to nutraceutical and food industries in developing functional food and probiotics based therapies for the treatment and prevention of obesity
TL;DR: GA contributes to the antiobesity effect of BTE as an active constituent by inhibiting pancreatic lipase activity, which is strongly correlated with the body weight.
Abstract: The antiobesity effects of Chinese black tea (Pu-erh tea) and of gallic acid (GA) were investigated using in vitro and in vivo assays. Chinese black tea extract (BTE) and GA inhibited pancreatic lipase activity in a dose-dependent manner in vitro; the IC(inhibitory concentration)(50) values were 101.6 and 9.2 µg/mL, respectively. Black tea extract (50, 100 mg/kg body weight (b.w.)) and GA (15, 45 mg/kg b.w.) significantly suppressed the elevation of blood triglyceride after oral administration of a corn oil emulsion (8 mL oil/kg b.w.) to male ddY mice. Moreover, the antiobesity effects of BTE and GA were also evaluated in a mouse model of diet-induced obesity. Female ddY mice were divided into seven groups; normal diet (ND) group, high fat diet (HFD) group, BTE (0.2% and 0.6% of diets) groups, and GA (0.007%, 0.02% and 0.1% of diets) groups; the experimental groups were fed the test diets for 12 weeks. The BTE 0.6% and GA 0.1% groups showed significant suppression of weight gain. The weight of parametrial adipose tissue was strongly correlated with the body weight. These results suggest that GA contributes to the antiobesity effect of BTE as an active constituent by inhibiting pancreatic lipase activity.
TL;DR: Activation of S100A8/TLR4 signalling was elucidated in an animal model of diabetic glomerular injury accompanied with hyperlipidaemia, which may provide novel therapeutic targets in progressive diabetic nephropathy.
Abstract: Hyperlipidaemia is an independent risk factor for the progression of diabetic nephropathy, but its molecular mechanism remains elusive. We investigated in mice how diabetes and hyperlipidaemia cause renal lesions separately and in combination, and the involvement of Toll-like receptor 4 (TLR4) in the process. Diabetes was induced in wild-type (WT) and Tlr4 knockout (KO) mice by intraperitoneal injection of streptozotocin (STZ). At 2 weeks after STZ injection, normal diet was substituted with a high-fat diet (HFD). Functional and histological analyses were carried out 6 weeks later. Compared with treatment with STZ or HFD alone, treatment of WT mice with both STZ and HFD markedly aggravated nephropathy, as indicated by an increase in albuminuria, mesangial expansion, infiltration of macrophages and upregulation of pro-inflammatory and extracellular-matrix-associated gene expression in glomeruli. In Tlr4 KO mice, the addition of an HFD to STZ had almost no effects on the variables measured. Production of protein S100 calcium binding protein A8 (calgranulin A; S100A8), a potent ligand for TLR4, was observed in abundance in macrophages infiltrating STZ-HFD WT glomeruli and in glomeruli of diabetic nephropathy patients. High-glucose and fatty acid treatment synergistically upregulated S100a8 gene expression in macrophages from WT mice, but not from KO mice. As putative downstream targets of TLR4, phosphorylation of interferon regulatory factor 3 (IRF3) was enhanced in kidneys of WT mice co-treated with STZ and HFD. Activation of S100A8/TLR4 signalling was elucidated in an animal model of diabetic glomerular injury accompanied with hyperlipidaemia, which may provide novel therapeutic targets in progressive diabetic nephropathy.
TL;DR: In diet-induced obesity, early activation of TLR-mediated inflammatory signalling cascades by CD antigen genes, leads to increased expression of pro-inflammatory cytokines and chemokines, resulting in chronic low-grade inflammation.
Abstract: Visceral white adipose tissue (WAT) hypertrophy, adipokine production, inflammation and fibrosis are strongly associated with obesity, but the time-course of these changes in-vivo are not fully understood. Therefore, the aim of this study was to establish the time-course of changes in adipocyte morphology, adipokines and the global transcriptional landscape in visceral WAT during the development of diet-induced obesity. C57BL/6 J mice were fed a high-fat diet (HFD) or normal diet (ND) and sacrificed at 8 time-points over 24 weeks. Excessive fat accumulation was evident in visceral WAT depots (Epidydimal, Perirenal, Retroperitoneum, Mesentery) after 2–4 weeks. Fibrillar collagen accumulation was evident in epidydimal adipocytes at 24 weeks. Plasma adipokines, leptin, resistin and adipsin, increased early and time-dependently, while adiponectin decreased late after 20 weeks. Only plasma leptin and adiponectin levels were associated with their respective mRNA levels in visceral WAT. Time-course microarrays revealed early and sustained activation of the immune transcriptome in epididymal and mesenteric depots. Up-regulated inflammatory genes included pro-inflammatory cytokines, chemokines (Tnf, Il1rn, Saa3, Emr1, Adam8, Itgam, Ccl2, 3, 4, 6, 7 and 9) and their upstream signalling pathway genes (multiple Toll-like receptors, Irf5 and Cd14). Early changes also occurred in fibrosis, extracellular matrix, collagen and cathepsin related-genes, but histological fibrosis was only visible in the later stages. In diet-induced obesity, early activation of TLR-mediated inflammatory signalling cascades by CD antigen genes, leads to increased expression of pro-inflammatory cytokines and chemokines, resulting in chronic low-grade inflammation. Early changes in collagen genes may trigger the accumulation of ECM components, promoting fibrosis in the later stages of diet-induced obesity. New therapeutic approaches targeting visceral adipose tissue genes altered early by HFD feeding may help ameliorate the deleterious effects of diet-induced obesity.
TL;DR: The evidence obtained in this study suggests that carvacrol appears to inhibit visceral adipogenesis probably by suppressing bone morphogenic protein-, fibroblast growth factor 1- and galanin-mediated signaling, and it also attenuates the production of pro-inflammatory cytokines in visceral adipose tissues by inhibiting toll like receptor 2 (TLR2)- and TLR4- mediated signaling.
Abstract: Carvacrol (2-methyl-5-isopropylphenol) is a monoterpene phenolic constituent of the essential oil produced by numerous aromatic plants and spices. The main objective of this study was to investigate effects of carvacrol in mice fed with a high-fat diet (HFD), which is an important model of obesity, and to study the potential underlying mechanisms focusing on the gene expression involved in adipogenesis, thermogenesis and inflammation. Male C57BL/6N mice were divided in three groups: those who received a normal diet, those fed with HFD and those fed with 0.1% carvacrol-supplemented diet (CSD). Body weight, visceral fat-pads and biochemical parameters were determined. Adipose tissue genes and protein expression levels were also assessed through reverse transcription polymerase chain reaction and Western blot analyses. Mice fed with CSD exhibited significantly reduced body weight gain, visceral fat-pad weights and plasma lipid levels compared with mice fed with HFD. Furthermore, HFD-induced up-regulations of adipose tissue genes and protein associated with the signaling cascades that lead to adipogenesis and inflammation were significantly reversed by dietary carvacrol supplementation. In summary, the major novel finding in our experimental conditions is that carvacrol prevented obesity in HFD-fed mice by decreasing body weight, visceral fat-pad weights and lowering plasma lipid levels. The evidence obtained in this study suggests that carvacrol appears to inhibit visceral adipogenesis probably by suppressing bone morphogenic protein-, fibroblast growth factor 1- and galanin-mediated signaling, and it also attenuates the production of pro-inflammatory cytokines in visceral adipose tissues by inhibiting toll like receptor 2 (TLR2)- and TLR4-mediated signaling.
TL;DR: Exposure to thousands of structurally diverse dietary phytochemicals appears to significantly modulate human drug metabolizing enzymes and transporters, and when taken with conventional medications, botanical dietary supplements may give rise to clinically significant herb-drug interactions.
Abstract: Phytochemicals have been components of man's diet for millennia and are believed to have played a significant role in steering the functional development of xenobiotic metabolizing enzymes and transporters within the human gastrointestinal tract. Only recently, however, have plant secondary metabolites been recognized as modulators of human drug disposition. Despite exposure to thousands of structurally diverse dietary phytochemicals, only a few appear to significantly modulate human drug metabolizing enzymes and transporters. In some instances, these interactions may have beneficial effects like cancer prevention, whereas others may dramatically affect the pharmacokinetics of concomitantly administered drugs. In today's global economy, the opportunity for exposure to more exotic phytochemicals is significantly enhanced. Formulated as concentrated phytochemical extracts, botanical dietary supplements are vehicles for a host of plant secondary metabolites rarely encountered in the normal diet. When taken with conventional medications, botanical dietary supplements may give rise to clinically significant herb-drug interactions. These interactions stem from phytochemical-mediated induction and/or inhibition of human drug metabolizing enzymes and transporters.
TL;DR: The lutein-supplemented diet attenuated light-induced visual impairment by protecting the photoreceptor cells' DNA and induced EYA for DNA repair, which could suppress DNA damage and Photoreceptor cell apoptosis.
Abstract: Lutein, a xanthophyll of a carotenoid, is anticipated as a therapeutic product to prevent human eye diseases. However, its biological mechanism is still unclear. Here, we show the molecular mechanism of lutein's effect to reduce photodamage of the retina. We analyzed the light-exposed retinas of Balb/c mice given lutein-supplemented or normal diet. Visual function was measured by electroretinogram, and histological changes were observed. Immunohistochemical and immunoblot analyses were performed to analyze molecular mechanism. The reactive oxygen species induced in the retina was evaluated by fluorescent probes. In the mice after light exposure, reduction of a-wave and b-wave amplitudes in electroretinogram, indicating visual impairment, and thinning of the photoreceptor cell layer owing to apoptosis were both attenuated by lutein diet. Interestingly, γ-H2AX, a marker for double-strand breaks (DSBs) in DNA, was up-regulated in the photoreceptor cells after light exposure, but this increase was attenuated by lutein diet, suggesting that DSBs caused by photodamage contributed to the photoreceptor cell death and that this change was suppressed by lutein. Moreover, the expression of eyes absent (EYA), which promotes DNA repair and cell survival, was significantly up-regulated with lutein diet in the light-exposed retina. Therefore, lutein induced EYA for DNA repair, which could suppress DNA damage and photoreceptor cell apoptosis. Lutein reduced light-induced oxidative stress in the retina, which might contribute to promote DNA repair. The lutein-supplemented diet attenuated light-induced visual impairment by protecting the photoreceptor cells' DNA.
TL;DR: Changes in extracellular phosphorus concentrations may directly modulate vascular function and thereby modulate the vascular smooth muscle response to physiological or pathological stimuli in normal and CKD mice.
Abstract: Aims Increased serum phosphorus levels are associated with cardiovascular disease in patients with chronic kidney disease (CKD) and in the general population. High phosphate levels may play a direct role in vascular dysfunction. We investigated here the effects of phosphate loading and of the phosphate binder sevelamer-HCl on vascular function.
Methods and results CKD and non-CKD C57/BL6 mice were used to study the effects of CKD, phosphate, and sevelamer-HCl on vascular function and structure. In vitro , phosphate exhibited a direct vasoconstrictor effect on aortic rings. This effect was smaller in vessels from CKD than non-CKD mice and it was abolished by reactive oxygen species inhibitor dimethylthiourea. A high-phosphate diet (1.3%) increased phenylephrine-induced contraction and lowered acetylcholine-induced relaxation of aortic rings ex vivo , both in non-CKD and CKD mice. It also induced endothelial cell detachment. Sevelamer-HCl exposure in vitro normalized the endothelial dysfunction induced by 3.0 mM phosphate and restored endothelial integrity. Sevelamer-HCl treatment of CKD mice under normal diet (0.65% phosphate) improved the endothelial dysfunction, aortic systolic expansion rate, and pulse wave velocity, and it reduced the endothelial expression of adhesion molecules.
Conclusion Changes in extracellular phosphorus concentrations may directly modulate vascular function and thereby modulate the vascular smooth muscle response to physiological or pathological stimuli in normal and CKD mice. Whether serum phosphorus lowering and/or dietary phosphate restriction can improve arterial function in humans remains to be established.
TL;DR: Tonsillotomy appears to be a safe technique that may offer some advantages over tonsillectomy in terms of postoperative morbidity, but differences in hemorrhage and dehydration were not evident in high-quality studies.
Abstract: Objective. Intracapsular tonsillotomy continues to gain accep- tance as an alternative to traditional tonsillectomy. Despite large clinical studies, there is a lack of consensus as to which technique offers lower complication rates. This study seeks to analyze the available data and surmise the compli- cation rates of partial tonsillectomy as compared with tradi- tional tonsillectomy. Data Sources. MEDLINE was searched using multiple search terms. Review Methods. After the MEDLINE search, the following inclusion criteria were applied: English language, human sub- jects, and related to partial tonsillectomy. Multiple tonsillot- omy techniques were included. The results of these studies were summated and the results analyzed. Subgroup analysis was then performed. Results. Thirty-three studies met inclusion criteria. Tonsillotomy had a lower postoperative bleeding rate, lower postoperative dehydration rate requiring medical care, reduced days of analgesic use, and reduced days to return to normal diet compared with tonsillectomy. When separated into higher versus lower quality studies, the differences in bleeding and dehydration were negligible, while differences in return to diet and days of analgesic use persisted. Mean intraoperative blood loss was similar for both techniques. Insufficient data were available to assess tonsil regrowth rates. Conclusions. Tonsillotomy appears to be a safe technique that may offer some advantages over tonsillectomy in terms of postoperative morbidity, but differences in hemorrhage and dehydration were not evident in high-quality studies. Data regarding tonsil regrowth rates and efficacy in treating sleep- disordered breathing are not yet sufficient for formal analysis, which may preclude widespread acceptance of this technique.