Positive Effects of Voluntary Running on Metabolic Syndrome-Related Disorders in Non-Obese Hereditary Hypertriacylglycerolemic Rats

Skop, V.; Malínská, Hana; Trnovská, Jaroslava; Hüttl, Martina; Cahová, Monika; Błachnio-Zabielska, Agnieszka; Baranowski, Marcin; Burian, Martin; Oliyarnyk, Olena; Kazdová, Ludmila

doi:10.1371/journal.pone.0122768

Cited by 8 publications

(15 citation statements)

References 72 publications

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“…Cardiac hypotrophy could be related to the fact that hypertriglyceridemia and metabolic syndrome are associated with increased lipid accumulation in nonadipose tissues. Ectopically stored lipids and their metabolites (diacylglycerols, ceramides, and fatty acyl-CoAs) in the liver, heart, muscles, and kidney lead to lipotoxicity, which may result in tissue injury [ 17 , 18 ]. We found increased levels of kidney and liver injury markers, such as alanine-aminotransferase, which also demonstrates myocardial damage [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

The Vasoactive Role of Perivascular Adipose Tissue and the Sulfide Signaling Pathway in a Nonobese Model of Metabolic Syndrome

et al. 2021

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The aim of this study was to evaluate the mutual relationship among perivascular adipose tissue (PVAT) and endogenous and exogenous H2S in vasoactive responses of isolated arteries from adult normotensive (Wistar) rats and hypertriglyceridemic (HTG) rats, which are a nonobese model of metabolic syndrome. In HTG rats, mild hypertension was associated with glucose intolerance, dyslipidemia, increased amount of retroperitoneal fat, increased arterial contractility, and endothelial dysfunction associated with arterial wall injury, which was accompanied by decreased nitric oxide (NO)-synthase activity, increased expression of H2S producing enzyme, and an altered oxidative state. In HTG, endogenous H2S participated in the inhibition of endothelium-dependent vasorelaxation regardless of PVAT presence; on the other hand, aortas with preserved PVAT revealed a stronger anticontractile effect mediated at least partially by H2S. Although we observed a higher vasorelaxation induced by exogenous H2S donor in HTG rats than in Wistar rats, intact PVAT subtilized this effect. We demonstrate that, in HTG rats, endogenous H2S could manifest a dual effect depending on the type of triggered signaling pathway. H2S within the arterial wall contributes to endothelial dysfunction. On the other hand, PVAT of HTG is endowed with compensatory vasoactive mechanisms, which include stronger anti-contractile action of H2S. Nevertheless, the possible negative impact of PVAT during hypertriglyceridemia on the activity of exogenous H2S donors needs to be taken into consideration.

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Section: Discussionmentioning

confidence: 99%

The Vasoactive Role of Perivascular Adipose Tissue and the Sulfide Signaling Pathway in a Nonobese Model of Metabolic Syndrome

et al. 2021

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“…Due to the paucity of lipidomics-focused studies on human liver biopsies in the NAFLD context, data from studies in rodent NAFLD models, which are more abundant, may provide the best information on sphingolipids in NAFLD. Among studies where NAFLD sphingolipidomes can be compared to controls, there are to date about nine performed in murine models [10, 11, 17, 28–33], three on rat [34–36], and one on rabbit [37]. Of the mouse studies, eight presented sphingolipidomics contrasting a control diet with those on a NAFLD-inducing diet, and one utilized the leptin receptor deficient ob/ob mouse [33].…”

Section: Sphingolipid Profiling In Nafldmentioning

confidence: 99%

Non-alcoholic fatty liver disease: Insights from sphingolipidomics

Montefusco

Allegood

Spiegel

et al. 2018

Biochemical and Biophysical Research Communications

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Non-alcoholic fatty liver disease (NAFLD) is a major clinical concern and its treatment consumes abundant resources. While accumulation of lipids in hepatocytes initiates the disease, this in itself is not necessarily harmful; rather, initiation of inflammation and subsequent fibrosis and cirrhosis are critical steps in NAFLD pathology. Mechanisms linking lipid overload to downstream disease progression are not fully understood; however, bioactive lipid metabolism may underlie instigation of proinflammatory signaling. With the advent of high-throughput, sensitive, and quantitative mass spectrometry-based methods for assessing lipid profiles in NAFLD, several trends have emerged, including that increases in specific sphingolipids correlate with the transition from the relatively benign condition of simple fatty liver to the much more concerning inflamed state. Continued studies that implement sphingolipid profiling will enable the extrapolations of candidate enzymes and pathways involved in NAFLD, either in biopsies or plasma from human samples, and also in animal models, from which data are much more abundant. While most data thus far are derived from targeted lipidomics approaches, unbiased, semi-quantitative approaches hold additional promise for furthering our understanding of sphingolipids as markers of and players in NAFLD.

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“…Within cells, proteins are under constant surveillance by the proteolytic systems that promote the degradation of proteins damaged by highly reactive molecules, thus operating a protein quality control and preserving muscle health (Kaushik and Cuervo, ). Interestingly, reduced oxidative stress (Škop et al, ) and increase in proteasome‐mediated proteolysis has been found following both acute (Pasiakos et al, ) and chronic endurance exercise (Cunha et al, ) in healthy conditions.…”

Section: Introductionmentioning

confidence: 99%

Voluntary physical activity counteracts Chronic Heart Failure progression affecting both cardiac function and skeletal muscle in the transgenic Tgαq*44 mouse model

et al. 2019

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Physical activity is emerging as an alternative nonpharmaceutical strategy to prevent and treat a variety of cardiovascular diseases due to its cardiac and skeletal muscle beneficial effects. Oxidative stress occurs in skeletal muscle of chronic heart failure (CHF) patients with possible impact on muscle function decline. We determined the effect of voluntary‐free wheel running (VFWR) in preventing protein damage in Tgαq*44 transgenic mice (Tg) characterized by a delayed CHF progression. In the early (6 months) and transition (12 months) phase of CHF, VFWR increased the daily mean distance covered by Tg mice eliminating the difference between Tg and WT present before exercise at 12 months of age (WT Pre‐EX 3.62 ± 1.66 vs. Tg Pre‐EX 1.51 ± 1.09 km, P < 0.005; WT Post‐EX 5.72 ± 3.42 vs. Tg Post‐EX 4.17 ± 1.8 km, P > 0.005). This effect was concomitant with an improvement of in vivo cardiac performance [(Cardiac Index (mL/min/cm 2 ): 6 months, untrained‐Tg 0.167 ± 0.005 vs. trained‐Tg 0.21 ± 0.003, P < 0.005; 12 months, untrained‐Tg 0.1 ± 0.009 vs. trained‐Tg 0.133 ± 0.005, P < 0.005]. Such effects were associated with a skeletal muscle antioxidant response effective in preventing oxidative damage induced by CHF at the transition phase (untrained‐Tg 0.438 ± 0.25 vs. trained‐Tg 0.114 ± 0.010, P < 0.05) and with an increased expression of protein control markers (MuRF‐1, untrained‐Tg 1.12 ± 0.29 vs. trained‐Tg 14.14 ± 3.04, P < 0.0001; Atrogin‐1, untrained‐Tg 0.9 ± 0.38 vs. trained‐Tg 7.79 ± 2.03, P < 0.01; Cathepsin L, untrained‐Tg 0.91 ± 0.27 vs. trained‐Tg 2.14 ± 0.55, P < 0.01). At the end‐stage of CHF (14 months), trained‐Tg mice showed a worsening of physical performance (decrease in daily activity and weekly distance and time of activity) compared to trained age‐matched WT in association with oxidative protein damage of a similar level to that of untrained‐Tg mice (untrained‐Tg 0.62 ± 0.24 vs. trained‐Tg 0.64 ± 0.13, P > 0.05). Prolonged voluntary physical activity performed before the onset of CHF end‐stage, appears to be a useful tool to increase cardiac function and to reduce skeletal muscle oxidative damage counteracting physical activity decline.

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Positive Effects of Voluntary Running on Metabolic Syndrome-Related Disorders in Non-Obese Hereditary Hypertriacylglycerolemic Rats

Cited by 8 publications

References 72 publications

The Vasoactive Role of Perivascular Adipose Tissue and the Sulfide Signaling Pathway in a Nonobese Model of Metabolic Syndrome

The Vasoactive Role of Perivascular Adipose Tissue and the Sulfide Signaling Pathway in a Nonobese Model of Metabolic Syndrome

Non-alcoholic fatty liver disease: Insights from sphingolipidomics

Voluntary physical activity counteracts Chronic Heart Failure progression affecting both cardiac function and skeletal muscle in the transgenic Tgαq*44 mouse model

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