ArticleThe Journal of clinical investigation2016
Activation of mTORC1 is essential for β-adrenergic stimulation of adipose browning.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
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Who cites it
127 citing papers in PubMed, 193 citations in OpenAlex.
- Fueling or Fighting Cancer? The Thermogenic Paradox of Brown Adipose Tissue.Current obesity reports · 2026Review
- Advances in Adipose Tissue Biology.Endocrine reviews · 2026Review
- Exercise and cold exposure as dual physiological stressors in MASLD: AMPK-mediated metabolic adaptation and interorgan crosstalk.Frontiers in physiology · 2026Review
- Brown adipose tissue in ruminants: development, thermogenic function, and nutritional regulation.Frontiers in veterinary science · 2026Review
- Periodic fasting and refeeding re-shapes lipid saturation, storage, and distribution in brown adipose tissue.PLoS biology · 2026Article
- Mechanisms of Variation in Abdominal Adipose Color Among Male Kazakh Horses Through Non-Coding RNA Sequencing.Biology · 2025Article
- The role of adipose tissue in critical illness-induced skeletal muscle wasting-new considerations for treatment approaches.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Natural killer cells from endurance-trained older adults show improved functional and metabolic responses to adrenergic blockade and mTOR inhibition.Scientific reports · 2025Article
- Salt-inducible Kinase Regulation of Adipose Tissue Metabolism.Endocrinology · 2025Review
- Extensive location bias of the GPCR-dependent translatome via site-selective activation of mTOR.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pro-renin Receptor (PRR) as a Target to Reduce Non-alcoholic Fatty Liver Disease Post Liver Transplantation.Current medicinal chemistry · 2025Review
- Extensive location bias of the GPCR-dependent translatome via site-selective activation of mTOR.bioRxiv : the preprint server for biology · 2024Article
- CMKLR1 senses chemerin/resolvin E1 to control adipose thermogenesis and modulate metabolic homeostasis.Fundamental research · 2024Article
- mTORC1 in energy expenditure: consequences for obesity.Nature reviews. Endocrinology · 2024Review
- mTORC1 hyperactivation and resultant suppression of macroautophagy contribute to the induction of cardiomyocyte necroptosis by catecholamine surges.Physiological reports · 2024Article
- ATF4 expression in thermogenic adipocytes is required for cold-induced thermogenesis in mice via FGF21-independent mechanisms.Scientific reports · 2024Article
- Depletion of JunB increases adipocyte thermogenic capacity and ameliorates diet-induced insulin resistance.Nature metabolism · 2024Article
- Mitophagy Responds to the Environmental Temperature and Regulates Mitochondrial Mass in Adipose Tissues.Advances in experimental medicine and biology · 2024Review
- Article
- A sustainable nutritional solution for fattening pigs based on 25-hydroxycholecalciferol and triterpenoids added to a low Ca diet containing phytase improves growth performance via the activation of muscle protein synthesis without compromising bone mineralization.Translational animal science · 2024Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
A classic metabolic concept posits that insulin promotes energy storage and adipose expansion, while catecholamines stimulate release of adipose energy stores by hydrolysis of triglycerides through β-adrenergic receptor (βARs) and protein kinase A (PKA) signaling. Here, we have shown that a key hub in the insulin signaling pathway, activation of p70 ribosomal S6 kinase (S6K1) through mTORC1, is also triggered by PKA activation in both mouse and human adipocytes. Mice with mTORC1 impairment, either through adipocyte-specific deletion of Raptor or pharmacologic rapamycin treatment, were refractory to the well-known βAR-dependent increase of uncoupling protein UCP1 expression and expansion of beige/brite adipocytes (so-called browning) in white adipose tissue (WAT). Mechanistically, PKA directly phosphorylated mTOR and RAPTOR on unique serine residues, an effect that was independent of insulin/AKT signaling. Abrogation of the PKA site within RAPTOR disrupted βAR/mTORC1 activation of S6K1 without affecting mTORC1 activation by insulin. Conversely, a phosphomimetic RAPTOR augmented S6K1 activity. Together, these studies reveal a signaling pathway from βARs and PKA through mTORC1 that is required for adipose browning by catecholamines and provides potential therapeutic strategies to enhance energy expenditure and combat metabolic disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.