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Postprandial exercise regulates tissue-specific triglyceride uptake through bifurcated regulation of tissue LPL by Angiopoietin-like proteins [RNA-seq]

ABSTRACT: We performed RNA-seq in the liver of wild-type (WT) mice in response to a single bout aerobic exercise. Exercise induced the downregulation of insulin signaling pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE269016 | GEO | 2024/08/08

REPOSITORIES: GEO

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Postprandial exercise regulates tissue-specific triglyceride uptake through angiopoietin-like proteins.

Project description:Fuel substrate switching between carbohydrates and fat is essential for maintaining metabolic homeostasis. During aerobic exercise, the predominant energy source gradually shifts from carbohydrates to fat. While it is well known that exercise mobilizes fat storage from adipose tissues, it remains largely obscure how circulating lipids are distributed tissue-specifically according to distinct energy requirements. Here, we demonstrate that aerobic exercise is linked to nutrient availability to regulate tissue-specific activities of lipoprotein lipase (LPL), the key enzyme catabolizing circulating triglyceride (TG) for tissue uptake, through the differential actions of angiopoietin-like (ANGPTL) proteins. Exercise reduced the tissue binding of ANGPTL3 protein, increasing LPL activity and TG uptake in the heart and skeletal muscle in the postprandial state specifically. Mechanistically, exercise suppressed insulin secretion, attenuating hepatic Angptl8 transcription through the PI3K/mTOR/CEBPα pathway, which is imperative for the tissue binding of its partner ANGPTL3. Constitutive expression of ANGPTL8 hampered lipid utilization and resulted in cardiac dysfunction in response to exercise. Conversely, exercise promoted the expression of ANGPTL4 in white adipose tissues, overriding the regulatory actions of ANGPTL8/ANGPTL3 in suppressing adipose LPL activity, thereby diverting circulating TG away from storage. Collectively, our findings show an overlooked bifurcated ANGPTL-LPL network that orchestrates fuel switching in response to aerobic exercise.

| S-EPMC11343597 | biostudies-literature

Postprandial exercise regulates tissue-specific triglyceride uptake through bifurcated regulation of tissue LPL by Angiopoietin-like proteins [RNA-seq]

Project description:Postprandial exercise regulates tissue-specific triglyceride uptake through bifurcated regulation of tissue LPL by Angiopoietin-like proteins [RNA-seq]

| PRJNA1119962 | ENA

Expression data from wild type mice and REDD1 null mice following acute aerobic exercise

Project description:Regulated in DNA Damage and Development 1 (REDD1) is a stress induced protein whose expression is highly induced in skeletal muscle following a single bout of aerobic exercise. However, the role of this induction is unknown We used microarrays to detail the change in gene signature within skeletal muscle following a single bout of aerobic exercise in wild type and REDD1 null mice

2017-10-05 | GSE97415 | GEO

Muscle Transcriptome Profile of Resistance Exercise is Augmented by Aerobic Exercise

Project description:10 male subjects performed ~45 min one-legged cycling and 4 x 7 maximal concentric-eccentric knee extensions for each leg 15 min later. Thus, one limb performed aerobic and resistance exercise (AE+RE), while the opposing leg did resistance exercise only (RE). Biopsies were obtained from m. vastus lateralis of each leg 3 h after the resistance exercise bout. Gene expression analysis was carried out on the Affymetrix HuGene-2.1-st platform.

2016-05-24 | GSE74194 | GEO

Transcription profiling time series of human skeletal muscle samples from metabolic syndrome patients following defined exercise (STRRIDE study)

Project description:STRRIDE is an exercise intervention study of different doses and intensities in overweight women and men with the metabolic syndrome. We profiled biopsies from 3 female and 3 male STRRIDE subjects in the âhighâ exercise group (2,200 kCal/wk). Muscle biopsies were profiled at entry (0h), and after 9 months of aerobic training (24 hrs post-last bout, 96 hrs post last bout, and 336h (14 days) de-training). Included also are pilot expression data from 3 male subjects.<br><br>Note that files GSM19162.txt and GSM20659.txt as downloaded from GEO are identical.

2007-08-02 | E-GEOD-1295 | biostudies-arrayexpress

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks

Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.

2014-05-23 | GSE57880 | GEO

Phosphoproteomic analysis of three exercise modalities in human skeletal muscle

Project description:To characterize phosphorylation-based signaling events across different exercise modalities we subjected eight healthy young men (age, 26.3±1.3 years; BMI, 23.5±0.7 kg/m2; maximal oxygen uptake (VO2 max), 42.6±1.5 ml/kg/min) that did not perform regular physical activity apart from local bicycling to an acute bout of endurance (90 min ~60% of VO2 max), sprint (3 x 30-s all-out cycling), or resistance exercise (6 sets of 10 RM knee extensions) in the fasting state. All participants completed the three types of exercise in a randomized crossover design with 14 days washout between each exercise bout.

2022-07-18 | PXD031049 | Pride

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks

Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays

2014-05-23 | E-GEOD-57880 | biostudies-arrayexpress

High and low exercise responders

Project description:Aerobic exercise capacity is a strong predictor of disease and survivability but the utility of exercise intervention is largely dependent on how one’s genome interacts with an exercise-training environment. A newly developed rat model selectively bred for inherited differences in response to aerobic exercise training shows to be a useful resource to sort out the networks of genes responsible for signalling exercise-induced changes that benefit cardiac function.

2012-01-01 | GSE20997 | GEO

Human skeletal muscle transcriptional response to exercise

Project description:The aim of this investigation was to evaluate the effect of training on the global transcriptional response of skeletal muscle to an acute bout of resistance exercise. Seven young healthy men and women underwent a 12-week supervised progressive unilateral arm resistance exercise (RE) training program. One week after the last session of training, subjects performed an acute bout of bilateral arm RE in which the trained and the untrained arm exercised at the same relative intensity. A muscle biopsy was obtained 4h post exercise from the biceps brachii of the trained and untrained arm. Trained and untrained muscle samples were analyzed for mRNA levels of over 20,000 annotated genes using Affymetrix U133 Plus 2.0 microarrays.

2011-12-15 | E-GEOD-28998 | biostudies-arrayexpress

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