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Metabolic and transcriptional adaptations improve physical performance of zebrafish

ABSTRACT: Metabolic and transcriptional adaptations improve physical performance of zebrafish

PROVIDER: PRJNA758884 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15667940.fastq.gz	Fastqsanger.gz
	SRR15667941.fastq.gz	Fastqsanger.gz
	SRR15667942.fastq.gz	Fastqsanger.gz
	SRR15667943.fastq.gz	Fastqsanger.gz
	SRR15667944.fastq.gz	Fastqsanger.gz

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Metabolic and transcriptional adaptations improve physical performance of zebrafish

Project description:Background: Obesity is a worldwide public health problem with increasing prevalence and affects 80% of diabetes mellitus type 2 cases. Zebrafish (Danio rerio) are an established model organism for studying obesity and diabetes including diabetic microvascular complications. We aimed to determine whether physical activity is an appropriate tool to examine training effects in zebrafish and to analyse metabolic and transcriptional processes in trained zebrafish. Methods: A 2- and 8-weeks experimental training phase protocol with adult zebrafish in a swim tunnel system was established. We examined zebrafish basic characteristics before and after training such as body weight, body length and maximum speed and considered overfeeding as an additional parameter in the 8-weeks training protocol. Ultimately, the effects of training and overfeeding on blood glucose, muscle core metabolism and liver gene expression using RNA-Seq were investigated. Results: Zebrafish maximum speed was correlated with body length and was significantly increased after 2 weeks of training. Maximum swim speed further increased after 8 weeks of training in both the normalfed and the overfed groups, but training was found not to be sufficient in preventing weight gain in overfed fish. Metabolome and transcriptome profiling in trained fish exhibited increased blood glucose levels in the short-term and upregulated energy supply pathways in the long-term. Conclusion: Swim training is a valuable tool to study effects of physical activity in zebrafish, which is accompanied by metabolic and transcriptional adaptations.

2021-12-06 | GSE183023 | GEO

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Project description:Cancer cachexia is a disorder characterized by both involuntary weight loss and impaired physical performance. Decline in physical performance of patients with cachexia is associated with poor quality of life, and currently there are no effective pharmacological interventions that restore physical performance. Here we examined the effect of GDF15 neutralization in a mouse model of cancer-induced cachexia (TOV21G) that manifested weight loss and muscle function impairments. With comprehensive assessments, our results demonstrated that cachectic mice treated with the anti-GDF15 antibody mAB2 exhibited body weight gain with near-complete restoration of muscle mass and markedly improved muscle function and physical performance. Mechanistically, the improvements induced by GDF15 neutralization were primarily attributed to increased caloric intake, while altered gene expressions in cachectic muscles were restored in both caloric intake-dependent and -independent manners. The findings implicate the potential of GDF15 neutralization as an effective therapy to enhance physical performance of patients with cachexia.

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Short-Term Adaptations in Skeletal Muscle Mitochondrial Oxidative Capacity and Metabolic pathways to Breaking Up Sedentary Behaviors with Short-Frequent Bouts of Physical Activity Compared to a Matched Daily Single-Continuous Bout in Obese Adults

Project description:We compared the short-term (4-day) adaptations in skeletal muscle mitochondrial function and gene expression between short-frequent bouts of physical activity and time matched single-continuous physical activity.

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Muscle cannabinoid 1 receptor regulates Il-6 and myostatin expression, governing physical performance and whole-body metabolism.

Project description:Cannabinoid 1 receptor (CB1R) plays a critical role in the regulation of whole-body energy metabolism because of its involvement in controlling food intake thorough a central mechanism, and controlling distribution of fuel and utilization in the periphery, particularly in fat and liver. Additionally, inhibition of CB1R improves insulin secretion from pancreatic beta cells and insulin sensitivity in both pancreatic beta cells and hepatocytes. We now developed a skeletal muscle-specific CB1R-knockout (Skm-CB1R-/-) mouse to study the specific role of CB1R in muscle. Muscle-CB1R ablation prevented diet-induced and age-induced insulin resistance by increasing insulin receptor signaling. Ablation of CB1R in muscle also led to IL-6 secretion and reduced myostatin expression, and enhanced AKT and MAPKs signaling. These changes in myokines induced the expression of myogenic genes, increasing muscle mass and whole-body lean/fat ratio in both obesity and aging, with no change in total body weight. Skm-CB1R-/- mice had increased energy expenditure and their muscle had improved mitochondrial performance, which led to improved physical endurance. These results collectively show that muscle-CB1R is involved in regulating whole-body insulin sensitivity and physical performance.

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Project description:Insufficient physical activity is associated with increased relative risk of cardiometabolic disease and is an independent risk factor for mortality. Experimentally reducing physical activity rapidly induces insulin resistance, impairs glucose handling, and drives metabolic inflexibility. These adaptations manifest during the early stages of physical inactivity, even when energy balance is maintained, suggesting that inactivity-mediated metabolic reprogramming is an early event that precedes changes in body composition. To identify mechanisms that promote metabolic adaptations associated with physical inactivity, we developed a mouse model of physical activity reduction that permits the study of inactivity in animals prior to the onset of overt changes in body composition. Adult mice were randomized into three groups: an inactive control group (standard housing), an active control group (treadmill running for 6-weeks), and an activity reduction group (treadmill running for 4-weeks, followed by 2-weeks of inactivity). Transcriptional profiling of gastrocnemius muscle was performed.

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Cellular Feimin enhances exercise performance by suppressing muscle thermogenesis

Project description:Exercise can rapidly increase core body temperature, and research has indicated that elevated internal body temperature can independently contribute to fatigue during physical activity. However, the precise mechanisms responsible for regulating thermogenesis in muscles during exercise have remained unclear. Here, we demonstrate that cellular Feimin (cFeimin) enhances exercise performance by inhibiting muscle thermogenesis during physical activity. Mechanistically, we found that AMPK phosphorylates cFeimin and facilitates its translocation into the cell nucleus during exercise. Within the nucleus, cFeimin binds to the forkhead transcription factor FOXC2, leading to the suppressed expression of Sarcolipin (Sln), which is a key regulator of muscle thermogenesis. In addition, our results further reveal that short-term AMPK agonist treatments can enhance exercise performance through the activation of the AMPK-cFeimin signaling pathway. In summary, these results underscore the crucial role of cFeimin in enhancing exercise performance by modulating SLN-mediated thermogenesis.

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