scholarly journals Effects of voluntary exercise training on liver fat accumulation - Measurement of over time CT imaging -

2017 ◽  
Vol 66 (4) ◽  
pp. 283-291 ◽  
Author(s):  
Saki Yoshimura ◽  
Yuki Tomiga ◽  
Shihoko Nakashima ◽  
Ai Ito ◽  
Shotaro Kawakami ◽  
...  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Siham Yasari ◽  
Denis Prud'homme ◽  
Frédérique Tesson ◽  
Marek Jankowski ◽  
Jolanta Gutkowska ◽  
...  

The present study was designed to investigate the impact of exercise training on lipogenic gene expression in liver and lipid partitioning following the ingestion of a high fructose load. Female rats were exercise-trained for 8 wk or kept sedentary before being submitted to a fasting/refeeding protocol. Rats were further subdivided as follow: rats were fasted for 24 h, refed a standard diet for 24 h, starved for another 24 h, and refed with a standard or a high-fructose diet 24 h before sacrifice. Fructose refeeding was associated with an increase in hepatic lipid content, endocannabinoid receptor 1, sterol regulatory element-binding protein1c, and stearoyl-CoA desaturase1 gene expression in both Sed and TR rats. However, desaturation indexes measured in liver (C16 : 1/C16 : 0 and C18 : 1/C18 : 0) and plasma (C18 : 1/C18 : 0) were higher (P<0.01) in TR than in Sed rats following fructose refeeding. It is concluded that exercise training does not significantly affect fat accumulation and the molecular expression of genes involved in lipogenesis after fasting and fructose refeeding but does modify the partitioning of lipids so as to provide more unsaturated fatty acids in liver without affecting liver fat content.


2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Jean-Marc Lavoie ◽  
Abdolnaser Pighon

One segment of the population that is particularly inclined to liver fat accumulation is postmenopausal women. Although nonalcoholic hepatic steatosis is more common in men than in women, after menopause there is a reversal in gender distribution. At the present time, weight loss and exercise are regarded as first line treatments for NAFLD in postmenopausal women, as it is the case for the management of metabolic syndrome. In recent years, there has been substantial evidence coming mostly from the use of the animal model, that indeed estrogens withdrawal is associated with modifications of molecular markers favouring the activity of metabolic pathways ultimately leading to liver fat accumulation. In addition, the use of the animal model has provided physiological and molecular evidence that exercise training provides estrogens-like protective effects on liver fat accumulation and its consequences. The purpose of the present paper is to present information relative to the development of a state of NAFLD resulting from the absence of estrogens and the role of exercise training, emphasizing on the contribution of the animal model on these issues.


Circulation ◽  
2000 ◽  
Vol 101 (18) ◽  
pp. 2134-2137 ◽  
Author(s):  
Yoko Eto ◽  
Katsunori Yonekura ◽  
Makoto Sonoda ◽  
Naoto Arai ◽  
Masataka Sata ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
pp. e001431
Author(s):  
Long Li ◽  
Caoxin Huang ◽  
Hongyan Yin ◽  
Xiaofang Zhang ◽  
Dongmei Wang ◽  
...  

IntroductionExercise training has been shown to be the most effective strategy to combat obesity and non-alcoholic fatty liver disease. However, exercise promotes loss of adipose tissue mass and improves obesity-related hepatic steatosis through mechanisms that remain obscure.Research design and methodsTo study the role of interleukin-6 (IL-6) in high-fat diet (HFD)-induced adiposity and hepatic steatosis during treadmill running, IL-6 knockout (IL-6 KO) mice and wild-type (WT) mice were randomly divided into lean, obese (fed a HFD) and trained obese groups (fed a HFD and exercise trained).ResultsAfter 20 weeks of HFD feeding and 8 weeks of treadmill running, we found that exercise obviously reduced HFD-induced body weight gain, inhibited visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) expansion and almost completely reversed obesity-related intrahepatic fat accumulation in WT mice. However, IL-6 knockout (IL-6 KO) mice are refractory to the benefits of treadmill training on body weight, VAT and SAT mass elevation, and hepatic steatosis. Moreover, a panel of lipolytic-related and thermogenic-related genes, including ATGL, HSL and PGC-1α, was upregulated in the VAT and SAT of WT mice that received exercise training compared with untrained mice, which was not observed in IL-6 KO mice. In addition, exercise training resulted in a significant inhibition of hepatic peroxisome proliferator-activated receptor gamma (PPAR-γ) expression in WT mice, and these effects were not noted in IL-6 KO mice.ConclusionThese results revealed that IL-6 is involved in the prevention of obesity and hepatic fat accumulation during exercise training. The mechanisms underlying these antiobesity effects may be associated with enhanced lipolysis and thermogenesis in white adipose tissue. The improvement in hepatic steatosis by exercise training may benefit from the marked inhibition of PPAR-γ expression by IL-6.


Microbiome ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jordi Mayneris-Perxachs ◽  
Marina Cardellini ◽  
Lesley Hoyles ◽  
Jèssica Latorre ◽  
Francesca Davato ◽  
...  

Abstract Background The gut microbiome and iron status are known to play a role in the pathophysiology of non-alcoholic fatty liver disease (NAFLD), although their complex interaction remains unclear. Results Here, we applied an integrative systems medicine approach (faecal metagenomics, plasma and urine metabolomics, hepatic transcriptomics) in 2 well-characterised human cohorts of subjects with obesity (discovery n = 49 and validation n = 628) and an independent cohort formed by both individuals with and without obesity (n = 130), combined with in vitro and animal models. Serum ferritin levels, as a markers of liver iron stores, were positively associated with liver fat accumulation in parallel with lower gut microbial gene richness, composition and functionality. Specifically, ferritin had strong negative associations with the Pasteurellaceae, Leuconostocaceae and Micrococcaea families. It also had consistent negative associations with several Veillonella, Bifidobacterium and Lactobacillus species, but positive associations with Bacteroides and Prevotella spp. Notably, the ferritin-associated bacterial families had a strong correlation with iron-related liver genes. In addition, several bacterial functions related to iron metabolism (transport, chelation, heme and siderophore biosynthesis) and NAFLD (fatty acid and glutathione biosynthesis) were also associated with the host serum ferritin levels. This iron-related microbiome signature was linked to a transcriptomic and metabolomic signature associated to the degree of liver fat accumulation through hepatic glucose metabolism. In particular, we found a consistent association among serum ferritin, Pasteurellaceae and Micrococcacea families, bacterial functions involved in histidine transport, the host circulating histidine levels and the liver expression of GYS2 and SEC24B. Serum ferritin was also related to bacterial glycine transporters, the host glycine serum levels and the liver expression of glycine transporters. The transcriptomic findings were replicated in human primary hepatocytes, where iron supplementation also led to triglycerides accumulation and induced the expression of lipid and iron metabolism genes in synergy with palmitic acid. We further explored the direct impact of the microbiome on iron metabolism and liver fact accumulation through transplantation of faecal microbiota into recipient’s mice. In line with the results in humans, transplantation from ‘high ferritin donors’ resulted in alterations in several genes related to iron metabolism and fatty acid accumulation in recipient’s mice. Conclusions Altogether, a significant interplay among the gut microbiome, iron status and liver fat accumulation is revealed, with potential significance for target therapies.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Aragon Herrera ◽  
S Feijoo-Bandin ◽  
M Otero Santiago ◽  
S Moranha Fernandez ◽  
L Anido Varela ◽  
...  

Abstract Background Empagliflozin is a potent, highly selective sodium glucose cotransporter-2 (SGLT2) inhibitor used as an effective and well-tolerated antihyperglycaemic agent. Beyond lowering glucose, empagliflozin exerts a favorable effect on a number of nonglycaemic outcomes, including modest reductions in bodyweight and blood pressure, and it has cardioprotective and renoprotective properties in patients with T2D and established cardiovascular disease (EMPA-REG OUTCOME). Purpose Since liver fat content represents a risk factor for cardiovascular diseases, and empagliflozin has been recently suggested to be able to contribute to the early treatment of nonalcoholic fatty liver disease in T2D, we aimed to study the effect of the empagliflozin treatment in the liver metabolome of type 2 diabetic rats. Methods Male ZDF-Leprfa/fa rats were treated with 30 mg/kg/d of empagliflozin p.o for six weeks. Metabolic profiling of the hepatic tissue was analyzed using UHPLC-MS based platforms. We performed a hematoxylin/eosin staining to determine the tissue integrity and liver fat accumulation, and a Masson's trichrome staining to analyze liver fibrosis. All animals were maintained and euthanized following protocols approved by the Animal Care Committee of the University of Santiago de Compostela in accordance with European Union Directive 2010/63. Results Empaglifozin treatment reduced blood glucose levels to normal (128.2±6.51 mg/dL), while untreated control rats showed high glucose levels (404.3±17.49 mg/dL). Hepatic histological analysis did not show differences regarding neither fat accumulation nor fibrosis between empagliflozin treated and control rats. Circulating levels of cholesterol, HDL, LDL, GTP, GGT triglycerides remained unaltered after empaglifozin treatment vs. control. 384 metabolites were analyzed in the liver tissue samples, observing significantly increased levels of 10 types of glycerolipids, 24 phosphatidylcholines, 8 amino acids, 1 polyunsaturated fatty acid, 4 lysophosphatidylethanolamines, 7 lysophosphatidylinositols, 1 carboxylic acid and 1 nucleoside in the empagliflozin treated rats with respect to the control group. In addition, treatment with empagliflozin produced a significant decrease of 1 glycerolipid, 1 phosphatidylcholine, 1 bile acid, 1 nucleoside and the NAD oxidoreduction coenzyme. Conclusions We demonstrated that empagliflozin significantly modify the liver content of the different lipid species, with the most relevant altered metabolic classes belonging to glycerophospholipids, especially monoacyl-species, and aromatic amino acids. Considering the suggested potential beneficial effect of the treatment with empagliflozin in the prevention of liver fibrosis, our metabolomics data can help to evaluate the impact and the mechanism of action of SGLT2 inhibitors at hepatic level. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Boehringer Ingelheim


2017 ◽  
Vol 123 (4) ◽  
pp. 876-883 ◽  
Author(s):  
Robert H. Brown ◽  
Robert J. Henderson ◽  
Elizabeth A. Sugar ◽  
Janet T. Holbrook ◽  
Robert A. Wise

Brown RH, Henderson RJ, Sugar EA, Holbrook JT, Wise RA, on behalf of the American Lung Association Airways Clinical Research Centers. Reproducibility of airway luminal size in asthma measured by HRCT. J Appl Physiol 123: 876–883, 2017. First published July 13, 2017; doi:10.1152/japplphysiol.00307.2017.—High-resolution CT (HRCT) is a well-established imaging technology used to measure lung and airway morphology in vivo. However, there is a surprising lack of studies examining HRCT reproducibility. The CPAP Trial was a multicenter, randomized, three-parallel-arm, sham-controlled 12-wk clinical trial to assess the use of a nocturnal continuous positive airway pressure (CPAP) device on airway reactivity to methacholine. The lack of a treatment effect of CPAP on clinical or HRCT measures provided an opportunity for the current analysis. We assessed the reproducibility of HRCT imaging over 12 wk. Intraclass correlation coefficients (ICCs) were calculated for individual airway segments, individual lung lobes, both lungs, and air trapping. The ICC [95% confidence interval (CI)] for airway luminal size at total lung capacity ranged from 0.95 (0.91, 0.97) to 0.47 (0.27, 0.69). The ICC (95% CI) for airway luminal size at functional residual capacity ranged from 0.91 (0.85, 0.95) to 0.32 (0.11, 0.65). The ICC measurements for airway distensibility index and wall thickness were lower, ranging from poor (0.08) to moderate (0.63) agreement. The ICC for air trapping at functional residual capacity was 0.89 (0.81, 0.94) and varied only modestly by lobe from 0.76 (0.61, 0.87) to 0.95 (0.92, 0.97). In stable well-controlled asthmatic subjects, it is possible to reproducibly image unstimulated airway luminal areas over time, by region, and by size at total lung capacity throughout the lungs. Therefore, any changes in luminal size on repeat CT imaging are more likely due to changes in disease state and less likely due to normal variability. NEW & NOTEWORTHY There is a surprising lack of studies examining the reproducibility of high-resolution CT in asthma. The current study examined reproducibility of airway measurements. In stable well-controlled asthmatic subjects, it is possible to reproducibly image airway luminal areas over time, by region, and by size at total lung capacity throughout the lungs. Therefore, any changes in luminal size on repeat CT imaging are more likely due to changes in disease state and less likely due to normal variability.


2020 ◽  
Vol 6 (3) ◽  
pp. 164-169
Author(s):  
Zahra Entezari ◽  
◽  
Ayyub Babaei ◽  
Saleh Rahmati-Ahmadabad ◽  
◽  
...  

Background: Depression is a common mood disorder that in the long-term impairs thoughts, behavior, feelings, and health. Chronic unpredictable stress is one of the factors that can cause depression. Objectives: To investigate the effect of voluntary exercise training on immobility behavior (caused by chronic unpredictable stress) and serum corticosterone concentration. Materials & Methods: A total of 24 male rats were randomly and equally assigned to four groups of healthy-control, healthy-exercise, depressed-control, and depressed-exercise. Depressed-control and depressed-exercise groups were first exposed to three weeks of chronic unpredictable stress. After this period, the exercise groups performed four weeks of voluntary exercise training. Twentyfour hours after the last training session, a forced swim test was taken from the rats and their blood samples were taken 24 hours later. The obtained data were analyzed using a 2-way analysis of variance (significance level: P<0.05). The Pearson correlation coefficient was used to examine the relationship between study variables. All statistical analyses were performed in SPSS v. 22. Results: Chronic stress increased immobility behavior (P=0.001) and serum corticosterone concentration (P=0.001). In contrast, exercise training reduced immobility behavior (P=0.001) and serum corticosterone (P=0.001). The immobility time (P=0.001) and serum corticosterone concentration in the depressed-exercise group were higher than those in the healthy-exercise group (P=0.001). There was a positive correlation between immobility behavior and serum corticosterone concentration (r=0.85 and P=0.001). Conclusion: While the chronic stress increases the immobility behavior and serum corticosterone concentration, voluntary exercise training can reduce immobility behavior and serum corticosterone and adjust some depression symptoms.


2016 ◽  
Vol 48 (5) ◽  
pp. 384-391 ◽  
Author(s):  
Massimiliano Ruscica ◽  
Nicola Ferri ◽  
Chiara Macchi ◽  
Marica Meroni ◽  
Claudia Lanti ◽  
...  
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