Effect of Bangle (Zingiber purpureum) extract and low-intensity exercise on mTOR phosphorylation and autophagy flux in skeletal muscles of rats on a high-fat diet

2018 ◽  
Vol 47 ◽  
pp. 554-561 ◽  
Author(s):  
Shin Sato ◽  
Saori Kataoka ◽  
Megumi Sato ◽  
Akane Takahashi ◽  
Toshio Norikura ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Skeletal Muscles ◽  
High Fat ◽  
Autophagy Flux ◽  
Low Intensity ◽  
Mtor Phosphorylation ◽  
Low Intensity Exercise

scholarly journals Effects of Steady Low-Intensity Exercise on High-Fat Diet Stimulated Breast Cancer Progression Via the Alteration of Macrophage Polarization

2020 ◽  
Vol 19 ◽  
pp. 153473542094967
Author(s):  
Min Kyoon Kim ◽  
Yesl Kim ◽  
SeungHwa Park ◽  
Eunju Kim ◽  
Yerin Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
High Fat Diet ◽  
Tumor Volume ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
High Fat ◽  
Low Intensity ◽  
M2 Macrophage Polarization ◽  
Low Intensity Exercise

Physical inactivity and high-fat diet, especially high saturated fat containing diet are established risk factors for breast cancer that are amenable to intervention. High-fat diet has been shown to induce tumor growth and metastasis by alteration of inflammation but steady exercise has anti-tumorigenic effects. However, the mechanisms underlying the effects of physical activity on high-fat diet stimulated breast cancer initiation and progression are currently unclear. In this study, we examined how the intensity of physical activity influences high fat diet-stimulated breast cancer latency and progression outcomes, and the possible mechanisms behind these effects. Five-week-old female Balb/c mice were fed either a control diet or a high-fat diet for 8 weeks, and then 4T1 mouse mammary tumor cells were inoculated into the mammary fat pads. Exercise training occurred before tumor cell injection, and tumor latency and tumor volume were measured. Mice with a high-fat diet and low-intensity exercise (HFLE) had a longer tumor latency period, slower tumor growth, and smaller tumor volume in the final tumor assessment compared with the control, high-fat diet control (HFDC), and high-fat diet with moderate-intensity exercise (HFME) groups. Steady low- and moderate-intensity exercise had no effect on cell proliferation but induced apoptosis by activating caspase-3 through the alteration of Bcl-2, Bcl-xL, and Bax expression. Furthermore, steady exercise reduced M2 macrophage polarization in breast tumor tissue, which has been linked to tumor growth. The myokine, myostatin, reduced M2 macrophage polarization through the inhibition of the JAK-STAT signaling pathway. These results suggest that steady low-intensity exercise could delay breast cancer initiation and growth and reduce tumor volume through the induction of tumor cell apoptosis and the suppression of M2 macrophage polarization.

scholarly journals Transcriptional regulation of pyruvate dehydrogenase kinase 4 in skeletal muscle during and after exercise

2004 ◽  
Vol 63 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Henriette Pilegaard ◽  
P. Darrell Neufer
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Pyruvate Dehydrogenase ◽  
High Fat Diet ◽  
Prolonged Exercise ◽  
Pyruvate Dehydrogenase Kinase ◽  
High Fat ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
The Impact

The pyruvate dehydrogenase complex (PDC) has a key position in skeletal muscle metabolism as it represents the entry of carbohydrate-derived fuel into the mitochondria for oxidation. PDC is regulated by a phosphorylation–dephosphorylation cycle, in which the pyruvate dehydrogenase kinase (PDK) phosphorylates and inactivates the complex. PDK exists in four isoforms, of which the PDK4 isoform is predominantly expressed in skeletal and heart muscle. PDK4 transcription and PDK4 mRNA are markedly increased in human skeletal muscle during prolonged exercise and after both short-term high-intensity and prolonged low-intensity exercise. The exercise-induced transcriptional response of PDK4 is enhanced when muscle glycogen is lowered before the exercise, and intake of a low-carbohydrate high-fat diet during recovery from exercise results in increased transcription and mRNA content of PDK4 when compared with intake of a high-carbohydrate diet. The activity of pyruvate dehydrogenase (PDH) is increased during the first 2 h of low-intensity exercise, followed by a decrease towards resting levels, which is in line with the possibility that the increased PDK4 expressed influences the PDH activity already during prolonged exercise. PDK4 expression is also increased in response to fasting and a high-fat diet. Thus, increased PDK4 expression when carbohydrate availability is low seems to contribute to the sparing of carbohydrates by preventing carbohydrate oxidation. The impact of substrate availability on PDK4 expression during recovery from exercise also underlines the high metabolic priority given to replenishing muscle glycogen stores and re-establishing intracellular homeostasis after exercise.

Hypoxic Exercise Training Promotes apelin/APJ Expression in Skeletal Muscles of High Fat Diet-Induced Obese Mice

2016 ◽  
Vol 24 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Weixiu Ji ◽  
Lijing Gong ◽  
Jianxiong Wang ◽  
Hui He ◽  
Ying Zhang
Keyword(s):  
Exercise Training ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Obese Mice ◽  
High Fat ◽  
Hypoxic Exercise

scholarly journals Thrombospondin 1 Mediates High-Fat Diet-Induced Muscle Fibrosis and Insulin Resistance in Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4548-4559 ◽  
Author(s):  
Mayumi Inoue ◽  
Yibin Jiang ◽  
Richard H. Barnes ◽  
Masakuni Tokunaga ◽  
Gabriel Martinez-Santibañez ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Matrix Protein ◽  
Extracellular Matrix Protein ◽  
Male Mice ◽  
High Fat ◽  
Adipose Tissues ◽  
Early Stages ◽  
Thrombospondin 1

Thrombospondin 1 (THBS1 or TSP-1) is a circulating glycoprotein highly expressed in hypertrophic visceral adipose tissues of humans and mice. High-fat diet (HFD) feeding induces the robust increase of circulating THBS1 in the early stages of HFD challenge. The loss of Thbs1 protects male mice from diet-induced weight gain and adipocyte hypertrophy. Hyperinsulinemic euglycemic clamp study has demonstrated that Thbs1-null mice are protected from HFD-induced insulin resistance. Tissue-specific glucose uptake study has revealed that the insulin-sensitive phenotype of Thbs1-null mice is mostly mediated by skeletal muscles. Further assessments of the muscle phenotype using RNA sequencing, quantitative PCR, and histological studies have demonstrated that Thbs1-null skeletal muscles are protected from the HFD-dependent induction of Col3a1 and Col6a1, coupled with a new collagen deposition. At the same time, the Thbs1-null mice display a better circadian rhythm and higher amplitude of energy expenditure with a browning phenotype in sc adipose tissues. These results suggest that THBS1, which circulates in response to a HFD, may induce insulin resistance and fibrotic tissue damage in skeletal muscles as well as the de-browning of sc adipose tissues in the early stages of a HFD challenge. Our study may shed new light on the pathogenic role played by a circulating extracellular matrix protein in the cross talk between adipose tissues and skeletal muscles during obesity progression.

Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease

1997 ◽  
Vol 273 (1) ◽  
pp. E37-E45 ◽  
Author(s):  
S. Ikemoto ◽  
M. Takahashi ◽  
N. Tsunoda ◽  
K. Maruyama ◽  
H. Itakura ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Skeletal Muscles ◽  
Unsaturation Index ◽  
Sodium Cholate ◽  
Fat Absorption ◽  
High Fat ◽  
Cholesterol Accumulation ◽  
Triglyceride Accumulation ◽  
Responsive Element

The effects of sodium cholate on high-fat diet-induced hyperglycemia and obesity were investigated. Insulin resistance was estimated by measuring 2-deoxyglucose uptake in epitrochlearis muscles incubated in vitro. Addition of 0.5% cholate to high-safflower oil diet completely prevented high fat-induced hyperglycemia and obesity in C57BL/6J mice with a slight decrease of energy intake but with no inhibition of fat absorption. Furthermore, the addition of cholate decreased blood insulin levels and prevented high-fat diet-induced decrease of glucose uptake in epitrochlearis. However, there was no change in the unsaturation index of fatty acids in skeletal muscles and in GLUT-4 levels by cholate. In liver, cholate addition resulted in cholesterol accumulation and completely prevented high-fat diet-induced triglyceride accumulation. The changes of triglyceride level in the liver were paralleled to the changes of acyl-CoA synthetase (ACS) mRNA. ACS catalyzes the formation of acyl-CoA from fatty acid, and acyl-CoA is utilized for triglyceride formation in liver. ACS has a sterol-responsive element 1 in its promoter region. These data indicate that the favorable effects of cholate could be partly the result of downregulation of ACS mRNA.

scholarly journals Increased Insulin Sensitivity by High-Altitude Hypoxia in Mice with High-Fat Diet-Induced Obesity Is Associated with Activated AMPK Signaling and Subsequently Enhanced Mitochondrial Biogenesis in Skeletal Muscles

Obesity Facts ◽  
2020 ◽  
Vol 13 (5) ◽  
pp. 455-472
Author(s):  
Kang Song ◽  
Yifan Zhang ◽  
Qin Ga ◽  
Zhenzhong Bai ◽  
Ri-Li Ge
Keyword(s):  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Protein Kinase ◽  
High Altitude ◽  
Mitochondrial Biogenesis ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Acid Oxidation ◽  
High Fat ◽  
Low Altitude

<b><i>Background:</i></b> This study aimed to investigate whether and how high altitude-associated ambient hypoxia affects insulin sensitivity in mice fed a high-fat diet (HFD). <b><i>Methods:</i></b> Mice were randomly divided into a control group (with normal diet feeding and low-altitude housing), LA/HFD group (with HFD feeding and low-altitude housing), and HA/HFD group (with HFD feeding and high-altitude housing). <b><i>Results:</i></b> After 8 weeks, mice in the HA/HFD group showed improved insulin sensitivity-related indices compared with the LA/HFD group. In mice residing in a low-altitude region, HFD significantly impaired mitochondrial respiratory function and mitochondrial DNA content in skeletal muscles, which was partially reversed in mice in the HA/HFD group. In addition, the fatty acid oxidation-related enzyme gene <i>CPT1</i> (carnitine palmitoyltransferase 1) and genes related to mitochondrial biogenesis such as peroxisome proliferator-activated receptor-γ coactivator-1α (<i>PGC-1α</i>), nuclear respiratory factor 1 (<i>NRF1</i>), and mitochondrial transcription factor A (<i>Tfam</i>) were upregulated in the skeletal muscles of mice housed at high altitude, in comparison to in the LA/HFD group. Furthermore, AMPK (adenosine monophosphate-activated protein kinase) signaling was activated in the skeletal muscles, as evidenced by a higher expression of phosphorylated AMPK (p-AMPK) and protein kinase B (p-AKT) in the HA/HFD group than in the LA/HFD group. <b><i>Conclusion:</i></b> Our study suggests that high-altitude hypoxia improves insulin sensitivity in mice fed an HFD, which is associated with AMPK activation in the skeletal muscle and consequently enhanced mitochondrial biogenesis and fatty acid oxidation. This work provides a molecular explanation for why high altitude is associated with a reduced incidence of insulin resistance in the obese population.

scholarly journals PO-128 Effects of 30%, 50%, 70%VO2 max treadmill exercises on gut microbiome of atherosclerotic mice

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Wenting Shi ◽  
Jin Li ◽  
Pengyi Zhang
Keyword(s):  
Gut Microbiome ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Exercise Group ◽  
High Fat ◽  
Vo2 Max ◽  
Adult Mice ◽  
Medium Intensity ◽  
Before And After ◽  
Low Intensity Exercise

Objective  To observe the dynamic changes of gut microbiome in mice before and after different intensities of treadmill exercises, and to explore the effects of different intensities of treadmill exercises on gut microbiome of atherosclerotic (AS) mice. Methods  The 50 male ApoE-/- mice aged 8 weeks were randomly divided into 2 groups, 10 mice in the general feeding group and the other 40 mice in the AS group, which were fed with normal and high-fat diet for 4 weeks respectively. Weight and blood test were taken before and after 4 weeks feeding. The serum Triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein (HDL) levels were examined by blood test in ApoE-/- mice model, and atherosclerotic disease degeneration score of adult mice was used to determine the success of modeling after 4 weeks feeding. Then two mice selected from the normal and high-fat group respectively selected to test the maximum oxygen uptake (VO2 max) by the reformative Bedford method, and the running platform speed and slope corresponding to 30%, 50% and 70%VO2 max were determined. The 40 AS mice were randomly divided into the model blank group, the low-intensity exercise group, the medium-intensity exercise group and the high-intensity exercise group according to their weight for 4 weeks of exercises, respectively. The low-intensity exercise group was 30% VO2 max, with a slope of 10 degrees and a speed of 10 m/min. The medium intensity exercise group was 50% VO2 max with a slope of 10 degrees and a speed of 15 m/min. The high-intensity exercise group was 70% VO2 max with a slope of 10 degrees and a speed of 20 m/min. The exercises were performed for 4 weeks, 5 days a week, 20 minutes a day. The fresh feces were collected from 5 groups of mice before and after 4 weeks treadmill exercises. The number of gut Lactobacillus, Bacteroides, Firmicutes, Bifidobacterium, Verrucomicrobiaceae, Akkermansia , Escherichia coli, Collinsella and Clostridium in AS mice were analyzed by 16s sequencing.  Results 1. The TG, TC and LDL-C were significantly increased in the blood serum of the mice after the modeling, and the HDL-C was decreased, and the atherosclerotic disease degeneration score was significantly increased in the adult mice, and the modeling was successful. 2. The different intensity treadmill exercises can increase the number of gut probiotics in mice and decrease the number of harmful bacteria. The beneficial bacteria in gut tract of AS mice with moderate intensity of 50% VO2max was observed in the experiment: Bacteroides, Bifidobacterium and Verrucomicrobiaceae, Akkermansia were significantly increased, P<0.05. The harmful bacteria:Lactobacillus, Escherichia coli, Collinsella and Clostridium were significantly decreased, P<0.05. The ratio of Firmicutes / Bacteroidetes was increased. Conclusions  1. High-fat diet can lead to AS in ApoE-/- mice. 2. The different intensity treadmill exercises can reduce the weight of AS mice. 3. The number and abundance of probiotics of gut microbiome of AS mice could be promoted by different intensity treadmill exercises, among which the medium intensity aerobic exercise can significantly increase the number of beneficial bacteria such Bacteroidetes, Bifidobacteria, Verrucomicrobiaceae and Akkermansia, meanwhile, the structure of gut microbiome in AS mice was improved as well.

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