Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA241325 | ENA |
REPOSITORIES: ENA
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Project description:The aim of the study was to investigate how short-term fasting affects whole-body energy homeostasis and skeletal muscle energy/nutrient-sensing pathways and transcriptome in humans. For this purpose, twelve young healthy men were studied during a 24-hour fast. Skeletal muscle biopsies were collected and analyzed at baseline and after 4, 10 and 24h of fasting. As expected, fasting induced a time-dependent decrease in plasma insulin and leptin levels, whereas levels of ketone bodies and free fatty acids increased. This was associated with a metabolic shift from glucose towards lipid oxidation. Transcriptome profiling identified genes that were significantly regulated by fasting in skeletal muscle at both early and late time-points. Collectively, our study provides a comprehensive map of the main energy/nutrient-sensing pathways and transcriptomic changes during short-term adaptation to fasting in human skeletal muscle
2014-12-02 | GSE55924 | GEO
Project description:Adaptation of the islet β-cell insulin secretory response to changing insulin demand is critical for blood glucose homeostasis, yet the mechanisms underlying this adaptation are unknown. Here, we show that nutrient cues adapt insulin secretion by modulating chromatin state and transcription of genes regulating β-cell nutrient sensing and metabolism. Feeding stimulates histone acetylation at sites occupied by the chromatin-modifying enzyme Lsd1 in islets. We demonstrate that β-cell-specific deletion of Lsd1 leads to insulin hypersecretion, aberrant expression of nutrient response genes, and histone hyperacetylation, features we also observed in the db/db model of chronically increased insulin demand. Moreover, genetic variants associated with fasting glucose levels and type 2 diabetes risk are enriched at LSD1-bound sites in human islets, suggesting interindividual variation in β-cell functional adaptation in humans. These findings reveal nutrient state-dependent modulation of the islet epigenome and identify Lsd1 as a regulator of feeding-stimulated chromatin modification and adaptive insulin secretion.
2023-02-24 | GSE134901 | GEO
Project description:The adaptive mechanisms in response to excess energy supply are still poorly known in humans. Our aims were to define metabolic responses and changes in gene expression in skeletal muscle of healthy volunteers during fat overfeeding.
2016-08-29 | GSE50484 | GEO
Project description:Body fat distribution is a heritable risk factor for cardiovascular and metabolic disease. In humans, rare Inhibin beta E (INHBE, activin E) loss-of-function variants are associated with lower waist-to-hip ratio and protection from type 2 diabetes. Hepatic fatty acid sensing promotes INHBE expression during fasting and in obese individuals, yet it is unclear how the hepatokine activin E governs body shape and energy metabolism. Here, we uncover activin E as a negative feedback regulator of adipose lipolysis that restrains excessive fat breakdown during fasting. By suppressing β-agonist-induced lipolysis, activin E promotes visceral fat accumulation, adipocyte hypertrophy and contributes to adipose dysfunction in mice. Mechanistically, we demonstrate that activin E elicits its effect on adipose tissue through ACVR1C, activating SMAD2/3 signaling and suppressing PPARG target genes. Conversely, loss of activin E or ACVR1C increases fat utilization, lowers adiposity and drives gene signatures indicative of healthy adipose function. Our studies identify activin E-ACVR1C as metabolic rheostat promoting liver-adipose crosstalk to preserve fat mass during prolonged fasting, a mechanism that is maladaptive in obese individuals.
2023-07-14 | GSE231444 | GEO
Project description:AMP-activated protein kinase (AMPK) is a major regulator of cellular energy homeostasis that coordinates metabolic pathways in order to balance nutrient supply with energy demand. AMPK elicits acute and diverse metabolic effects by directly phosphorylating various targets. AMPK activation also promotes metabolic reprogramming in longer term via effects on gene expression. The aim of this study is to elucidate molecular mechanism(s) by which AMPK activation modulates metabolic adaptation through its impact on gene regulation.
2019-03-04 | GSE104170 | GEO
Project description:The adaptive mechanisms in response to excess energy supply are still poorly known in humans. Our aims were to define metabolic responses and changes in gene expression in skeletal muscle of healthy offsprings of type 2 diabetic patients during one week of high fructose diet.
2018-06-24 | GSE70218 | GEO
Project description:Autophagy represents a key regulator of aging and metabolism upon cell autonomous sensing of energy deprivation. We find that fasting in mice activates autophagy in liver paralleled by activation of hypothalamic AgRP neurons. Optogenetic and chemogenetic activation of AgRP neurons induces autophagy, alters phosphorylation of autophagy regulators and promotes ß-oxidation in the liver. AgRP neuron dependent induction of liver autophagy relies on NPY expression in these neurons. AgRP neuron projections in the paraventricular nucleus of the hypothalamus (PVH) and the lateral hypothalamus (LHA) mediate AgRP neuron-dependent control of liver autophagy. Conversely, inhibiting AgRP neurons during energy deprivation abrogates induction of hepatic autophagy and re-wiring of metabolism. Finally, AgRP neuron activation increases circulating corticosterone concentrations, and reduction of hepatic glucocorticoid receptor expression attenuates AgRP neuron-dependent activation of hepatic autophagy. Collectively, our study reveals a fundamental regulatory principle of non-cell autonomous control of liver autophagy in control of metabolic adaptation during nutrient deprivation.
2023-04-18 | PXD029247 | Pride
Project description:The liver is key for maintaining metabolic homeostasis between feeding and fasting in healthy conditions. However, this is dysregulated during high fat diet feeding. What are the transcriptomic changes required for rapid adaptation of the liver to respond to feeding and fasting and how is this altered in the development of metabolic disease?
2022-09-26 | GSE151750 | GEO
Project description:The liver of dairy cows naturally displays a series of metabolic adaptation during the periparturient period in response to the increasing nutrient requirement of lactation. The hepatic adaptation is partly regulated by insulin resistance and it is affected by the prepartal energy intake level of cows. We aimed to investigate the metabolic changes in the liver of dairy cows during the periparturient at gene expression level and to study the effect of prepartal energy level on the metabolic adaptation at gene expression level.B13:N13
2017-10-05 | GSE97437 | GEO
Project description:The mechanistic underpinnings of the fasting response in skeletal muscle is still poorly understood. We therefore investigated the role of the transcriptional coactivator PGC-1beta (peroxisome proliferator-activated receptor gamma coactivator 1beta) in this context. To do so, the fasting response in quadriceps muscle was assessed in fed and 24 hours fasted mice and compared between wildtype and PGC-1beta muscle-specific knockout mice (both on a C57Bl6/J background). Morphological, functional and transcriptional parameters were determined. The results indicate that PGC-1beta significantly contributes to the metabolic remodelling of skeletal muscle to fasting by promoting catabolic pathways that help to improve energy production and sequester substrates for gluconeogenesis. Accordingly, muscle-specific knockouts for PGC-1beta exhibit mitigated protein degradation and muscle fiber atrophy. These findings contribute to our understanding of muscle plasticity in different metabolic contexts.
2022-11-18 | GSE210904 | GEO