ReviewTrends in cell biology2023
The adipocyte supersystem of insulin and cAMP signaling.
Review in Trends in cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- TRPC6 loss triggers mitochondrial dysfunction that drives white adipose tissue vulnerability to obesity and insulin resistance.Experimental & molecular medicine · 2026Article
- Canagliflozin regulates adipocyte lipolysis in vitro via a SGLT2 independent signaling pathway.International journal of obesity (2005) · 2026Article
- Chinese Yam Polysaccharide Ameliorates Obesity by Promoting Lipolysis Via the cAMP/PKA Signaling Pathway.Chemistry & biodiversity · 2026Article
- Chronic Stress Induces Hepatic Steatosis via Brain-Hepatic Sympathetic Axis Mediated Catecholamine Resistance.International journal of biological sciences · 2026Article
- Transcriptome analysis reveals reduced lipid accumulation and mitochondrial metabolic remodeling in ADCY3-overexpressing adipocytes.Functional & integrative genomics · 2025Article
- The Functional Interaction Between PRDM16 and the SREBP Pathway Controls Lipid Metabolism.International journal of molecular sciences · 2025Article
- How Genes Meet Diet in LCHAD Deficiency: Nutrigenomics of Fatty Acid Oxidation Disorder.International journal of molecular sciences · 2025Review
- Vitamin D receptor signalling regulates the diet-driven metabolic shift during weaning.Molecular metabolism · 2025Article
- Visceral adipose tissue-derived extracellular vesicles promote stress susceptibility in obese mice via miR-140-5p.Acta pharmacologica Sinica · 2025Article
- The role of compartmentalized β-AR/cAMP signaling in the regulation of lipolysis in white and brown adipocytes.The FEBS journal · 2025Review
- Myokines: metabolic regulation in obesity and type 2 diabetes.Life metabolism · 2024Review
- Activation of GPR81 by lactate drives tumour-induced cachexia.Nature metabolism · 2024Article
- The association between the AIP and undiagnosed diabetes in ACS patients with different body mass indexes and LDL-C levels: findings from the CCC-ACS project.Cardiovascular diabetology · 2024Article
- Transcriptional determinants of lipid mobilization in human adipocytes.Science advances · 2024Article
- ITGB1 alleviates osteoarthritis by inhibiting cartilage inflammation and apoptosis via activating cAMP pathway.Journal of orthopaedic surgery and research · 2023Article
- Activation of the cGAS-STING pathway by a mitochondrial DNA-targeted emissive rhodium(iii) metallointercalator.Chemical science · 2023Article
- Fuziline Ameliorates Glucose and Lipid Metabolism by Activating Beta Adrenergic Receptors to Stimulate Thermogenesis.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Adipose tissue signals to brain, liver, and muscles to control whole body metabolism through secreted lipid and protein factors as well as neurotransmission, but the mechanisms involved are incompletely understood. Adipocytes sequester triglyceride (TG) in fed conditions stimulated by insulin, while in fasting catecholamines trigger TG hydrolysis, releasing glycerol and fatty acids (FAs). These antagonistic hormone actions result in part from insulin's ability to inhibit cAMP levels generated through such G-protein-coupled receptors as catecholamine-activated β-adrenergic receptors. Consistent with these antagonistic signaling modes, acute actions of catecholamines cause insulin resistance. Yet, paradoxically, chronically activating adipocytes by catecholamines cause increased glucose tolerance, as does insulin. Recent results have helped to unravel this conundrum by revealing enhanced complexities of these hormones' signaling networks, including identification of unexpected common signaling nodes between these canonically antagonistic hormones.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.