oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Increased FAT/CD36 Cycling and Lipid Accumulation in Myotubes Derived from Obese Type 2 Diabetic Patients  [PDF]
Celine Aguer, Marc Foretz, Louise Lantier, Sophie Hebrard, Benoit Viollet, Jacques Mercier, Magali Kitzmann
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0028981
Abstract: Background Permanent fatty acid translocase (FAT/)CD36 relocation has previously been shown to be related to abnormal lipid accumulation in the skeletal muscle of type 2 diabetic patients, however mechanisms responsible for the regulation of FAT/CD36 expression and localization are not well characterized in human skeletal muscle. Methodology/Principal Findings Primary muscle cells derived from obese type 2 diabetic patients (OBT2D) and from healthy subjects (Control) were used to examine the regulation of FAT/CD36. We showed that compared to Control myotubes, FAT/CD36 was continuously cycling between intracellular compartments and the cell surface in OBT2D myotubes, independently of lipid raft association, leading to increased cell surface FAT/CD36 localization and lipid accumulation. Moreover, we showed that FAT/CD36 cycling and lipid accumulation were specific to myotubes and were not observed in reserve cells. However, in Control myotubes, the induction of FAT/CD36 membrane translocation by the activation of (AMP)-activated protein kinase (AMPK) pathway did not increase lipid accumulation. This result can be explained by the fact that pharmacological activation of AMPK leads to increased mitochondrial beta-oxidation in Control cells. Conclusion/Significance Lipid accumulation in myotubes derived from obese type 2 diabetic patients arises from abnormal FAT/CD36 cycling while lipid accumulation in Control cells results from an equilibrium between lipid uptake and oxidation. As such, inhibiting FAT/CD36 cycling in the skeletal muscle of obese type 2 diabetic patients should be sufficient to diminish lipid accumulation.
Differential effects of dietary protein sources on postprandial low-grade inflammation after a single high fat meal in obese non-diabetic subjects
Jens Holmer-Jensen, Toni Karhu, Lene S Mortensen, Steen B Pedersen, Karl-Heinz Herzig, Kjeld Hermansen
Nutrition Journal , 2011, DOI: 10.1186/1475-2891-10-115
Abstract: We conducted a randomized, acute clinical intervention study in a crossover design. We supplemented a fat rich mixed meal with one of four dietary proteins - cod protein, whey isolate, gluten or casein. 11 obese non-diabetic subjects (age: 40-68, BMI: 30.3-42.0 kg/m2) participated and blood samples were drawn in the 4 h postprandial period. Adiponectin was estimated by ELISA methods and cytokines were analyzed by multiplex assay.MCP-1 and CCL5/RANTES displayed significant postprandial dynamics. CCL5/RANTES initially increased after all meals, but overall CCL5/RANTES incremental area under the curve (iAUC) was significantly lower after the whey meal compared with the cod and casein meals (P = 0.0053). MCP-1 was initially suppressed after all protein meals. However, the iAUC was significantly higher after whey meal compared to the cod and gluten meals (P = 0.04).We have demonstrated acute differential effects on postprandial low grade inflammation of four dietary proteins in obese non-diabetic subjects. CCL5/RANTES initially increased after all meals but the smallest overall postprandial increase was observed after the whey meal. MCP-1 was initially suppressed after all 4 protein meals and the whey meal caused the smallest overall postprandial suppression.ClinicalTrials.gov ID: NCT00863564The global incidence of obesity is escalating at epidemic proportions. The obesity related co-morbidities include increased incidence of the metabolic syndrome, type-2 diabetes (T2DM), hypertension, dyslipidaemia and chronic low-grade inflammation [1,2].Interestingly, Hotamisligil et al [3] in 1993 suggested that chronic low-grade inflammation plays a role in the pathophysiology of obesity in general and of insulin resistance in particular. This has subsequently been supported by the demonstration of a correlation between circulating levels of inflammatory markers and both T2DM [4] and atherosclerosis in humans [5-8].White adipose tissue (WAT) is an important endocrine organ that sec
Increased Gut Permeability and Microbiota Change Associate with Mesenteric Fat Inflammation and Metabolic Dysfunction in Diet-Induced Obese Mice  [PDF]
Yan Y. Lam, Connie W. Y. Ha, Craig R. Campbell, Andrew J. Mitchell, Anuwat Dinudom, Jan Oscarsson, David I. Cook, Nicholas H. Hunt, Ian D. Caterson, Andrew J. Holmes, Len H. Storlien
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034233
Abstract: We investigated the relationship between gut health, visceral fat dysfunction and metabolic disorders in diet-induced obesity. C57BL/6J mice were fed control or high saturated fat diet (HFD). Circulating glucose, insulin and inflammatory markers were measured. Proximal colon barrier function was assessed by measuring transepithelial resistance and mRNA expression of tight-junction proteins. Gut microbiota profile was determined by 16S rDNA pyrosequencing. Tumor necrosis factor (TNF)-α and interleukin (IL)-6 mRNA levels were measured in proximal colon, adipose tissue and liver using RT-qPCR. Adipose macrophage infiltration (F4/80+) was assessed using immunohistochemical staining. HFD mice had a higher insulin/glucose ratio (P = 0.020) and serum levels of serum amyloid A3 (131%; P = 0.008) but reduced circulating adiponectin (64%; P = 0.011). In proximal colon of HFD mice compared to mice fed the control diet, transepithelial resistance and mRNA expression of zona occludens 1 were reduced by 38% (P<0.001) and 40% (P = 0.025) respectively and TNF-α mRNA level was 6.6-fold higher (P = 0.037). HFD reduced Lactobacillus (75%; P<0.001) but increased Oscillibacter (279%; P = 0.004) in fecal microbiota. Correlations were found between abundances of Lactobacillus (r = 0.52; P = 0.013) and Oscillibacter (r = ?0.55; P = 0.007) with transepithelial resistance of the proximal colon. HFD increased macrophage infiltration (58%; P = 0.020), TNF-α (2.5-fold, P<0.001) and IL-6 mRNA levels (2.5-fold; P = 0.008) in mesenteric fat. Increased macrophage infiltration in epididymal fat was also observed with HFD feeding (71%; P = 0.006) but neither TNF-α nor IL-6 was altered. Perirenal and subcutaneous adipose tissue showed no signs of inflammation in HFD mice. The current results implicate gut dysfunction, and attendant inflammation of contiguous adipose, as salient features of the metabolic dysregulation of diet-induced obesity.
Calorie Restriction with a High-Fat Diet Effectively Attenuated Inflammatory Response and Oxidative Stress-Related Markers in Obese Tissues of the High Diet Fed Rats
Seungae Park,Na-Young Park,Giuseppe Valacchi,Yunsook Lim
Mediators of Inflammation , 2012, DOI: 10.1155/2012/984643
Abstract: Obesity characterized by increased mass of adipose tissue leads to systemic inflammation. Calorie restriction (CR) improves parameters associated with immune response and antioxidant defense. We hypothesized that CR with a high fat diet (HFCR) regulates local and systemic inflammation and oxidative stress damage in a high fat diet induced obesity (HF group). We investigated effect of HFCR on inflammation and oxidative stress-related markers in liver and adipose tissues as well as adipokines in plasma. HFCR lowered liver triglyceride levels, total cholesterol levels, and the plasma leptin/adiponectin ratio to normal levels and improved glucose tolerance. HFCR also improved fatty liver and normalized adipocyte size and morphology. HFCR reduced lipid peroxidation and decreased the expression levels of inducible nitric oxide synthetase, cyclooxygenase-2, NF-E2-related factor, and heme oxygenase-1 in the liver. Moreover, HFCR suppressed the expression levels of C- reactive protein and manganese superoxide dismutase in the adipose tissue in the HF group. These results suggest that HFCR may have beneficial effects on inflammation and oxidative stress as well as lipid profiles in the HF diet induced obesity. Moreover, HFCR may be a good way to increase compliance in obese patients and to prevent obesity induced complications without changes in dietary pattern.
Increased Cardiovascular Reactivity to Acute Stress and Salt-Loading in Adult Male Offspring of Fat Fed Non-Obese Rats  [PDF]
Olena Rudyk, Péter Makra, Eugene Jansen, Michael J. Shattock, Lucilla Poston, Paul D. Taylor
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0025250
Abstract: Diet-induced obesity in rat pregnancy has been shown previously to be associated with consistently raised blood pressure in the offspring, attributed to sympathetic over-activation, but the relative contributions to this phenotype of maternal obesity versus raised dietary fat is unknown. Sprague-Dawley female rats were fed either a control (4.3% fat, n = 11) or lard-enriched (23.6% fat, n = 16) chow 10 days prior to mating, throughout pregnancy and lactation. In conscious adult (9-month-old) offspring cardiovascular parameters were measured (radiotelemetry). The short period of fat-feeding did not increase maternal weight versus controls and the baseline blood pressure was similar in offspring of fat fed dams (OF) and controls (OC). However, adult male OF showed heightened cardiovascular reactivity to acute restraint stress (p<0.01; Δ systolic blood pressure (SBP) and Δheart rate (HR)) with a prolonged recovery time compared to male OC. α1/β-adrenergic receptor blockade normalised the response. Also, after dietary salt-loading (8%-NaCl ad libitum for 1 week) male OF demonstrated higher SBP (p<0.05) in the awake phase (night-time) and increased low/high frequency ratio of power spectral density of HR variability versus OC. Baroreflex gain and basal power spectral density components of the heart rate or blood pressure were similar in male OF and OC. Minor abnormalities were evident in female OF. Fat feeding in the absence of maternal obesity in pregnant rats leads to altered sympathetic control of cardiovascular function in adult male offspring, and hypertension in response to stressor stimuli.
Oxidant/antioxidant status in obese adolescent females with acne vulgaris
Abulnaja Khalid
Indian Journal of Dermatology , 2009,
Abstract: Background and Objectives: Acne vulgaris is a distressing skin condition, which can carry with it significant psychological disability. Oxidant/antioxidant imbalance leads to increased production of free radicals, that cause many diseases. Some nutrients, along with systemic oxidative stress, have been implicated in acne vulgaris. The goal of the present study was to assess oxidant and antioxidant status in correlation with the incidence of acne vulgaris in adolescent obese females. Materials and Methods: A total of 60 adolescent females (age 16-22 years) were divided into four groups (15 each) as follows: The first included obese females with acne; the second included obese females without acne; the third included non obese with acne and the fourth included non obese without acne. Fasting serum Malondialdehyde (MDA), β-carotene, and Vitamins A, E, and C were measured. In addition, platelet monoamineoxidase (MAO), and erythrocyte catechol-o-methyltransferase (COMT) activities were determined. Results: It was found that serum MDA was statistically significantly decreased in obese and non obese subjects with acne, as compared to those without acne ( P < 0.05, P < 0.001) respectively. In contrast, the levels of β-carotene, vitamins A, E and C and the activity of MAO were significantly decreased in the obese and non obese with acne, as against the obese and non obese without acne. Interpretation: In obese subjects, increased fat content facilitates free radical production and lipid peroxidation, as indicated by increased MDA level, which is scavenged by the antioxidant vitamins. The decreased activity of MAO may be inhibited by free radicals and this causes psychological depression in adolescents. However there were non significant changes in the activity of COMT among the studied groups. Conclusion: The nutritional factors and a weakened antioxidant defense system may interplay, to increase the risk of psychological sequelae in acne vulgaris.
A High-Fat Meal, or Intraperitoneal Administration of a Fat Emulsion, Increases Extracellular Dopamine in the Nucleus Accumbens  [PDF]
Pedro Rada,Nicole M. Avena,Jessica R. Barson,Bartley G. Hoebel,Sarah F. Leibowitz
Brain Sciences , 2012, DOI: 10.3390/brainsci2020242
Abstract: Evidence links dopamine (DA) in the nucleus accumbens (NAc) shell to the ingestion of palatable diets. Less is known, however, about the specific relation of DA to dietary fat and circulating triglycerides (TG), which are stimulated by fat intake and promote overeating. The present experiments tested in Sprague-Dawley rats whether extracellular levels of NAc DA increase in response to acute access to fat-rich food or peripheral injection of a fat emulsion and, if so, whether this is related to caloric intake or elevated circulating lipids. When rats consumed more calories of a high-fat meal compared with a low-fat meal, there was a significant increase in extracellular accumbens DA (155% vs. 119%). Systemic injection of a fat emulsion, which like a high-fat diet raises circulating TG but eliminates the factor of taste and allows for the control of caloric intake, also significantly increased extracellular levels of DA (127%) compared to an equicaloric glucose solution (70%) and saline (85%). Together, this suggests that a rise in circulating TG may contribute to the stimulatory effect of a high-fat diet on NAc DA.
A Comparison of Inflammatory and Oxidative Stress Markers in Adipose Tissue from Weight-Matched Obese Male and Female Mice  [PDF]
Karen J. Nickelson,Kelly L. Stromsdorfer,R. Taylor Pickering,Tzu-Wen Liu,Laura C. Ortinau,Aileen F. Keating,James W. Perfield II
Journal of Diabetes Research , 2012, DOI: 10.1155/2012/859395
Abstract: Expansion of intra-abdominal adipose tissue and the accompanying inflammatory response has been put forward as a unifying link between obesity and the development of chronic diseases. However, an apparent sexual dimorphism exists between obesity and chronic disease risk due to differences in the distribution and abundance of adipose tissue. A range of experimental protocols have been employed to demonstrate the role of estrogen in regulating health benefits; however, most studies are confounded by significant differences in body weight and adiposity. Therefore, the purpose of this study was to compare weight-matched obese male and female mice to determine if the sex-dependent health benefits remain when body weight is similar. The development of obesity in female mice receiving a high-fat diet was delayed; however, subsequent comparisons of weight-matched obese mice revealed greater adiposity in obese female mice. Despite excess adiposity and enlarged adipocyte size, obese females remained more glucose tolerant than weight-matched male mice, and this benefit was associated with increased expression of adiponectin and reductions in immune cell infiltration and oxidative stress in adipose tissue. Therefore, the protective benefits of estrogen persist in the obese state and appear to improve the metabolic phenotype of adipose tissue and the individual. 1. Introduction Obesity is widely regarded as an independent risk factor for a range of chronic diseases including type 2 diabetes and cardiovascular disease [1, 2]. Low-grade systemic inflammation has been put forward as a unifying link between obesity and the onset of these obesity-associated diseases [3–5]. Expansion of intra-abdominal adipose tissue is associated with increased infiltration and activation of immune cells, and these events are a significant contributor to the systemic inflammation that occurs with obesity [6, 7]. While an exact explanation for the accumulation of immune cells in adipose tissue is unknown, one potential contributing factor is elevated oxidative stress [8, 9]. Therefore, decreasing intra-abdominal obesity and/or reducing adipose tissue oxidative stress and inflammation will positively influence chronic disease risk. Clear sex-based differences exist in adipose tissue distribution, inflammation, and ultimately the probability of developing a chronic disease [10–12]. Specifically, females tend to have a higher body fat content with the fat localized subcutaneously while males have less total body fat and their adipose tissue predominates in the visceral region. Furthermore,
Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults
Abigail D Peairs, Janet W Rankin, Yong Lee
Nutrition Journal , 2011, DOI: 10.1186/1475-2891-10-122
Abstract: Eleven overweight and obese subjects consumed three high fat milkshakes rich in monounsaturated fat (MFA), saturated fat (SFA), or long-chain omega 3 polyunsaturated fat (O3FA) in random order. Blood samples collected at baseline, 1, 2, 4, and 6 hours postprandial were analyzed for markers of inflammation (soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tumor necrosis factor- α (TNF-α), and C-reactive protein (CRP)), oxidative stress (8-epi-prostaglandin-F2α (8-epi) and nuclear factor-κB (NF-κB)), and metabolic factors (glucose, insulin, non-esterified free fatty acids, and triglycerides (TG)).O3FA enhanced NF-kB activation compared to SFA, but did not increase any inflammatory factors measured. Conversely, SFA led to higher ICAM-1 levels than MFA (p = 0.051), while MFA increased TG more than SFA (p < 0.05). CRP increased while TNF-α and 8-epi decreased with no difference between treatments.While most of the inflammatory factors measured had modest or no change following the meal, ICAM-1 and NF-κB responded differently by meal type. These results are provocative and suggest that type of fat in meals may differentially influence postprandial inflammation and endothelial activation.Cardiovascular disease and type 2 diabetes are associated with obesity and are also linked to inflammation and oxidative stress [1]. Weight loss is effective in reducing these conditions [2], however, as only 1 in 5 overweight people successfully maintain weight loss [3], alternative dietary strategies to improve health without weight loss are desirable.Most of each day is spent in the postprandial state. Increases in blood glucose and/or triglycerides following a meal stimulate oxidative stress, impair endothelial function, and cause a rise in circulating inflammatory factors [4]. Research suggests that the negative postprandial responses are exaggerated in obesity and diabetes [4-6]. The repeated acute stresses induced by food ingestion (par
Twenty-Four Hour Total and Dietary Fat Oxidation in Lean, Obese and Reduced-Obese Adults with and without a Bout of Exercise  [PDF]
Audrey Bergouignan, Elizabeth H. Kealey, Stacy L. Schmidt, Matthew R. Jackman, Daniel H. Bessesen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094181
Abstract: Background It has been hypothesized that obese and reduced-obese individuals have decreased oxidative capacity, which contributes to weight gain and regain. Recent data have challenged this concept. Objective To determine (1) whether total and dietary fat oxidation are decreased in obese and reduced-obese adults compared to lean but increase in response to an acute exercise bout and (2) whether regular physical activity attenuates these metabolic alterations. Design We measured 24-hr total (whole-room calorimetry) and dietary fat (14C-oleate) oxidation in Sedentary Lean (BMI = 21.5±1.6; n = 10), Sedentary Obese (BMI = 33.6±2.5; n = 9), Sedentary Reduced-Obese (RED-SED; BMI = 26.9±3.7; n = 7) and in Physically Active Reduced-Obese (RED-EX; BMI = 27.3±2.8; n = 12) men and women with or without an acute exercise bout where energy expended during exercise was not replaced. Results Although Red-SED and Red-EX had a similar level of fatness, aerobic capacity and metabolic profiles were better in Red-EX only compared to Obese subjects. No significant between-group differences were seen in 24-hr respiratory quotient (RQ, Lean: 0.831±0.044, Obese: 0.852±0.023, Red-SED: 0.864±0.037, Red-EX: 0.842±0.039), total and dietary fat oxidation. A single bout of exercise increased total (+27.8%, p<0.0001) and dietary (+6.6%, p = 0.048) fat oxidation across groups. Although exercise did not impact RQ during the day, it decreased RQ during sleep (p = 0.01) in all groups. Red-EX oxidized more fat overnight than Red-SED subjects under both resting (p = 0.036) and negative energy balance (p = 0.003) conditions, even after adjustment for fat-free mass. Conclusion Obese and reduced-obese individuals oxidize as much fat as lean both under eucaloric and negative energy balance conditions, which does not support the hypothesis of reduced oxidative capacity in these groups. Reduced-obese individuals who exercise regularly have markers of metabolic health similar to those seen in lean adults. Both the acute and chronic effects of exercise were primarily observed at night suggesting an important role of sleep in the regulation of lipid metabolism.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.